Nephrology Flashcards
cRenal blood flow normally drains ___ of the cardiac output
~20%
The most common clinical course of contrast nephropathy is characterized by a rise in SCr beginning ____ following exposure, peaking within ____ , and resolving within
24–48 h
3–5 days
1 week
Definition of AKI
AKI is currently defined by a rise from baseline of at least 0.3 mg/dL within 48 h or at least 50% higher than baseline within 1 week, or a reduction in urine output to < 0.5 mL/kg per h for longer than 6 h.
Diseases that may present with eosinophilluria (5)
Allergic interstitial nephritis
Atheroembolic dse
Pyelonephritis
Cystitis
Glomerulonephritis
Diseases that may present with RBC casts (4)
Glomerulonephritis
Vasculitis
malignant Hypertension
Thrombotic Microangiopathy
Diseases that may present with WBC casts (5)
Interstitial Nephritis
Glomerulonephritis
Plyelonephritis
Allograft Rejection
Malignant Infiltration of the kidney
Diseases that may present with RTE casts (5)
ATN
Tubulointerstitial nephritis
Acute cellular allograft reaction
Myoglobulinuria
Hemoglobinuria
Diseases that may present with granular casts (4)
ATN
GN
Vasculitis
TIN
Diseases that may present with crystalluria
Acute uric acid nephropathy
Caox
Drugs or toxin (acyclovir, indinavir, sulfadiazin, amoxicillin)
Fe Na of pre renal AKI
< 1%
Dose for furosemide challenge
1-1.5 mg/kg
UO of ________ after IV furosemide may identify patients at higher risk of progression to more severe AKI, and the need for renal replacement therapy
< 200 mL over 2 h a
Molecule can be detected shortly after ischemic or nephrotoxic injury in the urine and, therefore, may be an easily tested biomarker in the clinical setting
KIM-1
_____ is highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2 h of cardiopulmonary bypass– associated
NGAL
patients with AKI should achieve a total energy intake of ____ kcal/kg per day.
20–30 kcal/kg per day
Protein intake in AKI
_____ g/kg in noncatabolic AKI without the need for dialysis;
_____ g/kg per day in patients on dialysis;
and up to a maximum of ____ per day if hypercatabolic and receiving continuous renal replacement therapy
0.8–1.0 g/kg per day
1.0–1.5 g/kg
1.7 g/kg
Alkali supplementation may attenuate the catabolic state and possibly slow CKD progression and is recommended when the serum bicarbonate concentration falls below ____ mmol/L.
20–23
These PTH FGFR3 changes start to occur when the GFR falls below ___ mL/min.
60 mL/min
_____ is a devastating condition seen almost exclusively in patients with advanced CKD. It is heralded by livedo reticularis and advances to patches of ischemic necrosis, especially on the legs, thighs, abdomen, and breasts
Calciphylaxis
Blood thinner that is considered a risk factor for calciphylaxis
Warfarin
Warfarin is commonly used in HD patients in whom most direct oral anticoagulants (DOACs) are contraindicated, and one of the effects of warfarin therapy is to decrease the vitamin K–dependent regeneration of matrix GLA protein which is important in preventing vascular calcification
Target PTH level for CKD
150 and 300 pg/mL
2-9x the ULN
_______ is leading cause of morbidity and mortality in px at every stage of CKD
Cardiovascular disease
First line therapy for CKD to reduce BP
Salt restriction
In CKD patients with diabetes or proteinuria >1 g per 24 h, blood pressure should be reduced to ______ , if achievable without prohibitive adverse effects.
< 130/80 mmHg
normocytic, normochromic anemia is observed as early as stage ___ CKD and is almost universal by stage __
3,4
The primary cause is insufficient production of erythropoietin (EPO) by the diseased kidneys.
Adequate bone marrow iron stores should be available before treatment with ESA is initiated. Iron supplementation is usually essential to ensure an optimal response to ESA
Target Hb for CKD
10-11.5 g/dl
Peripheral neuropathy usually becomes clinically evident after the patient reaches stage __ CKD, although electrophysiologic and histologic evidence occurs earlier.
4
P-eripheral neuropathy, P-or
Initially, sensory nerves are involved more than motor, lower extremities more than upper, and distal parts of the extremities more than proximal. The “restless leg syndrome” is characterized by ill-defined sensations of sometimes debilitating discomfort in the legs and feet relieved by frequent leg movement
Class of OHAS that do not require dose reduction when EGFR is less than 50% of normal
SGLT 2 inhibitors
A skin condition unique to CKD patients called _____ consists of progressive subcutaneous induration, especially on the arms and legs.
nephrogenic fibrosing dermopathy
The condition is seen very rarely in patients with CKD who have been exposed to the magnetic resonance contrast agent gadolinium.
Current recommendations are that patients with CKD stage 3 (GFR 30–59 mL/min) should minimize exposure to gadolinium, and those with CKD stages 4–5 (GFR < 30 mL/min) should avoid the use of gadolinium agents unless it is medically necessary
Diseases where kidney size may be normal in the face of CKD (3)
diabetic nephropathy, amyloidosis, and HIV nephropathy
Discrepancy ___ cm in kidney length suggests either unilateral developmental abnormality or dse process or renovascular dse with arterial insufficiency affecting 1 kidney more than the other
> 1 cm
The most important complication of arteriovenous grafts is _______
thrombosis of the graft and graft failure
due principally to intimal hyperplasia at the anastomosis between the graft and recipient vein
_______ is the most common acute complication of hemodialysis, particularly among patients with diabetes mellitus.
Hypotension
_____ is the procedure of choice to rule out urinary obstruction or to confirm the presence of perirenal collections of urine, blood, or lymph.
Diagnostic ultrasound
The first rejection episode is usually treated with IV administration of
methylprednisolone, 500–1000 mg daily for 3 days.
Failure to respond is an indication for antibody therapy, usually with antithymocyte globulin.
Greater than ____mg/day of albuminuria represents frank proteinuria and more advanced renal disease
300 mg/24 h
Sustained - >1-2 g/day
___________ glomerulonephritis demonstrates hypercellularity of mesangial and endothelial cells, glomerular infiltrates of PMNs, granular subendothelial immune deposits of IgG, IgM, C3, C4 , and C5–9, and subepithelial deposits
PSGN
In PSGN In the first week of symptoms, ____ % of patients will have a depressed CH50 and decreased levels of C3 with normal levels of C4
90%
Treatment for PSGN
Treatment is supportive, with control of hypertension, edema, and dialysis as needed.
Antibiotic treatment for active streptococcal infection should be given to patients and their cohabitants. There is no role for immunosuppressive therapy, even in the setting of crescents.
Antibodies that that fix complement correlate best with the presence of renal disease in lupus nephritis
Anti-dsDNA
Hypocomplementemia is common in patients with acute lupus nephritis (70–90%) and declining complement levels may herald a flare.
Class of Lupus nephritis that presents with mesangial hypercellularity with expansion of the mesangia matrix
Class II
Class of Lupus nephritis that presents with focal endocapillary and extracapillary proliferation with focal subendothelial immune deposits and mild mesangial expansion
Class III
Class of Lupus nephritis that presents with diffuse endocapillary and extracapillary proliferation with diffuse subendothelial immune deposits and mesangial alterations
Class IV
Current evidence suggests that inducing a remission with administration of high-dose steroids and either cyclophosphamide or mycophenolate mofetil for 2–6 months, followed by maintenance therapy with lower doses of steroids and mycophenolate mofetil or azathioprine, best balances the likelihood of successful remission with the side effects of therapy
Class of Lupus nephritis that presents with thickened BM with diffuse subepithelial immune deposits
V
Patients with lupus nephritis class V, like patients with idiopathic membranous nephropathy (IMN), are predisposed to renal vein thrombosis and other thrombotic complications.
Class of lupus nephritis with Global sclerosis of nearly all glomerular capillaries
VI
Renal transplantation in renal failure from lupus, usually performed after ~6 months of inactive disease, results in allograft survival rates comparable to patients transplanted for other reasons.
Class of lupus nephritis with the most varied course
III
Henoch-Schönlein purpura is distinguished clinically from IgA nephropathy by (4).
prominent systemic ssx, a younger age (<20 years old), preceding infection, and abdominal complaints
Type I MPGN is associated with Hepatiti __ infection
B and C
Type I MPGN is immune complex–mediated and commonly associated with persistent hepatitis B and C, fungal and parasitic infections, SBE, autoimmune diseases such as lupus or cryoglobulinemia, or monoclonal gammopathies, including monoclonal gammopathy of renal significance (MGRS), where the only clinically apparent manifestations are in the kidney
Primary responders are patients who have a complete remission ( of____ proteinuria) after a single course of prednisone; steroid-dependent patients relapse as their steroid dose is tapered.
<0.2 mg/24 h
Response to steroids
Frequent relapsers have ____ relapses in ___ months following taper, and steroid-resistant patients fail to respond to steroid therapy.
two or more relapses in the 6 months
Adults are not considered steroid-resistant until after ___ months of therapy.
4 months or 16 weeks
First line therapy for MCD
Prednisone
Other immunosuppressive drugs, such as cyclophosphamide, chlorambucil, and mycophenolate mofetil, are saved for frequent relapsers, steroid-dependent patients, or steroidresistant patients.
Cyclosporine can induce remission, but relapse is also common when cyclosporine is withdrawn. The long-term prognosis in adults is less favorable when acute renal failure or steroid resistance occurs.
Electron microscopy, consistently demonstrates an effacement of the foot processes supporting the epithelial podocytes with weakening of slit-pore membranes. The pathogenesis of this lesion is unclear
Treatment of patients with primary FSGS should include
inhibitors of the renin-angiotensin system
Patients with primary FSGS with nephrotic-range proteinuria can be treated with steroids but respond far less often and after a longer course of therapy than patients with MCD. Proteinuria remits in only 20–45% of patients receiving a course of steroids over 6–12 months
The treatment of secondary FSGS typically involves
treating the underlying cause and controlling proteinuria.
GN that has the highest reported incidences of renal vein thrombosis, pulmonary embolism, and deep-vein thrombosis.
MGN AKA membranous nephropathy
Prophylactic anticoagulation is controversial but has
been recommended for patients with hypoalbuminemia
Therapy with immunosuppressive drugs is also recommended for patients with primary MGN and persistent proteinuria ____ g/day
(>3.0 g/24 h).
What microscopic finding is a sensitive indicator for the presence of diabetes but correlates poorly with the presence or absence of clinically significant nephropathy.
Thickening of the GBM
Mesangial expansion: correlates with clinical manifestation of DM nephropathy
Microalbuminuria appears ____ years after the onset of diabetes.
5–10
Morphologic changes = 1-2 yrs
More than ___% of patients with type 1 diabetes and nephropathy have diabetic retinopathy
90%
so the absence of retinopathy in type 1 patients with proteinuria should prompt consideration of a diagnosis other than diabetic nephropathy
There is a significant correlation between the presence of retinopathy and the presence of __________ nodules .
Kimmelstiel-Wilson
Characteristic lesion of HIVAN
The lesion in HIVAN is FSGS, characteristically revealing a collapsing glomerulopathy
Hydronephrosis may be absent on ultrasound when obstruction is less than ____ in duration or associated with volume contraction, staghorn calculi, retroperitoneal fibrosis, or infiltrative renal disease.
48 h
Ultrasonography is ~90% specific and sensitive for detection of hydronephrosis. False-positive results are associated with diuresis, renal cysts, or the presence of an extrarenal pelvis, a normal congenital variant.
Type of stone not influenced by pH
Calcium Oxalate
Uric acid stones form only when the urine pH is consistently _____ , whereas calcium phosphate stones are more likely to form when the urine pH is _____ .
≤5.5 or lower
≥6.5or higher
Cysteine solubility is increased when pH is inc
Size of stone with low probability of spontaneous passage
> = 6mm
The “gold standard” diagnostic test is ____ for urolithiasis
helical CT without contrast.
Urine volume needed to lessen risk of stone formation
> 2L/day
<1 L/day = more than 2x risk
______ also known as infection stones or triple-phosphate stones, form only when the upper urinary tract is infected with urease-producing bacteria such as Proteus mirabilis, Klebsiella pneumoniae, or Providencia species.
Struvite stones
Cystine stones may be treated with medication that covalently binds to cystine like ______ and a medication that raises urine pH.
eg tiopronin or penicillamine
Tiopronin is the preferred choice due to its better adverse event profile.
The preferred alkalinizing agent to achieve a urine pH of 7.5 is potassium citrate or bicarbonate as sodium salts may increase cystine excretion
Preferred alkalinizing agent for cystine stones
The preferred alkalinizing agent to achieve a urine pH of 7.5 is potassium citrate or bicarbonate as sodium salts may increase cystine excretion
Pentad for TTP
MAHA, thrombocytopenia, neurologic symptoms, fever, and renal failure.
Which has deficiency of ADAMST13? HUS or TTP?
TTP
The treatment of adult TTP with ADAMTS13 antibodies is daily plasmapheresis, which can be lifesaving. Plasmapheresis with fresh frozen plasma is given until the platelet count rises, but in relapsing patients, it normally is continued well after the platelet count improves. There is an anecdotal role in relapsing patients for using splenectomy, steroids, immunosuppressive drugs, bortezomib, or rituximab.
Patients without antibodies and a genetic deficiency of ADAMTS13 production can be treated with fresh frozen plasma alone.
Patients with Shiga toxin–mediated HUS are not given antibiotics and are treated with supportive care because antibiotics are thought to accelerate the release of the toxin and the diarrhea is usually self-limited. Patients with complement-mediated TMA/HUS are treated with eculizumab, an anticomplement therapy.
First line therapy for scleroderma renal crisis
ACE-inhibition
____ and _____ account for ~90% of cases of acute intrinsic renal failure
Ischemic and toxic Acute tubular necrosis (ATN)
BUN: crea ratio of prerenal azotemia
> 20:1
Causes of hypercoagulable state in nephrotic syndrome
urinary losses of antithrombin III
reduced proteins S and C
hyperfibrinogenemia
enhanced platelet aggregation.
Cause of hyperlipidemia in nephrotic syndrome
inc hepatic lipoprotein synthesis.
Hematuria with dysmorphic RBCs, RBC casts, and protein excretion > ____mg/day is virtually diagnostic of glomerulonephritis.
> 500 mg/d
RBC casts form as RBCs that enter the tubule fluid and become trapped in a cylindrical mold of gelled Tamm-Horsfall protein.
Recommended as the best method for distinguishing between central and nephrogenic diabetes insipidus.
plasma AVP level
AVP secretion is stimulated as systemic osmolality increases above a threshold level of ____
~285 mOsm/kg
. Thirst and thus water ingestion are also activated at ~285 mOsm/kg, beyond which there is an equivalent linear increase in the perceived intensity of thirst as a function of circulating osmolality
Serum uric acid is often low (<_____) in patients with SIAD
4 mg/dL
in contrast, patients with hypovolemic hyponatremia will often be hyperuricemic, due to a shared activation of proximal tubular Na+-Cl– and urate transport
Most common malignancy associated with SIADH
small cell lung CA
Overly rapid correction of hyponatremia (>________ in 24h and ____ in 48h) is also associated with a disruption in integrity of the bloodbrain barrier, allowing the entry of immune mediators that may contribute to demyelination.
> 8–10 mM in 24 h or 18 mM in 48 h
_______ has long been a cornerstone of the therapy of chronic hyponatremia.
Water deprivation
chronic hyponat duration > 48h
The urine-to-plasma electrolyte ratio (urinary [Na+] + [K+]/plasma [Na+]) can be exploited as a quick indicator of electrolyte-free water excretion;
o patients with a ratio of >1 should be more aggressively restricted _______
o those with a ratio of ~1 should be restricted to _______,
o those with ratio <1 should be restricted to _____
(<500 mL/d)
500–700 mL/d
1 L/d
________ is perhaps most appropriate for the management of significant and persistent SIAD (e.g., in small-cell lung carcinoma) that has not responded to water restriction and/or oral furosemide and salt tablets
Oral tolvaptan
Many patients with SIAD respond to combined therapy with oral furosemide, 20 mg twice a day (higher doses may be necessary in renal insufficiency), and oral salt tablets; furosemide serves to inhibit the renal countercurrent mechanism and blunt urinary concentrating ability, whereas the salt tablets counteract diuretic-associated natriuresis.
Treatment of acute symptomatic hyponatremia should include hypertonic 3% saline (513 mM) to acutely increase plasma Na+ concentration by _____ to a total of ____; this modest increase is typically sufficient to alleviate severe acute symptoms
1–2 mM/h
4–6 mM
A bolus of 100 mL of hypertonic saline is more effective than an infusion, rapidly improving both serum sodium and mental status
The rate of correction should be comparatively slow in chronic
hyponatremia (<6-8 mM in the first 24 h and <6 mM each subsequent 24h), so as to avoid ODS; lower target rates are appropriate in patients at particular risk for ODS, such as alcoholics or hypokalemic patients.
__________ is the most frequent manifestation of hypernatremia
Altered mental status
ranging from mild confusion and lethargy to deep coma.
Patients with NDI will fail to respond to DDAVP, with a urine osmolality that increases by __% or < ____mOsm/kg from baseline, in combination with a normal or high circulating AVP level
<50%
< 150 mOsm/kg
A rare exception to the slow correction of hypernatremia is patients with acute hypernatremia (<48 h) due to sodium loading, who can safely be corrected rapidly at a rate of _____
1 mM/h
It is imperative to correct hypernatremia slowly to avoid cerebral edema, typically replacing the calculated free water deficit over 48 h. Notably, the plasma Na+ concentration should be corrected by no more than 10 mM/d, which may take longer than 48 h in patients with severe hypernatremia (>160 mM).
Class of diuretics that may reduce polyuria due to NDI, ostensibly by inducing hypovolemia and increasing proximal tubular water reabsorption.
Thiazides
Random testing of plasma renin activity (PRA) and aldosterone is a helpful screening tool in hypokalemic and/or hypertensive patients, with an aldosterone:PRA ratio of ____ suggestive of primary hyperaldosteronism.
> 50
Critical diagnostic test in Giterlman vs Barter syndrome
urinary calcium excretion
Patients with GS are uniformly hypomagnesemic and exhibit marked hypocalciuria (hece hypercalcemic), rather than the hypercalciuria typically seen in BS
ECG findings are most marked when serum K+ is <_____
2.7mmol/L
Urine K value that will differentiate extrarenal from renal losses
< 15 mmol / day for extrarenal losses
TTKG in hypokalemia level that connotes inc K secretion
> 4
TTKG level in hypokalemia that connotes INCREASED tubular flow
< 2
2bular
Urine calcium/crea for Barters
> 0.20
B for bente
Urine calcium/crea for Gitelman
< 0.15
Classically, the ECG manifestations in hyperkalemia progress from tall peaked T waves (_____), to a loss of P waves (____) to a widened QRS complex (____), and, ultimately, a to a sine wave pattern ( )
5.5–6.5 mM (t wave)
6.5–7.5 mM (loss of p wave)
7.0–8.0 mM ( QRS)
>8.0 mM (sine)
Electrolyte imblances that may potentiate digoxin
Hypokalemia and hypercalcemia
In hyperkalemic patients with glucose concentrations of ≥ _____mg/dL, insulin should be administered without glucose, again with close monitoring of glucose concentrations
200–250
TTKG level in hyperkalemia that connotes reduced tubular flow
> 8
TTKG level in hyperkalemia that connotes decreased distal K secretion
< 5
Drug that you should give if TTKG < 5 in hyperkalemia to test for tubular resistance
Fludrocortisone
F-ive, F-ludrocortisone
Hypercalcemia associated with granulomatous disease (e.g., sarcoidosis) or lymphomas is caused by ___________
enhanced conversion of 25(OH)D to the potent 1,25(OH)2 D.
The first step in the diagnostic evaluation of hyper- or hypocalcemia is to ensure that ____________
the alteration in serum calcium levels is not due to abnormal albumin concentrations
When serum albumin concentrations are reduced, a corrected calcium concentration is calculated by adding 0.2 mM (0.8 mg/dL) to the total calcium level for every decrement in serum albumin of 1.0 g/dL below the reference value of 4.1 g/dL for albumin, and, conversely, for elevations in serum albumin
Chronic hypercalcemia is most commonly caused by __________ , as opposed to the second most common etiology of hypercalcemia, an underlying ______.
primary hyperparathyroidism
malignancy
Initial therapy of significant hypercalcemia begins with ________
volume expansion because hypercalcemia invariably leads to dehydration
4–6 L of IV saline may be required over the first 24 h, keeping in mind that underlying comorbidities may require the use of loop diuretics to enhance Na and Ca excretion
In patients with 1,25(OH)2 D-mediated hypercalcemia, ______ are the preferred therapy, as they decrease 1,25(OH)2 D production.
glucocorticoids
Formula for plasma osmolality
Plasma osmolality is calculated according to the following expression: Posm = 2Na + Glu + BUN (all in mmol/L), or, using conventional laboratory values in which glucose and BUN are expressed in milligrams per deciliter: Posm = 2Na+ Glu/18 + BUN/2.8.
When the measured osmolality exceeds the calculated osmolality by >10–15 mmol/kg H2 O, one of two circumstances prevails. Either the serum sodium is spuriously low, as with hyperlipidemia or hyperproteinemia (pseudohyponatremia), or osmolytes other than sodium salts, glucose, or urea have accumulated in plasma
Type of RTA that is most often due to generalized proximal tubular dysfunction manifested by glycosuria, generalized aminoaciduria, and phosphaturia
Proximal RTA (type 2 RTA)
Associated with Fanconi syndrome
Tx: Alkali supplementatio + K and Vit D
Type of RTA with the typical findings including hypokalemia, a non-AG metabolic acidosis, low urinary NH4 + excretion (positive UAG, low urine [NH4 +]), and inappropriately high urine pH (pH > 5.5).
classic distal RTA (type 1 RTA)
Remember low urinary NH4 exretion!!!
Most patients have hypocitraturia and hypercalciuria, so nephrolithiasis, nephrocalcinosis, and bone disease are common.
bONE (b1)
Tx: Alkali supplementation + Citrate
Type of RTA in which hyperkalemia is disproportionate to the reduction in (GFR) because of coexisting dysfunction of potassium and acid secretion.
distal RTA (type 4 RTA)
Most common form
______ syndrome results from an inherited gain of function mutation of genes that regulate the collecting duct Na+ channel (ENaC).
Liddle’s
most common acid-base disturbance in critically ill patients and, when severe, portends a poor prognosis
Chronic respiratory alkalosis
The compensatory reduction in plasma [HCO3 – ] is so effective in chronic respiratory alkalosis that the pH may not decline significantly from the normal value. Therefore, chronic respiratory alkalosis is the only acid-base disorder for which compensation can return the pH to the normal value
the most common cause of drug-induced respiratory alkalosis as a result of direct stimulation of the medullary chemoreceptor
Salicylates
mechanism that predominantly mediates potassium balance in CKD
Aldosterone dependent secretion in the
distal nephron
complication is prevented by supplemental bicarbonate in CKD
protein catabolism
Target blood pressure for patients with CKD and concomitant proteinuria?
<130/80
most common organisms implicated in peritonitis in px undergoing peritoneal dialysis
G+ cocci
main feature distinguishing pyelonephritis from cystitis?
fever
What is the threshold for diagnosing asymptomatic bacteriuria in urine culture expressed in bacterial CFU/mL?
10^5
type of AKI caused by cyclosporine
pre-renal
same with ACE I and NSAIDs
PPI = intrinsic
portion of the kidney is particularly
susceptible to ischemic damage?
outer medulla
and S3 segment
PSGN usually develops
After _____ weeks post impetigo/skin infection
After _____weeks post strep pharyngitis
2-6 weeks
1-3 weeks
Most common cause of nephrotic syndrome in the elderly
MGN
Biopsy: uniform thickening of the basement membrane along the peripheral capillary LOOPSon light microscopy, diffuse granular deposits of IgG and C3 on IF and subepithelial electron-dense deposits on EM
urine osmolality of pre renal AKI
> 500
urine crea/ plasma crea ratio of pre renal AKI
> 40
Vomiting, nausea, confusion, and seizures, usually at plasma Na+ concentration _____
<125 mM
The ultimate “gold standard” for the diagnosis of hypovolemic hyponatremia is __________
the demonstration that plasma Na+ concentration corrects after hydration with normal saline
Causes of low FeNa aside from pre-renal AKI
Rhabdomyolysis
Sepsis
Hemolysis
CIN
-sis + CIN
Myeloma light chains can also cause AKI by
Binding to Tamm-Horsfall protein to form obstructing intratubular casts
The presence of hematuria and RBC casts on urinalysis in the setting of azotemia, oliguria, edema and hypertension point to the possibility of which major renal syndrome?
Acute nephritis
If BM thickening is a sensitive indicator of DM but does not corrrelate with nephropathy, what histologic finding correlates well with DM nephropathy?
Mesangial expansion
Formula for corrected anion gap
CorrectedAnionGap=MeasuredAnionGap+2.5×(4.0−SerumAlbumin(g/dL))
*some sources use 4.5 as normal value for albumin
What is the mechanism of Vancomycin in causing acute kidney injury?
Intratubular obstruction
** same with acyclovir
Vitamin C supplementation increases risk for what kind of stone formation
CaOx
What is the recommended urine pH for uric acid stones
6.5
What are the containdications to kidney biopsy?
Contraindications for kidney biopsy
Not advisable for patients with bilaterally small
kidneys:
* Technically difficult and higher chances of bleeding
* Scarred tissue will not show underlying disease
* Disease-specific therapy no longer useful
Other contraindications:
* Uncontrolled hypertension
* Active UTI
* Bleeding diathesis (including anticoagulation)
* Severe obesity
A urine osmolality <___mOsm/kg is suggestive of polydipsia
100
from the earliest stages of microalbuminuria, it usually takes ___ years to reach ESRD.
10–20
GNs that presents with hypocomplementenemia (3)
MPGN
Lupus nephritis
PSGN
** extra: cryloglobulinemia also has decreased C4 + positive RF
Type of cast seen in pre renal AKI
granular/hyaline
Most common type of stone
Calcium oxalate
The majority of calcium oxalate stones grow on calcium phosphate at the tip of the renal papilla AKA
(Randall’s plaque).
Effect of pH on citrate reabsorption
Citrate reabsorption is influenced by the intracellular pH of proximal tubular cells. Metabolic acidosis, including that due to higher animal flesh intake, will lead to a reduction in citrate excretion by increasing reabsorption of filtered citrate.
This test serves as the cornerstone on which therapeutic recommendations are based for px with urolithiasis
The results from 24-h urine collections serve as the cornerstone on which therapeutic recommendations are based.
At least 2 samples needed
The following factors should be measured: total volume, calcium, oxalate, citrate, uric acid, sodium, potassium, phosphorus, pH, and creatinine. When available, the calculated supersaturation is also informative.
Risk factors for caox stones
Risk factors for calcium oxalate stones include higher urine calcium, higher urine oxalate, and lower urine citrate
Individuals with higher urine calcium excretion tend to absorb a higher percentage of ingested calcium. Nevertheless, dietary calcium restriction is not beneficial and, in fact, is likely to be harmful. Excessive calcium intake (>1200 mg/d) should be avoided
Mediation used to tx hypertension that can decrease Caox recurrence
A thiazide diuretic, in doses higher than those used to treat hypertension, can substantially lower urine calcium excretion. Several randomized controlled trials have demonstrated that thiazide diuretics, most commonly chlorthalidone, can reduce calcium oxalate stone recurrence by ~50%.
T/F
In px with urinary tract obstruction, pain severity is influenced more by the rate at which distention develops than by the degree of distention.
true
Flank pain, the symptom that most commonly leads to medical attention, is due to distention of the collecting system or renal capsule. Pain severity is influenced more by the rate at which distention develops than by the degree of distention.
T/F
Partial bilateral UTO often results in acquired distal renal tubular acidosis, hypokalemia, and renal salt wasting
False
Partial bilateral UTO often results in acquired distal renal tubular acidosis, HYPERkalemia, and renal salt wasting
Fluid of choice for post obstructive diuresis
. Often replacement with 0.45% saline is required
Management of cardiorenal syndrome
Continued use of diuretic therapy may be associated with a reduction in glomerular filtration rate and a worsening of the cardiorenal syndrome when right-sided filling pressures remain elevated.
In patients in the late stages of disease characterized by profound low cardiac output state, inotropic therapy or mechanical circulatory support has been shown to preserve or improve renal function in selected individuals in the short term until more definitive therapy such as assisted circulation or cardiac transplantation is implemented
Difference between Type 1 vs Type 2 HRS
Type 1 HRS is characterized by a progressive impairment in renal function and a significant reduction in creatinine clearance within 1–2 weeks of presentation.
Type 2 HRS is characterized by a reduction in glomerular filtration rate with an elevation of serum creatinine level, but it is stable and is associated with a better outcome than that of type 1 HRS
HRS requires exclusion of other causes of acute renal failure, most notably volume depletion
Management of HRS
Diuretics should be stopped, and infusion of albumin 1 g/kg per day is recommended. Treatment is with vasoconstrictors such as terlipressin or low-dose norepinephrine (requires intensive care unit monitoring).
Midodrine, an α-agonist, along with octreotide and intravenous albumin are also commonly used in the United States.
The best therapy for HRS is liver transplantation; recovery of renal function is typical in this setting. In patients with either type 1 or type 2 HRS, the prognosis is poor unless transplant can be achieved within a short period of time.
Hypotension is the most common acute complication of hemodialysis, particularly among patients with _______
diabetes mellitus
Excessively rapid fluid removal (>13 mL/kg per h) should be avoided, as rapid fluid removal has been associated with adverse outcomes, including cardiovascular deaths.
Midodrine, an oral selective α1 adrenergic agent, has been advocated by some practitioners, although there is insufficient evidence of its safety and efficacy to support its routine use
Difference between two dialyzer reaction types
Dialyzer reactions can be divided into two types, A and B. Type A reactions are attributed to an IgEmediated intermediate hypersensitivity reaction to ethylene oxide used in the sterilization of new dialyzers. This reaction typically occurs soon after the initiation of a treatment (within the first few minutes) and can progress to full-blown anaphylaxis if the therapy is not promptly discontinued. Treatment with steroids or epinephrine may be needed if symptoms are severe.
The type B reaction consists of a symptom complex of nonspecific chest and back pain, which appears to result from complement activation and cytokine release
Difference between CAPD vs CCPD peritoneal dialysis
In CAPD, dialysate is manually infused into the peritoneal cavity and exchanged three to five times during the day. A nighttime dwell is frequently instilled at bedtime and remains in the peritoneal cavity through the night.
In CCPD, exchanges are performed in an automated fashion, usually at night; the patient is connected to an automated cycler that performs a series of exchange cycles while the patient sleeps. The number of exchange cycles required to optimize peritoneal solute clearance varies by the peritoneal membrane characteristics; as with hemodialysis, solute clearance should be tracked to ensure dialysis “adequacy.”
formal evaluation of peritoneal membrane characteristics that measures the transfer rates of creatinine and glucose across the peritoneal membrane
The peritoneal equilibrium test is a formal evaluation of peritoneal membrane characteristics that measures the transfer rates of creatinine and glucose across the peritoneal membrane
major complications of peritoneal dialysis p
The major complications of peritoneal dialysis are peritonitis, catheter-associated nonperitonitis infections, weight gain and other metabolic disturbances, and residual uremia (especially among patients with little or no residual kidney function).
How do you differentiate pre renal from renal cause of AKI based on FeNa, U/P ratio and urine osmolality
How do you differentiate PSGN vs Iga nephropathy with regard to timing of pharyngitis?
Postinfectious GN is to be distinguished from synpharyngitic hematuria, another glomerular syndrome that frequently produces gross hematuria, a heavier excretion of red blood, which may appear to the patient as a frightening hemorrhage. The patient may present with this concern so it is important for the clinician to recognize that as little as 10–20 mL of blood will turn a liter of urine red.
Synpharyngitic hematuria, usually with a viral pharyngitis, is most often related to IgA nephropathy rather than postinfectious GN.
Another feature that distinguishes IgA nephropathy from postinfectious GN is that the former usually demonstrates normal circulating C3 complement as opposed to low complement in PIGN.
IgA nephropathy can cause chronic microhematuria or bouts of gross hematuria or can occur in association with other immunologic conditions including celiac disease, rheumatoid arthritis, reactive arthritis, and ankylosing spondylitis. IgA nephropathy and staphylococcal-associated GN are more common in Asian populations
Acute allergic or immune interstitial nephritis (AIN) usually occurs __________ (duration) following exposure to an offending drug and may be associated with a rapid and potentially reversible loss of kidney function, which may occur in the setting of a change in dose or the restarting of a previously used medication
Acute allergic or immune interstitial nephritis (AIN) usually occurs 1 day to 2 weeks following exposure to an offending drug and may be associated with a rapid and potentially reversible loss of kidney function, which may occur in the setting of a change in dose or the restarting of a previously used medication.
Associated glomerular proteinuria sometimes occurs with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) or ampicillin.
Clinically, there may be fever, rash, and eosinophilia; the last is typical for certain penicillins, fluoroquinolones, and some biologic cancer drugs that act as checkpoint inhibitors (CPIs) but is atypical for NSAIDs.
most common cause of chronic interstitial nephritis
Perhaps the most common cause of chronic interstitial nephritis is prolonged analgesic use to treat chronic pain (not only NSAIDs but acetaminophen or combinations of phenacetin, aspirin, and caffeine) as part of the analgesic syndrome. T
3 defining features of nephrotic syndrome
Nephrotic syndrome (NS) has three defining features: edema, hypoalbuminemia (<3.5 g/dL), and proteinuria >3.5 g/day.
The syndrome is often associated with lipid abnormalities such as a high LDL, low HDL, and lipiduria.
The urine may contain large tubular epithelial cells that are engulfed with the lipid in a recognizable shape under polarized light. These oval fat bodies may also contain cholesterol monohydrate crystals, which appear as Maltese crosses.
A characteristic finding of rapid-onset hypoalbuminemia in NS is horizontal linear white lines in the nail bed, known as
A characteristic finding of rapid-onset hypoalbuminemia in NS is horizontal linear white lines in the nail bed, known as Muehrcke’s line
Exception to the low sodium excretion in prerenal AKI
The fractional excretion of sodium is usually >1–2%, whereas in oliguric prerenal syndromes the fractional excretion of sodium is usually <1%. Exception to the low sodium excretion would be in the case of hyperchloremic metabolic alkalosis, where chloride is being conserved and sodium excreted with bicarbonate
Stage of CKD in which the patient should be prepared and educated about transplant and dialysis
4
When the eGFR is <15–20 mL/min, the patient should already have had conversations about choices of eventual treatment and, if indicated, surgical preparation for peritoneal or hemodialysis
Based on CPG 2018, Among CKD 5 patients on low-flux hemodialysis, ___ times a week hemodialysis may be recommended.
3 (4 hrs each session)
same with hi flux
Based on CPG 2018, Initiation of hemodialysis at eGFR greater than ___ ml/min is not recommended among asymptomatic patients with CKD 5.
Initiation of hemodialysis at eGFR greater than 10 ml/min is not recommended among asymptomatic patients with CKD 5.
Based on CPG 2018, Among CKD 5 patients with CHF, initiating hemodialysis at eGFR <__ml/min may be recommended.
15
if no CHF <10
T/F
The mean GFR is lower in women than in men
True
Diagnostic test for monitoring albuminuria
Measurement of albuminuria is also helpful for monitoring nephron injury and the response to therapy in many forms of CKD, especially chronic glomerular diseases. The cumbersome 24-h urine collection has been replaced by measurement of urinary albumin-to-creatinine ratio (UACR) in one and preferably several spot first-morning urine samples as a measure pointing to glomerular injury.
Even in patients with negative conventional urinary dipstick tests for protein, persistent UACR >2.5 mg/mmol (male) or >3.5 mg/mmol (female) on two to three occasions serves as a marker not only for early detection of primary kidney disease but for systemic microvascular disease as well.
Leading causes of CKD
Diabetic nephropathy = #1
Glomerulonephritis
Hypertension-associated CKD (includes vascular and ischemic kidney disease and primary glomerular disease with associated hypertension)
Autosomal dominant polycystic kidney disease
Other cystic and tubulointerstitial nephropathy
T/F thiazide diuretics may be used across all stages of CKD
False
Thiazide diuretics have limited utility in stages 3–5 CKD, such that administration of loop diuretics, including furosemide, bumetanide, or torsemide, may be needed
Hyperparathyroidism stimulates bone turnover and leads to _________________. Bone histology shows abnormal osteoid, bone and bone marrow fibrosis, and, in advanced stages, the formation of bone cysts, sometimes with hemorrhagic elements so that they appear brown in color; hence, the term brown tumor.
Hyperparathyroidism stimulates bone turnover and leads to osteitis fibrosa cystica. Bone histology shows abnormal osteoid, bone and bone marrow fibrosis, and, in advanced stages, the formation of bone cysts, sometimes with hemorrhagic elements so that they appear brown in color; hence, the term brown tumor.
CXR findings of low pressure pulmonary edema from CKD
A form of “low-pressure” pulmonary edema can also occur in advanced CKD, manifesting as shortness of breath and a “bat wing” distribution of alveolar edema fluid on chest x-ray. This finding can occur even in the absence of ECFV overload and is associated with normal or mildly elevated pulmonary capillary wedge pressure. This process has been ascribed to increased permeability of alveolar capillary membranes as a manifestation of the uremic state, and it responds to dialysis
Causes of anemia in CKD
Subtle clinical manifestations of uremic neuromuscular disease usually become evident at stage ___ CKD
3
In women with CKD, estrogen levels are low, and menstrual abnormalities, infertility, and inability to carry pregnancies to term are common. When the GFR has declined to ~__ mL/min, pregnancy is associated with a high rate of spontaneous abortion, with only ~20% of pregnancies leading to live births, and pregnancy may hasten the progression of the kidney disease itself
40
Most useful imaging study for CKD
The most useful imaging study is a renal ultrasound, which can verify the presence of two kidneys, determine if they are symmetric, provide an estimate of kidney size, and rule out renal masses and evidence of obstruction
Which CCB has superior antiproteinuric and renoprotective effects
Among the calcium channel blockers, diltiazem and verapamil may exhibit superior antiproteinuric and renoprotective effects compared to the dihydropyridines.
AKI staging
Even in healthy adults, renal autoregulation usually fails once the systolic blood pressure falls below ____ mmHg
There is a limit, however, to the ability of these counterregulatory mechanisms to maintain GFR in the face of systemic hypotension. Even in healthy adults, renal autoregulation usually fails once the systolic blood pressure falls below 80 mmHg
most common causes of intrinsic AKI
The most common causes of intrinsic AKI are sepsis, ischemia, and nephrotoxins, both endogenous and exogenous
markedly elevated intraabdominal pressures, usually >__ mmHg, lead to renal vein compression and reduced GFR
20
the gold standard for direct visualization of the renal vasculature and is important for the diagnosis of renal artery stenosis, large vessel vasculitis, fibromuscular disease, or renal vein obstruction.
Renal angiography is the gold standard for direct visualization of the renal vasculature and is important for the diagnosis of renal artery stenosis, large vessel vasculitis, fibromuscular disease, or renal vein obstruction.
How does aminoglycosides and amp B cause intrinsic AKI?
Aminoglycosides and amphotericin B both cause tubular necrosis. Same with cisplatin and carboplatin
Nonoliguric AKI accompanies 10–30% of courses of aminoglycoside antibiotics, even when plasma levels are in the therapeutic range.
Aminoglycosides are freely filtered across the glomerulus and then accumulate within the renal cortex, where concentrations can greatly exceed those of the plasma. AKI typically manifests after 5–7 days of therapy and can present even after the drug has been discontinued. Hypomagnesemia is a common finding
Amphotericin B causes renal vasoconstriction from an increase in tubuloglomerular feedback as well as direct tubular toxicity mediated by reactive oxygen species. Nephrotoxicity from amphotericin B is dose and duration dependent. This drug binds to tubular membrane cholesterol and introduces pores. Clinical features of amphotericin B nephrotoxicity include polyuria, hypomagnesemia, hypocalcemia, and nongap metabolic acidosis.
Electrolyte abnormalities associated with ifosfamide
Ifosfamide may cause hemorrhagic cystitis and tubular toxicity, manifested as type II renal tubular acidosis (Fanconi syndrome), polyuria, hypokalemia, and a modest decline in GFR
MOA of AKI from ethylene glycol
Ethylene glycol, present in automobile antifreeze, is metabolized to oxalic acid, glycolaldehyde, and glyoxylate, which may cause AKI through direct tubular injury and tubular obstruction
Think of ethylene glycol if + oxalate crystals and AKI + HAGMA
Treatment for rhabdomyolysis
Early and aggressive volume repletion is mandatory in patients with rhabdomyolysis, who may initially require 10 L of fluid per day. Alkaline fluids (e.g., 75 mmol/L sodium bicarbonate added to 0.45% saline) may be beneficial in preventing tubular injury and cast formation, but carry the risk of worsening hypocalcemia.
Diuretics may be used if fluid repletion is adequate but unsuccessful in achieving urinary flow rates of 200–300 mL/h. There is no specific therapy for established AKI in rhabdomyolysis, other than dialysis in severe cases or general supportive care to maintain fluid and electrolyte balance and tissue perfusion
Metabolic acidosis is generally not treated unless severe (pH <____ AND serum bicarbonate <___ mmol/L).
Metabolic acidosis is generally not treated unless severe (pH <7.20 and serum bicarbonate <15 mmol/L).
T/F Anemia in AKI can be tx by erythropoiesis-stimulating agents
The anemia seen in AKI is usually multifactorial and is not improved by erythropoiesis-stimulating agents, due to their delayed onset of action and the presence of bone marrow resistance in critically ill patients
ESA only in CKD
More severe hypercalcemia (>_____mg/dL), particularly if it develops acutely, may result in lethargy, stupor, or coma, as well as gastrointestinal symptoms (nausea, anorexia, constipation, or pancreatitis)
More severe hypercalcemia (>12–13 mg/dL), particularly if it develops acutely, may result in lethargy, stupor, or coma, as well as gastrointestinal symptoms (nausea, anorexia, constipation, or pancreatitis)
Although there are many potential causes of hypocalcemia, _____________ are the most common etiologies
impaired PTH production and impaired vitamin D production
Hypoparathyroidism is a cardinal feature of autoimmune endocrinopathies
A suppressed (or “inappropriately low”) PTH level in the setting of hypocalcemia establishes absent or reduced PTH secretion (hypoparathyroidism) as the cause of the hypocalcemia. Further history will often elicit the underlying cause (i.e., parathyroid agenesis vs destruction)
Carpal spasm may be induced by inflation of a blood pressure cuff to ___ mmHg above the patient’s systolic blood pressure for 3 min (Trousseau’s sign).
Carpal spasm may be induced by inflation of a blood pressure cuff to 20 mmHg above the patient’s systolic blood pressure for 3 min (Trousseau’s sign).
The MDRD equation is better correlated with true GFR when the GFR is <____ mL/min per 1.73 m2 .
The MDRD equation is better correlated with true GFR when the GFR is <60 mL/min per 1.73 m2 .
Patients with atheroembolic acute renal failure often have a normal urinalysis, but the urine may contain
eosinophils and casts
Next step when px with hematuria presents with proteinuria
The dipstick measurement detects only albumin and gives false-positive results at pH
The dipstick measurement detects only albumin and gives false-positive results at pH >7.0 or when the urine is very concentrated or contaminated with blood.
Hematuria is defined as ______ RBCs per high-power field (HPF) and can be detected by dipstick
Hematuria is defined as two to five RBCs per high-power field (HPF) and can be detected by dipstick
Gross hematuria with blood clots usually is not an intrinsic renal process; rather, it suggests a postrenal source in the urinary collecting system
1st diagnostic test when px presents with polyuria
If the urine volume is >3 L/d and urine osmolality is >300 mosmol/L, a solute diuresis is clearly present and a search for the responsible solute(s) is mandatory
Poorly controlled diabetes mellitus with glucosuria is the most common cause of a solute diuresi
Winter’s equation
Paco2 = (1.5 × [HCO3 −]) + 8 ± 2 (Winter’s equation)
Cause of HAGMA
An increase in the AG is most often due to an increase in unmeasured anions but, less commonly, may be due to a decrease in unmeasured cations (calcium, magnesium, potassium).
Indications for bicarbonate therapy in DKA
Bicarbonate therapy in diabetic ketoacidosis (DKA) is reserved for adult patients with severe acidemia (pH <7.00) and/or evidence of shock. In such circumstances, bicarbonate may be administered IV, as a slow infusion of 50 meq of NaHCO3 diluted in 300 mL of a saline solution, over 30–45 min, during the initial 1–2 h of therapy. Bolus administration should be avoided.
4 principal causes of HAGMA
There are four principal causes of a high-AG acidosis: (1) lactic acidosis, (2) ketoacidosis, (3) ingested toxins, and (4) acute and chronic kidney failure
2 types of lactic acidosis
An increase in plasma l-lactate may be secondary to poor tissue perfusion (type A)—circulatory insufficiency (shock, cardiac failure), severe anemia, mitochondrial enzyme defects, and inhibitors (carbon monoxide, cyanide)—or to aerobic disorders (type B)—malignancies, nucleoside analogue reverse transcriptase inhibitors in HIV, diabetes mellitus, renal or hepatic failure, thiamine deficiency, severe infections (cholera, malaria), seizures, or drugs/toxins (biguanides, ethanol, and the toxic alcohols: ethylene glycol, methanol, or propylene glycol)
Treatment for ethylene glycol toxicity
This includes the prompt institution of IV isotonic fluids, thiamine and pyridoxine supplements, fomepizole, and usually, hemodialysis. Both fomepizole and ethanol compete with EG for metabolism by alcohol dehydrogenase. Fomepizole (4-methylpyrazole; 15 mg/kg IV over 30 min as a loading dose, then 10 mg/kg for four doses every 12 h) is the agent of choice and offers the advantages of a predictable decline in EG levels without excessive obtundation, as seen during ethyl alcohol infusion. Fomepizole should be continued until blood pH is normal or the osmolar gap is <10 mOsm/kg H2 O. Hemodialysis is indicated when the arterial pH is <7.3, a high-AG acidosis is present, the osmolar gap exceeds 20 mOsm/kg H2 O, or there is evidence of end organ damage such as CNS manifestations and kidney failure
Treatment of methanol intoxication is similar to that for EG intoxication, including general supportive measures, fomepizole, and hemodialysis
Treatment for metab acidosis in CKD
Because of the association of metabolic acidosis in advanced CKD with muscle catabolism, bone disease, and more rapid progression of CKD, both the “uremic acidosis” of end-stage renal disease and the non-AG metabolic acidosis of stages 3 and 4 CKD require oral alkali replacement to increase and maintain the [HCO3 −] to a value >22 mmol/L. This can be accomplished with relatively modest amounts of alkali (1.0–1.5 mmol/kg body weight per day) and has been shown to slow the progression of CKD. Either NaHCO3 tablets (650-mg tablets contain 7.8 meq) or oral sodium citrate (Shohl’s solution) is effective. Moreover, addition of fruits and vegetables (citrate) to the diet may increase the plasma [HCO3 – ] and slow progression
How do you differentiate NAGMA from RTA vs diarrhea?
Metabolic acidosis due to gastrointestinal losses with a high urine pH can be differentiated from RTA because urinary NH4 + excretion is typically low in RTA and high with diarrhea. Urinary NH4 + levels are not routinely measured by clinical laboratories but can be estimated by calculating the urine anion gap (UAG): UAG = [Na+ + K+]u – [Cl−]u . When [Cl−]u > [Na+ + K+]u , the UAG is negative by definition. This suggests that the urine ammonium level is appropriately increased, suggesting an extrarenal cause of the acidosis
Fanconi syndrome is associated with what type of RTA?
Proximal RTA (type 2 RTA) is most often due to generalized proximal tubular dysfunction manifested by glycosuria, generalized aminoaciduria, and phosphaturia (Fanconi syndrome).
Type of RTA associated with nephrolithiasis and nephrocalcinosis
The typical findings in acquired or inherited forms of classic distal RTA (type 1 RTA) include hypokalemia, a non-AG metabolic acidosis, low urinary NH4 + excretion (positive UAG, low urine [NH4 +]), and inappropriately high urine pH (pH >5.5). Most patients have hypocitraturia and hypercalciuria; nephrolithiasis, nephrocalcinosis, and bone disease are common
Type of RTA associated with hyperkalemia
In generalized distal RTA (type 4 RTA), hyperkalemia is disproportionate to the reduction in glomerular filtration rate (GFR) because of coexisting dysfunction of potassium and acid secretion. Urinary ammonium excretion is invariably depressed, and kidney function may be compromised secondary to diabetic nephropathy, obstructive uropathy, or chronic tubulointerstitial disease
How do you correct potassium in Type 2 RTA
An oral solution of sodium and potassium citrate (citric acid 334 mg, sodium citrate 500 mg, and potassium citrate 550 mg per 5 mL) may be prescribed for this purpose (Virtrate or Cytra-3).
In Type 1 RTA, which should be corrected first, hypokalemia or acidosis?
. In classical distal RTA (type 1), hypokalemia should be corrected first. When accomplished, alkali therapy with either sodium citrate (Shohl’s solution) or NaHCO3 tablets (650-mg tablets contain 7.8 meq) should be initiated to correct and maintain the serum [HCO3 – ] in the range of 24–26 meq/L. Type 1 RTA patients typically respond to chronic alkali therapy readily, and the benefits of adequate alkali therapy include a decrease in the frequency of nephrolithiasis, improvement in bone density, resumption of normal growth patterns in children, and preservation of kidney function in both adults and children
how does hypokalemia cause alkalosis?
renal generation of NH4 + (ammoniagenesis) is upregulated directly by hypokalemia. Chronic K+ deficiency also upregulates the H+, K+- ATPases in the distal tubule and collecting duct to increase K+ absorption while simultaneously increasing H+ secretion.
How do you correct metabolic alkalosis due to ECV contraction
Isotonic saline is recommended to reverse the alkalosis when ECFV contraction is present. If associated conditions, such as congestive heart failure, preclude infusion of isotonic saline, renal HCO3 − loss can be accelerated by administration of acetazolamide (125–250 mg IV), a carbonic anhydrase inhibitor, which is usually effective in patients with adequate renal function.
Vasopressin secretion, water ingestion, and renal water transport collaborate to maintain human body fluid osmolality between _______
Vasopressin secretion, water ingestion, and renal water transport collaborate to maintain human body fluid osmolality between 280 and 295 mOsm/kg
More reliable signs of hypovolemia on physical examination
On examination, diminished skin turgor and dry oral mucous membranes are less than ideal markers of a decreased ECFV in adult patients; more reliable signs of hypovolemia include a decreased jugular venous pressure (JVP), orthostatic tachycardia (an increase of >15–20 beats/min upon standing), and orthostatic hypotension (a >10–20 mmHg drop in blood pressure on standing).
two key effectors in the defense of serum osmolality
Water intake and circulating AVP constitute the two key effectors in the defense of serum osmolality
Causes of euvolemic hyponatremia
if UNa >20, renal losses
Causes of hypervolemic hyponatremia
if UNa >20, renal losses
T/F
The degree of hyponatremia provides an indirect index of the associated neurohumoral activation and is an important prognostic indicator in hypervolemic hyponatremia.
True
Formula for corrected sodium in hyperglycemia
Serum glucose should also be measured; plasma Na+ concentration falls by ~1.6–2.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced water efflux from cells; this “true” hyponatremia resolves after correction of hyperglycemia
Therapy with vaptans must be initiated in a hospital setting, with a liberalization of fluid restriction (>___ L/d) and close monitoring of plasma Na+ concentration.
Therapy with vaptans must be initiated in a hospital setting, with a liberalization of fluid restriction (>2 L/d) and close monitoring of plasma Na+ concentration.
Abnormalities in liver function tests have been reported with chronic tolvaptan therapy; hence, the use of this agent should be restricted to <1–2 months.
subset of px with highest risk of developing hypernatremia
Elderly individuals with reduced thirst and/or diminished access to fluids are at the highest risk of developing hypernatremia.
Rate of correction of hypernatremia in adults
In critically ill adults, however, recent evidence does not indicate that rapid correction of hypernatremia is associated with a higher risk for mortality, seizure, alteration of consciousness, and/or cerebral edema. Given that restricting the rate of correction to <10 mM/d has no physiologic sequelae, it seems prudent to restrict correction in adults to this rate; however, should that rate be exceeded, hypernatremia does not need to be reinduced.
**sequelae more common in pedia px
Majority of potassium is excreted via
urine (90%)
TPP develops more frequently in patients of Asian or Hispanic origin; this shared predisposition has been linked to genetic variation in _____, a muscle-specific, thyroid hormone–responsive K+ channel.
TPP develops more frequently in patients of Asian or Hispanic origin; this shared predisposition has been linked to genetic variation in Kir2.6, a muscle-specific, thyroid hormone–responsive K+ channel.
What beta lactams are associated with hypokaleia
High doses of penicillin-related antibiotics (nafcillin, dicloxacillin, ticarcillin, oxacillin, and carbenicillin) can increase obligatory K+ excretion by acting as nonreabsorbable anions in the distal nephron
T/F licorice is associated with hyperkalemia
False. Hypokalemia
Recessive loss-of-function mutations in the 11βHSD-2 gene are thus associated with cortisol-dependent activation of the MLR and the syndrome of apparent mineralocorticoid excess (SAME), encompassing hypertension, hypokalemia, hypercalciuria, and metabolic alkalosis, with suppressed PRA and suppressed aldosterone. A similar syndrome is caused by biochemical inhibition of 11βHSD-2 by glycyrrhetinic/ glycyrrhizinic acid and/or carbenoxolone. Glycyrrhizinic acid is a natural sweetener found in licorice root, typically encountered in licorice and its many guises or as a flavoring agent in tobacco and food products. More recently, the antifungals itraconazole and posaconazole have been shown to inhibit 11βHSD-2, leading to hypertension and hypokalemia.
Loss of the transport functions of the TALH and DCT nephron segments causes hereditary hypokalemic alkalosis and ______ and _______ respectively
Loss of the transport functions of the TALH and DCT nephron segments causes hereditary hypokalemic alkalosis and Bartter’s syndrome (BS) and Gitelman’s syndrome (GS), respectively
When excessive activity of the sympathetic nervous system is thought to play a dominant role in redistributive hypokalemia what should be given to reduc the risk of rebound hyperkalemia
When excessive activity of the sympathetic nervous system is thought to play a dominant role in redistributive hypokalemia, as in TPP, theophylline overdose, and acute head injury, high-dose propranolol (3 mg/kg) should be considered; this nonspecific β-adrenergic blocker will correct hypokalemia without the risk of rebound hyperkalemia
most important infectious cause of adrenal insufficiency
HIV has surpassed tuberculosis as the most important infectious cause of adrenal insufficiency
How does brugada type 1 pattern from hyperkalemia differ from genetic brugada syndrome based on ecg?
Hyperkalemia can also cause a type I Brugada pattern in the electrocardiogram (ECG), with a pseudo–right bundle branch block and persistent coved ST-segment elevation in at least two precordial leads. This hyperkalemic Brugada’s sign occurs in critically ill patients with severe hyperkalemia and can be differentiated from genetic Brugada’s syndrome by an absence of P waves, marked QRS widening, and an abnormal QRS axis.
Effect of hyperkalemia on pH
Hyperkalemia can cause metabolic acidosis
First step in managing px with severe hyperkalemia
The recommended dose is 10 mL of 10% calcium gluconate (3–4 mL of calcium chloride), infused intravenously over 2–3 min with cardiac monitoring. The effect of the infusion starts in 1–3 min and lasts 30–60 min; the dose should be repeated if there is no change in ECG findings or if they recur after initial improvement. Hypercalcemia potentiates the cardiac toxicity of digoxin; hence, intravenous calcium should be used with extreme caution in patients taking this medication; if judged necessary, 10 mL of 10% calcium gluconate can be added to 100 mL of 5% dextrose in water and infused over 20–30 min to avoid acute hypercalcemia.
What could be given to reduce hyperkalemia by means of Rapid reduction in plasma K+ concentration by redistribution into cells.
Insulin- Glucose
The recommended dose is 10 units of intravenous regular insulin followed immediately by 50 mL of 50% dextrose (D50W, 25 g of glucose total); the effect begins in 10–20 min, peaks at 30–60 min, and lasts for 4–6 h. Bolus D50W without insulin is never appropriate, given the risk of acutely worsening hyperkalemia due to the osmotic effect of hypertonic glucose. Hypoglycemia is common with insulin plus glucose; hence, this should be followed by an infusion of 10% dextrose at 50–75 mL/h, with close monitoring of plasma glucose concentration. In hyperkalemic patients with glucose concentrations of ≥200–250 mg/dL, insulin should be administered without glucose, again with close monitoring of glucose concentrations.
B2 agonists
β2 -Agonists, most commonly albuterol, are effective but underused agents for the acute management of hyperkalemia. Albuterol and insulin with glucose have an additive effect on plasma K+ concentration; however, ~20% of patients with ESRD are resistant to the effect of β2 -agonists; hence, these drugs should not be used without insulin. The recommended dose for inhaled albuterol is 10–20 mg of nebulized albuterol in 4 mL of normal saline, inhaled over 10 min; the effect starts at about 30 min, reaches its peak at about 90 min, and lasts for 2–6 h. Hyperglycemia is a side effect, along with tachycardia. β2 - Agonists should be used with caution in hyperkalemic patients with known cardiac disease.
Nephritic syndrome with gross subcapsular hemorrhages with a “flea-bitten” appearance, and microscopy on renal biopsy reveals focal proliferation around foci of necrosis associated with abundant mesangial, subendothelial, and subepithelial immune deposits of IgG, IgM, and C3 .
Endocarditis-associated glomerulonephritis is typically a complication of SBE, particularly in patients who remain untreated for a long time, have negative blood cultures, or have right-sided endocarditis. Common comorbidities are valvular heart disease, intravenous drug use, hepatitis C, and diabetes mellitus. Glomerulonephritis is unusual in acute bacterial endocarditis because it takes 10–14 days to develop immune complex–mediated injury, by which time the patient has been treated, often with emergent surgery. Grossly, the kidneys in SBE have subcapsular hemorrhages with a “flea-bitten” appearance, and microscopy on renal biopsy reveals focal proliferation around foci of necrosis associated with abundant mesangial, subendothelial, and subepithelial immune deposits of IgG, IgM, and C3 . Commonly patients present with a clinical picture of RPGN and have crescents on biopsy.
Treatment for endocarditis associated GN
Primary treatment is eradication of the infection with 4–6 weeks of antibiotics, and if accomplished expeditiously, the prognosis for renal recovery is good
Pathophysiology of Goodpasture syndrome
Patients who develop autoantibodies directed against glomerular basement antigens frequently develop a glomerulonephritis termed antiglomerular basement membrane (anti-GBM) disease. When they present with lung hemorrhage and glomerulonephritis, they have a pulmonary-renal syndrome called Goodpasture’s syndrome.
Treatment for Goodpasture syndrome
Prognosis at presentation is worse if there are >50% crescents on renal biopsy with advanced fibrosis, if serum creatinine is >5–6 mg/dL, if oliguria is present, or if there is a need for acute dialysis. Patients who present with hemoptysis should be treated for their lung hemorrhage, as it responds to plasmapheresis.
Treated patients with less severe disease typically respond to 8–10 treatments of plasmapheresis accompanied by oral prednisone and cyclophosphamide.
Maintenance therapy with low-dose immunosuppressants should be considered until antibody titers are negative. There are scarce data alternatively using rituximab, azathioprine, or mycophenolate mofetil. Kidney transplantation should wait for 6 months and until serum antibodies are undetectable.
Scoring system with predictive value for IgA Nephropathy
Mesangial hypercellularity (M), endocapillary hypercellularity (E), segmental glomerulosclerosis (S), tubular interstitial fibrosis (T), and crescents (C) have predictive value as established by the Oxford Classification and the MEST-C score
Treatment for IgA Nephropathy
There is no agreement on optimal treatment.
Both large studies that include patients with multiple glomerular diseases and small studies of patients with IgA nephropathy support the use of (ACE) inhibitors in patients with proteinuria or declining renal function.
In patients with persistent proteinuria after ACE inhibitor therapy, steroid treatment or other immunosuppressives have demonstrated conflicting results.
Tonsillectomy and fish oil have also been suggested in small studies to benefit select patients. When presenting as RPGN, patients typically receive steroids, cytotoxic agents, and plasmapheresis.
Patients with this disease classically present with fever, purulent rhinorrhea, nasal ulcers, sinus pain, polyarthralgias/arthritis, cough, hemoptysis, shortness of breath, hematuria, and subnephrotic proteinuria; occasionally, there may be cutaneous purpura and mononeuritis multiplex.
Granulomatosis with Polyangiitis
Previously known as Wegeners
Biopsy of involved tissue will show a small-vessel vasculitis and adjacent noncaseating granulomas. Renal biopsies during active disease demonstrate segmental necrotizing glomerulonephritis without immune deposits and have been classified as focal, mixed, crescentic, or sclerotic
** if with no lung dse/ sinusitis –> MPA / Microscopic polyangitis
small-vessel vasculitis that is associated with peripheral eosinophilia, cutaneous purpura, mononeuritis, asthma, and allergic rhinitis
EGPA
previously known as Churg Strauss
Treatment for MPGN
treatment with inhibitors of the renin-angiotensin system is prudent.
Evidence supports the efficacy of treatment of primary MPGN with steroids, particularly in children.
There are reports of efficacy with other immunosuppressive drugs. If defects in the complement pathway are found, treatment with eculizumab is of benefit.
In secondary MPGN, treating the associated infection, autoimmune disease, or neoplasms is of demonstrated benefit. Patients with primary MPGN are well known to be at risk for not only a histologic recurrence in the transplanted kidney but also a clinically significant recurrence with loss of graft function
Treatment for membranous nephropathy
In addition to the treatment of edema, dyslipidemia, and hypertension, inhibition of the renin-angiotensin system is recommended. Therapy with immunosuppressive drugs is also recommended for patients with primary MGN and persistent proteinuria (>3.0 g/24 h).
The choice of immunosuppressive drugs for therapy is controversial, but current recommendations are to treat with steroids and cyclophosphamide, chlorambucil, mycophenolate mofetil, or cyclosporine or rituximab, an anti-CD20 antibody directed at B cells. Attaining remission is associated with a good long-term prognosis.
When do you test for albuminuria in px with T1DM and T2DM
Microalbuminuria appears 5–10 years after the onset of diabetes. It is currently recommended to test patients with type 1 disease for microalbuminuria 5 years after diagnosis of diabetes and yearly thereafter and, because the time of onset of type 2 diabetes is often unknown, to test type 2 patients at the time of diagnosis of diabetes and yearly thereafter.
an X-linked inborn error of globotriaosylceramide metabolism secondary to deficient lysosomal α-galactosidase A (alpha-Gal A) activity, resulting in excessive intracellular storage of globotriaosylceramide. Affected organs include the vascular endothelium, heart, brain, and kidneys
Fabry’s dse
Renal biopsy reveals enlarged glomerular visceral epithelial cells packed with small clear vacuoles containing globotriaosylceramide; vacuoles may also be found in parietal and tubular epithelia
These vacuoles of electron-dense materials in parallel arrays (zebra bodies) are easily seen on electron microscopy. Ultimately, renal biopsies reveal FSGS. The nephropathy of Fabry’s disease typically presents in the third decade as mild to moderate proteinuria, sometimes with microscopic hematuria or nephrotic syndrome. Urinalysis may reveal oval fat bodies and birefringent glycolipid globules under polarized light (Maltese cross).
Presentation of Alport’s syndrome
Classically, patients with Alport’s syndrome develop hematuria, thinning and splitting of the GBMs, and mild proteinuria (<1–2 g/24 h), which appears late in the course, followed by chronic glomerulosclerosis leading to renal failure in association with sensorineural deafness
Primary treatment is control of systemic hypertension and use of ACE inhibitors to slow renal progression. Although patients who receive renal allografts usually develop antiGBM antibodies directed toward the collagen epitopes absent in their native kidney, overt Goodpasture’s syndrome is rare and graft survival is good.
Hypertensive nephrosclerosis is fivefold more frequent in African Americans than whites. Risk alleles associated with _____, a functional gene for apolipoprotein L1 expressed in podocytes, substantially explain the increased burden of ESRD among African Americans
Hypertensive nephrosclerosis is fivefold more frequent in African Americans than whites. Risk alleles associated with APOL1, a functional gene for apolipoprotein L1 expressed in podocytes, substantially explain the increased burden of ESRD among African Americans
How does HIVAN differ from other causes of nephrotic syndrome?
HIV patients with FSGS typically present with nephrotic-range proteinuria and hypoalbuminemia, but unlike patients with other etiologies for nephrotic syndrome, they do not commonly have hypertension, edema, or hyperlipidemia.
atment with inhibitors of the reninangiotensin system decreases the proteinuria. Effective antiretroviral therapy benefits both the patient and the kidney and improves survival of HIV-infected patients with HIVAN and, in some cases, HIVICKassociated chronic kidney disease or ESRD. In HIV-infected patients not yet on therapy, the presence of HIVAN is an indication to initiate therapy
Scistosoma species associated with renal dse
Schistosoma mansoni is most commonly associated with clinical renal disease
PPI causes what type of AKI
Intrinsic –> acute tubulointerstitial nephritis
Increased intraabdominal pressure > ___ mmHg can lead to renal vein compression and therefore decreased GFR
20
Abdominal compartment syndrome
Most evident signs/symptoms in CKD 3 and 4
Anemia
Easy fatigability
Malnutrition
Which of the following is TRUE regarding medication dose adjustment in CKD?
a.Maintenance doses of many drugs do not need to be adjusted in CKD
b.Loading dose of most drugs is not affected by CKD because renal elimination is not used in the calculation
c.For agents in which >20% excretion is by a nonrenal route, maintenance dose adjustment may not be needed
d.Gadolinium is the safest radiocontrast agent for patients with CKD needing immediate imaging
b.Loading dose of most drugs is not affected by CKD because renal elimination is not used in the calculation
This immunosuppressive drug used after kidney transplant is a macrolide with good absorption. It blocks cytokine production, but stimulates TGF-B production. Unlike its counterpart, this drug does not produce hirsutism:
a. Azathioprine
b. Cyclosporine
c. Sirolimus
d. Tacrolimus
d. Tacrolimus
A 34-year-old male with no symptoms consults for recent findings hypertension and adult polycystic kidney disease. What is a rational approach to slow down cyst growth in this patient?
a. Initiate lifetime aspirin and statin therapy
b. Rigorous BP control with Telmisartan to target lower than BP 110/75
c. Permissive BP target with Spironolactone to target of 130/80
d. Nerve blockade
c. Permissive BP target with Spironolactone to target of 130/80
Which of the following causes of hyperkalemia is consistent with decreased urinary K excretion and a TTKG >8?
a.Diabetes mellitus
b.NSAID use
c.Urinary tract obstruction
d.Advanced kidney failure
d.Advanced kidney failure
Hyperkalemia occurs due to impaired potassium excretion or excessive potassium release from cells. The Transtubular Potassium Gradient (TTKG) helps differentiate whether the kidneys are appropriately excreting potassium.
Normally, in hyperkalemia, TTKG should be >8 (indicating appropriate renal K+ excretion).
If TTKG <5 in hyperkalemia, it suggests inadequate renal K+ excretion, often due to hypoaldosteronism or kidney dysfunction.
However, in advanced kidney failure (option d), TTKG can remain >8 even with hyperkalemia.
This occurs because the remaining functioning nephrons compensate by increasing potassium excretion, but overall kidney function is still too impaired to fully correct the hyperkalemia.
Which of the following accounts for secondary hyperparathyroidism in CKD?
a.Increased renal secretion of phosphate
b.Negative feedback in the synthesis of PTH
c.Reduced calcitriol production
d.Hypoplasia of parathyroid gland
c.Reduced calcitriol production
A 52-year old male with known chronic kidney disease stage 3 from diabetic kidney disease presents with a blood pressure of 158 to 173/92 to 103 on both office and home blood pressure monitoring. He is already on optimal doses of Amlodipine and Telmisartan. What is the next possible add-on treatment for control of his blood pressure?
a. Carvedilol 6.25 mg BID
b. Enalapril 10 mg BID
c. Diltiazem 60 mg BID
d. Hydrochlorothiazide 25 mg OD
a. Carvedilol 6.25 mg BID
Already on ARB and DHP CCB
HCTZ limited use in ckd 3-5
What is the most common histology of urinary tract cancer?
a.Urothelial carcinoma
b.Squamous cell carcinoma
c.Glandular carcinoma
d.Plasmacytoid carcinoma
a.Urothelial carcinoma
A 27/F is brought to the emergency department for fever. Five weeks prior, she underwent kidney transplantation and was discharged well on prednisone, tacrolimus, mycophenolate mofetil, co-trimoxazole, and isoniazid. Which of the following diagnostic tests is the LEAST helpful in determining the patient’s fever etiology?
a. Chest CT
b. Hepatitis profile
c. CMV antigenemia assay
d. Urine PCR for BK polyoma virus
d. Urine PCR for BK polyoma virus
Seen after >6mos
Which of the following peritoneal fluid cell counts are diagnostic of peritoneal dialysis peritonitis?
a. WBC 50/mm3 with 75% neutrophils
b. WBC 95/mm3 with 60% neutrophils
c. WBC 105/mm3 with 55% neutrophils
d. WBC 250/mm3 with 45% neutrophils
c. WBC 105/mm3 with 55% neutrophils
WBC at least 100 and 50% neutros
Detection of calcium oxalate crystals in the urinalysis of a patient with AKI is most suggestive of what clinical condition?
a.Ethylene glycol intoxication
b.Tumor lysis syndrome
c.Allograft rejection
d.Hemolytic uremic syndrome
a.Ethylene glycol intoxication
According to Kidney Disease Improving Global Outcomes (KDIGO) guidelines, how much total energy intake should a patient with AKI receive?
a.15-20 kcal/kg
b.20-25 kcal/kg
c.20-30 kcal/kg
d.30-35 kcal/kg
c.20-30 kcal/kg
The dipstick is a quick way to test the presence of proteinuria. However, it can be false positive in which condition?
a.Concentrated urine
b.pH <7.0
c.Excessive intake of alcohol
d.Bence-Jones protein
a.Concentrated urine
Which stain is used to better identify basement membrane structure in kidney biopsies?
a.Jones methenamine silver
b.Congo red
c.Masson’s trichome
d.Hematoxylin and eosin
a.Jones methenamine silver
Congo red : amyloid deposits
Massons trichome: collagen deposition, assess degree of glomerulosclerosis and interstitial fibrosis
H&E: assess cllularity and architecture
On renal biopsy, this finding is an ominous pathologic sign of irreversibility and progression to renal failure:
a. Glomerular crescents
b. Interstitial fibrosis
c. Sclerotic glomeruli
d. Synechiae formation
b. Interstitial fibrosis
A 23-year-old male consulted for a 2-day history of gross hematuria. He recalls having a sore throat 3 days ago which spontaneously resolved without antibiotics. Urinalysis revealed RBC 20/hpf, with no protein, casts and crystals; hemoglobin 135 g/L, platelet count 345, C3 levels normal. What is the expected kidney biopsy finding?
a. Granular subepithelial immune complex deposition
b. Mesangial IgA deposits
c. Dense deposits of C3
d. Diffuse granular IgG, C3
b. Mesangial IgA deposits
IgA nephropathy since nepritic picture
A 54 year old male who previously worked as a miner consulted for hemoptysis at the ER. Pertinent PE included nasal ulcers and decreased breath sounds on both basal lung fields. Chest radiograph showed cavitation in the left upper base and bilateral pleural effusion. Other tests revealed microscopic hematuria and albuminuria. Renal biopsy revealed pauci-immune necrotizing glomerulonephritis. What is the most likely diagnosis?
a.Granulomatosis with polyangiitis
b.Microscopic polyangiitis
c.Churg-Strauss syndrome
d.Goodpasture’s disease
a.Granulomatosis with polyangiitis
URT and LRT involvement + kidney involvement
A 72 year old male with diabetes mellitus was admitted for sudden right visual field cuts and a rapid increase in baseline creatinine from a month ago. Further investigation revealed Hollenhorst plaques in the retina. Which is a proven strategy to prevent progression of disease?
a.Dialysis
b.Heparin
c.Insulin
d.Statin
d.Statin
Hollenhorst plaques = choleterol plaque
Which of the following conditions is associated with the development of chronic interstitial nephritis?
a.G6PD
b.HIV
c.Neurogenic bladder
d.Vesicoureteral reflux
d.Vesicoureteral reflux
Best histological correlate of renal failure in GN
presence of tubulointerstitial nephritis NOT the type of inciting glomerular injury
Prognosis of MCD
Children: complete remission 90-95% after 8 weeks of steroid
Adult: complete remission 80-85% after 20-24 weeks of steroid therapy
Most common autoantibody implicated in membranous nephropathy
70% ab against mtype phospholipase A2 (PLA2R)
T/F intensive control of blood sugar clearly prevents progression of DM nephropathy
True for T1DM but not for T2DM
What drug is associated with red green birefringent needle shaped crystals
Acyclovir
What drug is associated with sheaf of wheat crystals
Sulfodiazine/ Sulfonamides
Most common renal complication of lithium
nephrogenic DI
Causes of papillary necrosis
Analgesic nephropathy
DM with UTI
Prolonged NSAID use
Sickle cell nephropathy
Nephropathy with renal interstitial fibrosis with relative paucity of cellular infiltrates is caused by this acid
Artistocholic acid
AKA Chinese/Balkan nephropathy
Triad of Lead nephropathy
saturnine gout, hypertension, renal insufficiency
T/F Allopurinol and alkalinization may reverse gouty nephropathy
False
What type of nephropathy due to electrolyte imbalance leads to reversible vacuolar degeneration of proximal and distal tubular cells
Hypokalemic nephropathy
Formula for estimating background percentage sclerosis using age
(Age/2) - 10
Dietary factors associated with lower risk of nephrolithiasis
Ca (dietary NOT supplement)
K
phytate
Urologic intervention for stone with the highest likelihood of rendering the patient stone free
Percutaneous nephrolithostomy
If px with struvie has recurrent giving, you might considering giving this
Urease inhibitor Acetohydroxamic acid
Type of stone most common in ADPKD
Uric acid
more than half of stones in ADPKD are composed of uric acid
De novo diabetes mellius after transplant is more likely caused by which immunosuppressive agent?
Tacrolimus
Which of the following is true regarding the mean glomerular filtration rate (GFR)?
a.An increase in GFR is expected with aging
b.Mean GFR is lower in women than in men
c.A mild elevation in serum creatinine often signifies a substantial reduction in GFR in younger individuals
d.Relying on serum creatinine concentration is sufficient to stage chronic kidney disease (CKD)
b.Mean GFR is lower in women than in men
Which of the following disorders in CKD is associated with low bone turnover with low or normal parathyroid hormone (PTH) levels?
a.Osteitis fibrosa cystica
b.Secondary hyperparathyroidism
c.Osteomalacia
d.Adynamic bone disease
d.Adynamic bone disease
A: high PTH
B: High PTH
C: dec Vit D
A 45-year-old male with hypertension, dyslipidemia and chronic kidney disease (CKD) diagnosed 5 years ago consulted for chest pain. On examination, he was noted to be pale and edematous, with a BP of 170/100. Which of the following is considered a CKD-related risk factor for ischemic vascular disease?
a.Hypertension
b.Hypervolemia
c.Dyslipidemia
d.Anemia
d.Anemia
Non traditional risk factors
Anemia
Hyperphosphatemia
Hyperparathyroidism
Inc FGF 23
Sleep apnea
Systemic inflammation
A 34 year old male with hypertension and CKD presents his renal ultrasound result showing a discrepancy of >1 cm in kidney length. What is your next step?
a.Perform Doppler sonography
b.Repeat imaging after 3 months
c.Start Enalapril 10 mg BID
d.Perform a kidney biopsy
a.Perform Doppler sonography
r/o renal artery stenosis
Among the calcium channel blockers, which of the following may exhibit superior antiproteinuric and renoprotective effects:
a.Verapamil
b.Amlodipine
c.Nifedipine
d.Felodipine
a.Verapamil
NON-DHP better
Which of the following is considered the most common opportunistic infection in renal transplant patients within the peri-transplant period (<1 month)?
a. Herpes virus
b. Legionella
c. Nocardia
d. Viral hepatitis
a. Herpes virus
The progression of ADPKD has striking variability. End-stage renal disease (ESRD) typically occurs in late middle age. Risk factors include which of the following:
a.Hypertension
b.Small kidney size
c.Microscopic hematuria
d.Late diagnosis of ADPKD
a.Hypertension
Which of the following DOES NOT characterize persistent or significant hematuria?
a.>3 RBCs/HPF on three urinalyses
b.Single urinalysis with >100 RBCs
c.Single positive dipstick for hematuria
d.Gross hematuria
c.Single positive dipstick for hematuria
What is the dominant mechanism of metabolic acidosis in CKD?
a.Decreased ammonia production
b.Hyperkalemia
c.Decrease in HCO3 excretion
d.Hyperchloremia
a.Decreased ammonia production
Dec ammonia excretion –> inc retention of organic acids
Which of the following explains the mechanism of the effectiveness of angiotensin converting enzyme inhibitors and angiotensin II receptor blockers in reducing proteinuria?
a. Decreasing K secretion
b. Improves insulin resistance
c. Maintenance of MAP <90 mmHg
d. Reducing glomerular hypertension
d. Reducing glomerular hypertension
he first step in the diagnostic evaluation of hyper- or hypocalcemia is to:
a.Ensure that the alteration is not due to abnormal albumin concentrations
b.Ensure adequate hydration of the patient
c.Determine the baseline renal function
d.Rule out other electrolyte abnormalities
a.Ensure that the alteration is not due to abnormal albumin concentrations
Which of the following is TRUE about or is expected of laboratory tests in the setting of uremia?
a.Slow but steady rise of serum urea and potassium levels
b.Low to normal fibrinogen and ESR
c.Elevated levels of CRP
d.High serum albumin
c.Elevated levels of CRP
a. rises progressively
b. inc
d. low
Which of the following is TRUE regarding the stages of CKD?
a.Stages 1 to 3 CKD are usually asymptomatic
b.Majority of elderly patients in stage 2 or 3 CKD are stable and do not progress
c.Majority of the population would require screening for CKD stage because of the lack of symptoms
d.Clinical and laboratory complications become prominent at Stage 5 CKD
b.Majority of elderly patients in stage 2 or 3 CKD are stable and do not progress
What is the cell of origin of clear cell carcinoma?
a.Proximal tubule
b.Distal tubules
c.Cortical collecting duct
d.Medullary collecting duct
a.Proximal tubule
What is the standard management for stage I or II renal cell tumors?
a.Nephrectomy
b.Interferon-A adjuvant therapy
c.Chemotherapy
d.Radiotherapy
a.Nephrectomy
A 27 year old female medical student spent her afternoon in a 2-hour cycling session. She felt immense pain on both thighs the following day, prompting ER consult. She related a decrease in urine output for the past 6 hrs. On urinary catheterization, dark urine was drained. Tests revealed elevated creatinine and creatine kinase. The following are mechanisms of action that contributed to her acute kidney injury EXCEPT?
a. Tubular obstruction due to heme pigment casts
b. Volume depletion resulting in renal ischemia
c. Tubular injury from free chelatable iron
d. Immune deposition resulting in glomerulonephritis
d. Immune deposition resulting in glomerulonephritis
All of the following patients with recurrent UTI need further screening for urologic abnormalities EXCEPT: (Philippine CPG on the Diagnosis and Treatment of UTI in Adults. 2015 Update. Part 2. P23)
a.Persistent microscopic hematuria
b.Elevated serum creatinine
c.History of pyelonephritis
d.Multiple sexual partners
d.Multiple sexual partners
Conditions that may cause false positive hydronephrosis on ultrasound
Diuretics
Renal cysts
Extra renal pelvis
Conditions that may cause false negative hydronephrosis on ultrasound
Obstruction with volume contraction
Staghorn calculi
Retroperitoneal fibrosis
Infiltrative renal dse
The kidneys are unlikely to recover if complete obstruction is ___ weeks duration
8
A 32- year- old female is brought to the ER due to a two- week- history of progressive weakness, fatigue, increased sleeping time, nausea and headache. She was diagnosed with Papillary thyroid carcinoma a year prior and underwent total thyroidectomy and RAI but was lost to followup. Serum Na is 102mmo/L, K is 3.0mmol/L, TSH is 10.5mIU/L, and Tg is 2.1 ng/ml. What is the most likely cause of her symptoms?
A. SIADH
B. Metastatic recurrence of thyroid carcinoma to the brain
C. Hypothyroidism
D. Pituitary adenoma
C. Hypothyroidism
Which of the following is part of the commonly accepted criteria for initiating maintenance dialysis in patients with chronic kidney disease:
A. Bleeding diathesis
B. Hyponatremia unresponsive to conservative measures
C. Creatinine clearance 10-14 mL/min per 1.73m2
D. Hyperphosphatemia refractory to medical therapy
A. Bleeding diathesis
A 54 year old male patient diagnosed with small cell lung cancer underwent induction chemotherapy with Cisplatin + Etoposide. A few days later, he complained of decreasing urine output, tea colored-urine and rising creatinine levels. Which of the following is true about his condition?
A. Eosinophilia is present
B. FeNa <1%
C. Urinary myoglobin levels are elevated
D. Granular casts may be present
D. Granular casts may be present
The patient presents with acute kidney injury (AKI) after receiving Cisplatin + Etoposide for small cell lung cancer. His symptoms—decreasing urine output, tea-colored urine, and rising creatinine—suggest acute tubular necrosis (ATN), a common nephrotoxic effect of Cisplatin
Muddy brown granular casts are a hallmark finding in acute tubular necrosis (ATN), which is the most common cause of intrinsic AKI due to nephrotoxic agents like Cisplatin.
A 54/F, diagnosed hypertensive, maintained on Amlodipine 10mg once a day, complained of progressive dyspnea on exertion and generalized body weakness. There was also associated progressive edema starting at the ankles ascending up to the knee. At the clinic, you noticed that the left leg is markedly swollen, erythematous and tender compared to the right. Her BP is 160/100, HR100, RR-25, sats-92% on room air. Her CBC showed anemia (9.5 g/dL). Urinalysis showed: amber colored, specific gravity 1.020, protein +++, RBC 2-3/hpf, WBC 0-1/hpf. What is the most likely underlying renal pathology?
A. Minimal Change Disease
B. Membranous Glomerulonephritis
C. Focal Segmental Glomerulosclerosis
D. Ligh-chain deposition disease
B. Membranous Glomerulonephritis
MGN = most common cause of nephrotic syndrome in elderly
Highest reported renal vein thrombosis, DVT and PE
20-30% assoc with malignancy
A 24 year-old man presented to the emergency room with severe rightsided flank pain that radiates to the inguinal area. It was accompanied by nausea, vomiting and diaphoresis. Upon arrival at the ER, he was in distressing pain, only controlled with administration of intravenous fentanyl. A noncontrast CT scan of the KUB revealed a 0.5cm hyperdense calculi located at the distal 1/3 of the ureter. After 3 days, the patient was able to pass the calculi spontaneously. He was very concerned about recurrence of the stone, and expressed willingness for an extensive workup.
Which of the following tests in a 24-hour urine collection isrecommended for his case:
A. Total protein
B. Total glucose
C. Total bilirubin
D. Total creatinine
D. Total creatinine
After an episode of nephrolithiasis (kidney stones), a 24-hour urine collection is recommended to assess metabolic abnormalities and help prevent recurrence. One of the most crucial tests in the 24-hour urine collection is total creatinine, which serves as a marker of urine collection adequacy.
Additional Tests Recommended in 24-Hour Urine Collection for Nephrolithiasis:
Urinary Volume (goal: >2.5 L/day to prevent stones)
Calcium (hypercalciuria is a major risk factor for calcium oxalate/phosphate stones)
Oxalate (hyperoxaluria promotes calcium oxalate stone formation)
Citrate (a natural stone inhibitor; low levels increase risk)
Uric Acid (associated with uric acid and calcium stones)
Sodium (high sodium intake increases calcium excretion)
pH (acidic urine favors uric acid stones; alkaline urine favors calcium phosphate stones)
Analysis of the stone revealed majority of the stone is compose of calcium oxalate. Which of the following statements is true regarding management?
A. Low calcium diet is recommended
B. A loop diuretic is recommended to substantially lower urine calcium excretion
C. Reduction of sodium intake to <2.5g/day may reduce urinary excretion of calcium
D. Sodium bicarbonate may alkalize the urine and decrease stone formation
C. Reduction of sodium intake to <2.5g/day may reduce urinary excretion of calcium
A: not recommended
B: thiazide
D. CaOx not affected by pH
A 59-year-old man, hypertensive maintained on Amlodipine 10mg daily, and diagnosed with chronic hepatitis B, consults you for progressive dyspnea on exertion and generalized body weakness. You also elicited a history of progressive edema starting at the ankles ascending up to the knee since 2 weeks ago. You noticed that the left leg is markedly swollen, erythematous and tender compared to the right. BP is 160/100, HR-100, RR-25, sats-92% on room air. CBC showed anemia (9.5 g/dL). Urinalysis: amber colored, specific gravity 1.020, protein +++, RBC 20-30/hpf, WBC 0-1/hpf. If you are considering a renal disease, what is the most likely underlying renal pathology?
a. Minimal Change Disease
b. Membranous Glomerulonephritis
c. Focal Segmental Glomerulosclerosis
d. Light-chain deposition disease
b. Membranous Glomerulonephritis
three most common types of kidney disease resulting from HBV infection are:
●Membranous nephropathy
●Membranoproliferative glomerulonephritis (MPGN) ●Polyarteritis nodosa (PAN)
A 64-year-old male diabetic and hypertensive, has been admitted for last five days due to fungemia and is being treated with Amphotericin B. PE findings are as follows: weight 70kg, BP 130/90 mmHg, heart rate 94 bpm, RR 24 breaths/min, Temp 36.8OC, crackles at both bases, and grade 1 bipedal edema. Urine output was 2520mL in 24 hours. CBG range is 109-110mg/dL His serum creatinine was noted to have increase from 1.2mg/dL to 2.4mg/dL, while his serum magnesium was low. What other clinical features can be expected from this type of acute kidney injury?
a. Oliguria, hypocalcemia, and non-gap metabolic acidosis
b. Oliguria, hypokalemia, and non-gap metabolic acidosis
c. Polyuria, hypocalcemia, and non-gap metabolic acidosis
d. Polyuria, hypokalemia, and non-gap metabolic acidosis
d. Polyuria, hypokalemia, and non-gap metabolic acidosis
DIAGNOSIS: drug induced (amphotericin B) intrinsic AKI
● Non-oliguric (polyuria), FeNa > 1%, nephrogenic DI
● Hypokalemia due to renal K wasting
● NAGMA from distal RTA (type 1)
● Na and Mg wasting
A 28-year-old male came in due to history of hematuria. This was already his fourth episode. Urinalysis showed albumin +2, RBC 10-15/hpf. Renal biopsy was done revealing an immunofluorescent pattern of IgA. Which is correct about his case?
a. Acute renal failure and a rapidly progressive disease is expected
b. Complete remission is rare and will usually require lifetime immunosuppressive therapy
c. Monitoring of persistent proteinuria provides the greatest predictive power for adverse renal outcomes
d. There is high risk to develop ESRD within 6 months
Monitoring of persistent proteinuria provides the greatest predictive power for adverse renal outcomes
DIAGNOSIS: IgA nephropathy
● aka Berger’sdisease
● Most common cause of GN
a. Acute renal failure and a rapidly progressive disease is expected - slowly progressive disease over decades
b. Complete remission is rare and will usually require lifetime immunosuppressive therapy common but may still progress to ESRD over time if HTN, proteinuria not controlled
c. Monitoring of persistent proteinuria provides the greatest predictive power for adverse renal outcomes - higher proteinuria, lower eGFR and higher uric acid are independent risk factors for the development of ESRD in patients with IgA nephropathy
d. There is high risk to develop ESRD within 6 months - 50% of patients can develop ESRD within 30 yrs.
A 36-year-old female with no known co-morbidities came to the OPD complaining of 2-week history of progressive bipedal edema which started from the ankles, now extending to mid-thighs. She claims that she has tea-colored, frothy urine and headaches. On PE, BP is 150/80, HR 87, RR 24, T 36.7C. Which laboratory test finding is consistent with the patient’s diagnosis?
a. Anemia
b. High urine protein/creatinine ratio
c. Low total cholesterol
d. Normal albumin
b. High urine protein/creatinine ratio
DIAGNOSIS: GN
Significant proteinuria (>500 mg/day) is a hallmark of GN.
In which of the following cases is kidney biopsy generally contraindicated?
a. A 28-year-old APAS patient with BP of 120/80
b. A 34-year-old female SLE with hemoglobin of 9.8
c. A 57-year-old female with recurrent UTI with scarring of kidney
d. A CKD 3 patient with HBa1c 12%
c. A 57-year-old female with recurrent UTI with scarring of kidney
Active UTI - contraindication
Scarred kidneys = Contraindication
A 25-year-old female came in due to fatigue and malaise. Repeated urinalysis showed albumin +++, RBC 20-30, WBC 30-40. Renal biopsy was requested revealing mesangial proliferation with lobular segmentation and tram tracking. Which management will benefit this patient?
a. ACE inhibitor
b. Cyclophosphamide
c. Dipyridamole
d. Eculizumab
a. ACE inhibitor
DIAGNOSIS: MPGN Type I MPGN, the most proliferative of the three types, shows mesangial proliferation with lobular segmentation on renal biopsy and mesangial interposition between the capillary basement membrane and endothelial cells, producing a double contour sometimes called tram-tracking
An 18-year-old male developed muscle weakness and cramps of the lower extremities. BP 90/60. Serum K = 2.7meq/L, urine K = 10mmol/day. Thyroid function is normal. Serum HCO3 is 18. The hypokalemia is most likely due to:
a. Extrarenal loss of potassium
b. Gitelman’s syndrome
c. Hyperaldosteronism
d. Renal potassium wasting
a. Extrarenal loss of potassium
If urine K < 15= extrarenal losses
32 year old female, previously well, consults for persistent bilateral ank pains. She has been complaining of occasional dysuria with feeling of incomplete voiding the past 2 weeks. She has no signicant past medical conditions with no maintenance medications. Vital signs are stable and physical examination reveal tenderness on both CV angles. Initial laboratory results show: Crea 1.2 mg/dl (nv 0.7-1.3) Na 140 mmol/L (nv 8.5-10.2) Albumin 41 Intact PTH 250 pg/ml (nv 15-65) Vitamin D 22 ng/mL (nv 30-50) Uric acid 7.2 mg/dl (nv 3.5-7.1) CBC Hb 130 WBC 11,500 (seg 82, lym 16) K 3.9 mmol/L Platelet ct 380,000 Ca 12 mg/dl Urinalysis: SG 1.015, pH 6.5, no glucose, trace protein, +4 blood, +2 leukocytes, +2 nitrites, 50-100 rbc/hpf, 20-50 wbc/hpf, calcium crystals many Abdominal CT scan shows nephrocalcinosis in both kidneys with bilateral nonobstructing nephrolithiasis and ureterolithiasis. Which of the following is the most appropriate step?
a. Start allopurinol 300mg/tab 1 tab 1xd
b. Start Vitamin D3 2000 iu/cap 1 cap 1xd
c. Start hydrochlorothiazide 25mg/tab 1 tab 1xd
d. Start potassium citrate 30meq 1xd
c. Start hydrochlorothiazide 25mg/tab 1 tab 1xd
This strongly suggests Primary Hyperparathyroidism (PHPT), the most common cause of hypercalcemia with kidney stones.
Thiazide diuretics (e.g., HCTZ) reduce calcium excretion in urine by increasing calcium reabsorption in the distal tubule.
Prevents further calcium stone formation in PHPT.
Beneficial in hypercalciuria-related nephrolithiasis.
20 year old female with SLE complaining of “bubbly” urine. She denies dysuria, oliguria or fever. She is maintained on prednisone 5mg OD. Vital signs as follows: BP 160/90 mmHg, HR 92bpm, RR 20 cpm, Temp 37.4C with O2 99%. Systemic finding show grade 1 to 2 bipedal edema.
Labs show Crea 1.1 mg/dl (nv 0-.7-1.3)
Na 140 mmol/L K 4.1 mmol/L
CBC Hb 108 WBC 10,500 (seg 65, lym 28) Plt count 108,000
Urinalysis: cloudy, +2 protein, +4 blood, trace leukocytes, RBC >100/hpf, WBC 3- 5/hpf, many RBC casts
Kidney biopsy shows: mesangial proliferation with note of hypercellularity with expansion of mesangial matrix What is the next best step?
a. Start losartan and diuretic medications and observe
b. Increase prednisone to 60mg BID
c. Shift prednisone to high dose intravenous methylprednisolone pulse therapy
d. Start oral cyclophosphamide
a. Start losartan and diuretic medications and observe
Class II Lupus nephritis. No need for immunosuppresants and steroids
Which clinical scenario warrants a kidney biopsy?
a. 20/F with gross hematuria, dysuria, frequency of 1 day duration. Urinalysis show turbid urine with 30-50 RBCs and WBCs TNTC
b. 68/F diabetic of 20 years with pedal edema, bubbly urine, and new onset hypertension. Urinalysis show +3 proteinuria, RBC 1-3/hpf and WBC 3-5/hpf
c. 35/F, previously well with episodic gross hematuria after bouts of sore throat. Urinalysis show +3 protein, RBC TNTC/hpf, WBC 3-5/hpf, many casts
d. 40/F G1P0 28 weeks AOG complaining of headache with new onset hypertension and bipedal edema. Urinalysis show +4 protein, trace blood, trace leukocytes, RBC 3/hpf, WBC 5/hpf
c. 35/F, previously well with episodic gross hematuria after bouts of sore throat. Urinalysis show +3 protein, RBC TNTC/hpf, WBC 3-5/hpf, many casts
A kidney biopsy is warranted when there is suspicion of an underlying glomerular disease that requires histologic diagnosis for appropriate management.
The 35-year-old female with episodic gross hematuria after sore throat and significant proteinuria, RBCs TNTC, and many casts raises suspicion for IgA Nephropathy (Berger’s Disease) or Post-Streptococcal Glomerulonephritis (PSGN). A biopsy is necessary to confirm the diagnosis and guide management.
A 45 year old male, known type 2 diabetes mellitus for 5 years, is noted to have consistent microalbuminuria for the last 3 medical consultations. Which of the following is he MOST at risk for?
a. Cardiovascular complications
b. End stage renal disease
c. Hepato-renal syndrome
d. Complicated urinary tract infections
a. Cardiovascular complications
A 24 year old male residing in Payatas Quezon City complains of acute hemoptysis over the past week. He has been previously well with no drug history. He is a 3 pack year smoker. He also lives with his father who is taking anti-koch’s medication via DOTS for the past 2 months. Vital signs: BP 120/80 HR 72bpm, RR 26 cpm, temp 38.5C with O2 93%. Urinalysis shows +4 blood with rbc TNTC and many red blood cell casts. Which of the following is the most likely etiology?
a. Acute disseminated tuberculosis
b. Renal cell carcinoma with lung metastasis
c. Goodpasture disease
d. IgA nephropathy
c. Goodpasture disease
Goodpasture since with hemoptysis and kidney involvement
A 20 year old male college student consults for decreasing urine output, tea- colored urine and bipedal edema. He denies any previous medical condition except for impetigo 3 weeks ago. On PE, BP 160/90, HR 114bpm, RR 26 cpm, with note of periorbital and bipedal edema and scabs on all extremities. What is the classic nding expected in his urinalysis?
a. Muddy brown casts
b. Hyaline casts
c. Nephrotic range proteinuria
d. Red blood cell casts
d. Red blood cell casts
Dx: PSGN –> nephritic syndrome
a. Muddy brown casts —> ATN
b. Hyaline casts are non-specific and can be found in normal individuals, dehydration, or mild kidney disease.
C. Nephrotic range proteinuria is rare
A 25-year-old woman, previously healthy, is admitted for severe body weakness. She has been having diarrhea and vomiting for the last two days. On admission, vital signs taken are as follows: Temp = 37.1C, BP=80/60, HR=110bpm, RR=22/min. She has faint pulses and poor skin turgor. Her serum creatinine was 2.4mg/dL. Which of the following is most diagnostic of the underlying renal injury?
a. BUN/Creatinine ratio less than 20
b. Fractional excretion of sodium less than 1%
c. Urine Osmolality less than 500 mOsm/kg
d. Repeat serum creatinine after adequate hydration and with normal BP
d. Repeat serum creatinine after adequate hydration and with normal BP
Response to restoration of hemodynamics = diagnostic of pre renal
A 55-year-old woman was admitted for severe community-acquired pneumonia. After initial blood draw, she was started on Cefepime + Amikacin. Her baseline serum creatinine was 0.6mg/dL. Over the next 5 days, she was normotensive with resolution of fever. Urine output was sustained at around 1.5 to 2 liters per day. Repeat serum creatinine on her 5th hospital day was noted to be increased at 3.2mg/dL. What is a common finding given the likely diagnosis of azotemia?
a. Low FeNa
b. Hypomagnesemia
c. Hypocalcemia
d. Nongap metabolic acidosis
b. Hypomagnesemia
Aminoglycosides can cause renal magnesium wasting, leading to hypomagnesemia.
A 55-year-old man, admitted for shortness of breath, has a large mediastinal mass on chest Xray. A Chest CT scan with IV contrast was done. 3 days later, a routine blood examination showed a serum creatinine of 2.6 mg/dL. His serum creatinine on admission was 1.1 mg/dL. He has good urine output with normal vital signs during his connement. Which of the following likely contributes to the mechanism of the patient’s acute azotemia?
a. Thrombotic microangiopathy
b. Efferent arteriolar vasodilation due to loss of Angiotensin II activity
c. Afferent renal vasoconstriction due to prostaglandin depletion
d. Small vessel occlusion causing hypoxia in the renal outer medulla
d. Small vessel occlusion causing hypoxia in the renal outer medulla
Contrast-induced nephropathy (CIN) is caused by renal medullary hypoxia due to small vessel occlusion.
Mechanism:
Renal vasoconstriction → Contrast agents cause endothelial dysfunction, leading to reduced nitric oxide and increased endothelin, resulting in medullary ischemia.
Direct tubular toxicity → Contrast media damages tubular cells, increasing oxidative stress.
Ischemia of the renal outer medulla → The medulla is highly vulnerable to hypoxia, as it already functions in a low-oxygen environment.
Among patients receiving aggressive uid resuscitation for extensive uid losses, a decrease in renal output with rise in serum creatinine may indicate which complication of management?
a. Renal vein compression
b. Acute pulmonary congestion
c. Loss of counterregulatory mechanisms
d. Acute tubular injury
a. Renal vein compression
A 58-year-old man, with known diabetes and hypertension has the following laboratory results:
ABG: pH=7.30, pCO2=30 mmHg, HCO3=15 mmol/L
Serum Na = 136 mmol/L
Serum K =5.8 mEq/L
Serum Cl=115 mEq/L
Blood glucose = 128mg/dL Serum creatinine: 1.4mg/dL
These laboratory ndings are consistent with which of thefollowing?
a. Hyporeninemic hypoaldosteronism
b. Hypertensive nephrosclerosis
c. Proximal renal tubular acidosis
d. Distal renal tubular acidosis
a. Hyporeninemic hypoaldosteronism
C and D should have low K. Only Type 4 RTA has high K
A 35-year-old male was stabbed multiple times by an unknown assailant and was brought to the emergency department. On assessment, he was actively hemorrhaging, lethargic, with the following vital signs: BP 70/50 mmHg, HR 120 bpm, RR 12 cpm. He had a feeble pulse and peripheral cyanosis.
Which is a true statement on this case?
a. The osmotic threshold for AVP release is reduced.
b. The slope of the AVP response curve to osmolality is
decreased.
c. There is a reduction in the sensitivity of circulating AVP levels
to osmolality.
d. Serum Na+ is the sole determinant of AVP levels
a. The osmotic threshold for AVP release is reduced.
A 70-year-old male was brought to the ED due to changes insensorium. Work-up revealed: serum Na+ 118 mEq/L, BUN 65 mg/dL, random blood sugar 108 mg/dL. What is the computed serum osmolality?
a. 235 mOsm/kg H2O
b. 245 mOsm/kg H2O
c. 255 mOsm/kg H2O
d. 265 mOsm/kg H2O
d. 265 mOsm/kg H2O
2 Na + (BUN /2.8 )+ gluc/18
A 35 y/o HIV patient developed weakness and hypotension after stopping ketoconazole therapy for a fungal infection. Serum potassium was 6.4 mmol/l. What are the expected TTKG pre and
post fludrocortisone challenge?
a. TTKG <5 presteroid and > 8 post steroid
b. TTKG < 5 presteroid and < 8 post steroid
c. TTKG > 8 presteroid and no change post steroid
d. TTKG > 8 presteroid and < 8 post steroid
a. TTKG <5 presteroid and > 8 post steroid
Adrenal Insufficiency (Likely Primary Adrenal Insufficiency due to Ketoconazole Withdrawal in an HIV Patient)
This 35-year-old HIV patient developed weakness, hypotension, and hyperkalemia (K+ = 6.4 mmol/L) after stopping ketoconazole therapy.
Ketoconazole is a potent inhibitor of adrenal steroidogenesis, particularly cortisol and aldosterone synthesis.
What is the Corrected Anion Gap of this patient with the following labs?
Na: 150, Cl: 113, HCO3 11, Serum albumin: 2.5 g/dl ( nv of 4.5g/dl)
a. 21 b. 26 c. 31 d. 34
c. 31
AG = 150 - (113+11) = 26
corrected anion gap = AG + 2.5 x (4.5-2.5) –> 31
What is the mechanism of Vancomycin in causing acute
kidney injury?
a. Tubular membrane pore formation
b. Direct tubular injury by reactive oxygen species
c. Intratubular obstruction
d. Interstitial inflammation
c. Intratubular obstruction
Several antimicrobial agents are commonly associated with AKI. Vancomycin may be associated with AKI from tubular injury, particularly when trough levels are high and when used in combination with other nephrotoxic antibiotics. Vancomycin can also crystalize in tubules and cause intratubular obstruction
What is a reliable sign of hypovolemia in an adult patient?
a. Increased jugular venous pressure
b. 20 mmHg systolic blood pressure drop on sitting up
c. 30 bpm increase in HR on standing up
d. Dry oral mucosa
c. 30 bpm increase in HR on standing up
HYPOVOLEMIA
On examination, diminished skin turgor and dry oral mucous membranes are less than ideal markers of a decreased ECFV in adult patients; more reliable signs of hypovolemia include:
● a decreased jugular venous pressure (JVP)
● Orthostatic tachycardia (an increase of >15–20 beats/min upon standing)
● orthostatic hypotension (a >10–20 mmHg drop in blood pressure on standing)
In a patient with milk alkali syndrome, what is the likely mechanism for metabolic alkalosis?
a. Increase bicarbonate load
b. Gastrointestinal bicarbonate loss
c. Renal bicarbonate loss
d. Decrease hydrogen absorption
a. Increase bicarbonate load
JR, 77 years old male is being treated for hyponatremiafrom chronic diuretic use. Baseline serum Na was 107 mEqs/L.After 6hrs of correction with PNSS, serum Na was 128 mEqs/L. After 24 hrs, he developed diplopia and dysarthria that progressed to loss of consciousness. What is the possible
explanation of this condition?
a. Immune mediators entering the blood brain barrier
b. Thrombosis in middle cerebral artery
c. Hemorrhage in the pons and medulla
d. Apoptosis of neurons in the cerebellum
a. Immune mediators entering the blood brain barrier
Brain cells accommodate to a chronic increase in ECF osmolality (>48 h) by activating membrane transporters that mediate influx and intracellular accumulation of organic osmolytes (creatine, betaine, glutamate, myoinositol, and taurine); this results in an increase in ICF water and normalization of brain parenchymal volume
What is the mechanism of hypokalemia in magnesium deficiency?
a. Excitatory activity on muscle Na K ATPase
b. Increase in ENaC activity
c. Intracellular block of K efflux through the secretory K channel
d. Apoptosis of ROMK containing cells
c. Intracellular block of K efflux through the secretory K channel
HR, a 28-year-old female, presented with a 1-month history of progressive oedema. On examination, she was seen to have elevated blood pressure, distended abdomen with positive fluid wave on palpation, and grade 2 bipedal pitting oedema. Renal biopsy revealed focal and segmental scarring, most prominent in the glomeruli obtained from the corticomedullary junction. Increased incidence of this condition is most commonly associated with podocytic polymorphisms of which gene?
a. APOL1
b. NPHS1
c. NPHS2
d. TRPC6
a. APOL1
. TS, a 58-year-old diabetic male who has been on oral hypoglycemics for at least 8 years, consulted for a 4-month history of persistent bipedal oedema. Physical examination revealed normal blood pressure, but with periorbital and grade 2 bipedal pitting oedema. Diagnostic tests revealed a serum creatinine level of 2.9 mg/dL, and a spot urine albumin/creatinine ratio of 1442.8 mg/g. Which of the following statements regarding urine assays for proteinuria is accurate?
a. Dipstick evaluation detects the most acidic proteins, including those with a higher isoelectric point, such as albumin.
b. Microalbuminuria can be detected by a urinary dipstick protein analysis.
c. The ratio of total protein concentration to creatinine concentration is specific to albumin excretion, and excludes light-chain proteins.
d. Urine albumin or total protein should be normalized to urine creatinine concentration in order to discount the effects of urinary dilution or concentration.
d. Urine albumin or total protein should be normalized to urine creatinine concentration in order to discount the effects of urinary dilution or concentration.
A. Dipstick evaluation detects ONLY ALBUMIN, and gives FALSE-POSITIVE results at pH >7.0
B. Microalbuminuria IS BENEATH DETECTION by a urinary dipstick protein analysis.
C. The ratio of total protein concentration to creatinine concentration is NOT specific to albumin excretion, and MAY INDICATE light-chain proteins
MC, a 51-year-old female, consulted for severe right flank pain, radiating to the right labial area. This was accompanied by gross hematuria. A presumptive diagnosis of urolithiasis was made. Based on the initial presentation, and epidemiologic data, an imaging study would most likely show a stone lodged in which area?
a. Distal ureter
b. Proximal ureter
c. Renal pelvis
d. Urinary bladder
a. Distal ureter
BG, a 41-year-old male, was recently admitted for azotemia, proteinuria, and hematuria. History was unremarkable, apart from a recent travel to a malaria-endemic area. A kidney biopsy was done, consistent with mesangioproliferative glomerulonephritis. This finding is most consistent with:
a. Plasmodium falciparum malaria
b. Plasmodium malariae malaria
c. Plasmodium ovale malaria
d. Plasmodium vivax malaria
a. Plasmodium falciparum malaria
SG, a 27-year-old male, consulted for left flank pain, nausea and vomiting, low-grade fever with chills, and gross hematuria. Physical examination revealed some signs of dehydration, with direct tenderness over the left lower back. Diagnostic examination showed gross and microscopic pyuria, along with leukocytosis and neutrophilia. A non-obstructing stone, with a widest diameter of 0.9 cm, was seen in the left renal pelvis on sonogram. Which of the following suggests an indication for urologic intervention?
a. Concurrent urinary tract infection
b. Flank pain and tenderness
c. Nausea and vomiting, with dehydration
d. Renal stone > 0.5 cm in size
a. Concurrent urinary tract infection
RB, a 50-year-old male patient with chronic tophaceous gout, consulted for sonogram findings of non-obstructing bilateral nephrolithiases. He has been experiencing tolerable lower back pains, associated with position and movement. His urinalysis showed a pH of 5.0. What is the best initial pharmacologic management in this case?
a. Potassium citrate
b. Prophylactic antibiotics
c. Sambong supplementation
d. Tiopronin
a. Potassium citrate
JF, a 67-year old male, has been on heart failure medications for ischemic cardiomyopathy. On his latest series of consultations, the cardiologist noted progressive increase in his serum creatinine levels, translating into a steady decline in renal function. Which of the following statements is accurate regarding his condition?
a. Decreased intraabdominal pressure and abdominal congestion correlate with renal dysfunction.
b. Neurohormonal activation and release of arginine vasopressin has the most impact in reduced eGFR in cardiorenal syndrome.
c. Systemic venous congestion with decreased backward pressure plays a crucial role in cardiorenal syndrome
d. This is a consequence of reduced cardiac output in heart failure.
c. Systemic venous congestion with decreased backward pressure plays a crucial role in cardiorenal syndrome
GB, a 52-year-old diabetic male, was rushed into the ER for progressive angina for more than 24 hours,unrelieved by rest and nitrates. Review of history showed previously normal renal indices on his clinic visit less than a month ago. Initial PE showed an obese
male with an actual body weight of 110 kg, diaphoretic, with cold, clammy hands, hypotension, and tachycardia. Baseline laboratory tests in the ER revealed azotemia and markedly high urine specific gravity. The first 4hours were marked by a urine output of less than 30 cc/hour. Which of the following is a microvascular eventthat might have contributed to his renal condition atinitial presentation?
A. Diminished leukocyte endothelial adhesion.
B. Enhanced vasodilation in response to nitric oxide.
C. Impaired arteriolar vasodilation in response to Angiotensin I.
D. Significant endothelial and vascular smooth musclecellular damage
D. Significant endothelial and vascular smooth muscle
cellular damage
which of the following compensatory mechanisms is/are responsible for
maintaining normal glomerular filtration in the early phase of renal injury?
A. Arteriolar dilatation resulting from myogenic reflex in the setting of low perfusion pressure.
B. Capillary endothelial hypertrophy secondary to release to tissue growth factors.
C. Nitric oxide-mediated increase in intraglomerular pressure via afferent arteriolar dilatation.
D. Reflex afferent arteriolar constriction and efferent arteriolar dilatation
A. Arteriolar dilatation resulting from myogenic reflex in thesetting of low perfusion pressure.
Normal GFR is maintained in part by renal blood flow and the relative resistances of the afferent and efferent renal arterioles, which determine the glomerular plasma flow rate and the transcapillary hydraulic pressure gradient that drive glomerular ultrafiltration.
Mild degrees of hypovolemia and reductions in cardiac output elicit compensatory renal physiologic changes…. Mediators of this response include angiotensin II, norepinephrine, and vasopressin (also termed antidiuretic hormone). Glomerular filtration can be maintained despite reduced renal blood flow by angiotensin II–mediated renal efferent vasoconstriction, which maintains glomerular capillary hydrostatic pressure closer to normal and thereby prevents marked reductions in GFR if renal blood flow reduction is not excessive.
In addition, a myogenic reflex within the afferent arteriole leads to dilation in the setting of low perfusion pressure, thereby maintaining glomerular perfusion. Intrarenal biosynthesis of vasodilator prostaglandins (prostacyclin, prostaglandin E2), kallikrein and kinins, and possibly nitric oxide (NO) also increases in response to low renal perfusion pressure.
Which of the following patient and intervention variables would play an important role in the risk stratification for contrast- induced acute kidney injury
A. Albumin level prior to procedure
B. Blood urea nitrogen level
C. Hematocrit
D. Type of contrast agent
C. Hematocrit
which of the following nutritional recommendations has the most robust clinical evidence, and may therefore be advised to your aforementioned patient with CKD?
A. Adopt a healthy and diverse diet, with equal consumption of plant- and animal-based proteins.
B. Maintain a protein-intake of 0.8 g/kg body weight/day.
C. Sodium intake should be restricted to < 2 g of sodium chloride per day.
D. Strict adherence to a very low protein diet supplemented by ketoacid analogs of branched chain amino acids.
B. Maintain a protein-intake of 0.8 g/kg body weight/day.
The ADA suggests a protein intake of 0.8 mg/kg of body weight/day in individuals with diabetic kidney disease. Compared with higher levels of dietary protein intake, this level slowed GFR decline with evidence of a greater effect over time. Higher levels of dietary protein intake (>20% of daily calories from protein or >1.3 g/kg/day) have been associated with increased albuminuria, more rapid kidney function loss, and CVD mortality and therefore should be avoided.
BR, a 66-year-old male diabetic diagnosed with CKD checks in at the clinic for a routine follow-up. He reports no symptoms, but presents laboratory results as follows: eGFR of 22 ml/min/1.73 m2 (CKD-EPI 2021), HbA1c of 8%, arterial blood pH of 7.33, with a bicarbonate of 19 mmol/L, and serum potassium of 5.5 mmol/L. Which of the following is the most appropriate initial management to address the metabolic acidosis?
A. Advise a protein-restricted diet to reduce acid burden.
B. Discontinue his on-board potassium- sparing diuretic.
C. Initiate oral sodium bicarbonate supplementation.
D. Start insulin therapy
B. Discontinue his on-board potassium- sparing diuretic.
Metabolic acidosis is a common disturbance in CKD. The majority of patients can still acidify the urine, but they produce less ammonia and, therefore, cannot excrete the quantity of protons required to maintain acid-base balance in most diets. Hyperkalemia, if present, further depresses ammonia production. In most patients, the metabolic acidosis is mild; the pH is rarely <7.32 and can usually be corrected with oral sodium bicarbonate supplementation.
Secondary hyperparathyroidism secondary to chronic kidney disease is best addressed by:
A. Avoidance of lanthanum to prevent calcium deposits in the vascular endothelium
B. Dietary calcium restriction and reasonable phosphate intake
C. Low dietary phosphate intake and use of sevelamer
D. Surgical resection of the parathyroid glands
C. Low dietary phosphate intake and use of sevelamer
Secondary hyperparathyroidism (SHPT) in chronic kidney disease (CKD) occurs due to elevated phosphate levels, decreased calcium, and low calcitriol (active vitamin D).
Phosphate retention stimulates parathyroid hormone (PTH) secretion, worsening bone disease and vascular calcifications.
Managing SHPT in CKD involves controlling phosphorus levels to reduce PTH stimulation.
The optimal management of secondary hyperparathyroidism and osteitis fibrosa is prevention. Once the parathyroid gland mass is very large, it is difficult to control the disease. Careful attention should be paid to the plasma phosphate concentration in CKD patients, who should be counseled on a low-phosphate diet as well as the appropriate use of phosphate-binding agents, which are taken with meals and complex dietary phosphate to limit its GI absorption. Examples of phosphate binders are calcium acetate and calcium carbonate. A major side effect of calcium-based phosphate binders is calcium accumulation and hypercalcemia, especially in patients with low-turnover bone disease. Sevelamer and lanthanum are non-calcium-containing polymers that also function as phosphate binders; they do not predispose CKD patients to hypercalcemia and may attenuate calcium deposition in the vascular bed. Tenapanor is a sodium-proton inhibitor that decreases GI phosphate absorption & may be useful to manage hyperphosphatemia in CKD & dialysis patients.
CC, a 33-year-old male, was brought in for evaluation as a living kidney donor for a CKD patient. Which of the following clinical information constitutes an absolutely high risk for this patient to develop post-donation kidney disease and possible ESKD?
A. CC has an aunt on insulin for type 1 diabetes mellitus
B. CC was previously treated for minimal change disease when he was 8 years old.
C. During pre-employment evaluation 2 years ago, CC had a one-time BP measurement of 130/70 mmHg.
D. Further investigation revealed CC was adopted, and therefore has no recollection of significant blood-related familial illnesses.
B. CC was previously treated for minimal change disease when he was 8 years old.
A potential living kidney donor must have minimal risk for future kidney disease. Any condition predisposing the donor to CKD or ESKD is an absolute contraindication to donation.
“Maria dela Cruz”, a vagrant with no reliable informant or medical alert bracelet, was brought into the acute care unit after being witnessed to be in an apparent tonic-clonic seizure by roving security personnel at the Luneta Park. Initial evaluation revealed an unconscious female with no other significant physical findings. Baseline laboratory results revealed normal renal indices, but with a serum sodium level of 103 mmol/L.
Which of the following are appropriate diagnostic interventions for initial investigation?
A. Arterial blood gas, cranial computed tomography, serum vasopressin
B. Serum glucose, thyroid function test, urine osmolality
C. Urine specific gravity, urinary fractional sodium excretion
D. 12-lead electrocardiogram, urine glucose, serum sodium
B. Serum glucose, thyroid function test, urine osmolality
Serum glucose should also be measured; plasma Na+ concentration falls by ~1.6–2.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced water efflux from cells; this “true” hyponatremia resolves after correction of hyperglycemia. In the appropriate clinical setting, thyroid, adrenal, and pituitary function should also be tested; hypothyroidism and secondary adrenal failure due to pituitary insufficiency are important causes of euvolemic hyponatremia, whereas primary adrenal failure causes hypovolemic hyponatremia. Urine electrolytes and osmolality are crucial tests in the initial evaluation of hyponatremia.
A urine Na+ concentration <20–30 mM is consistent with hypovolemic hyponatremia, in the clinical absence of a hypervolemic, Na+-avid syndrome such as CHF (Fig. 53-5). In contrast, patients with SIAD will typically excrete urine with an Na+ concentration that is >30 mM. However, there can be substantial overlap in urine Na+ concentration values in patients with SIAD and hypovolemic hyponatremia, particularly in the elderly; the ultimate “gold standard” for the diagnosis of hypovolemic hyponatremia is the demonstration that plasma Na+ concentration corrects after hydration with normal saline.
Hypomagnesemia induces hypokalemia by which of the following mechanisms?
A. Inhibition of muscle Na+/K+-ATPase activity reduces influx into the myocytes, and secondary kaliuresis.
B. Magnesium depletion reduces potassium reabsorption in the distal nephron
C. Potassium and magnesium are selectively secreted in the proximal nephron.
D. Many disorders of the proximal nephron cause both potassium and magnesium wasting through co-transport mechanisms.
A. Inhibition of muscle Na+/K+-ATPase activity reduces influx into the myocytes, and secondary kaliuresis.
Magnesium depletion has inhibitory effects on muscle Na+/K+-ATPase activity, reducing influx into muscle cells and causing a secondary kaliuresis. In addition, magnesium depletion causes exaggerated K+ secretion by the distal nephron; this effect is attributed to a reduction in the magnesium dependent, intracellular block of K+ efflux through the secretory K+ channel of principal cells
Which of the following statements is ACCURATE regarding treatment of hyperkalemia?
A. Calcium reduces the action potential threshold, thereby causing immediate antagonism of the cardiac effects of hyperkalemia.
B. Insulin causes a gradual but sustained reduction in serum potassium concentration by shifting potassium into the cells.
C. Intravenous bicarbonate plays a significant role in the acute treatment of hyperkalemia, and attenuates hyperkalemia by sustained intravenous infusion.
D. Salbutamol and insulin with glucose have an additive potassium-lowering effect
D. Salbutamol and insulin with glucose have an additive potassium-lowering effect
Insulin lowers plasma K+ concentration by shifting K+ into cells. The recommended dose is 10 units of intravenous regular insulin followed immediately by 50 mL of 50% dextrose (D50W, 25 g of glucose total); the effect begins in 10–20 min, peaks at 30–60 min, and lasts for 4–6 h. Bolus D50W without insulin is never appropriate, given the risk of acutely worsening hyperkalemia due to the osmotic effect of hypertonic glucose. β2-Agonists, most commonly albuterol, are effective but underused agents for the acute management of hyperkalemia. Albuterol and insulin with glucose have an additive effect on plasma K+ concentration; however, ~20% of patients with ESRD are resistant to the effect of β2-agonists; hence, these drugs should not be used without insulin. The recommended dose for inhaled albuterol is 10–20 mg of nebulized albuterol in 4 mL of normal saline, inhaled over 10 min; the effect starts at about 30 min, reaches its peak at about 90 min, and lasts for 2–6 h. Hyperglycemia is a side effect, along with tachycardia. Β2- Agonists should be used with caution in hyperkalemic patients with known cardiac disease.
What is a unique characteristic feature in a patient’s kidney biopsy whose HbA1c levels range from 10 to 12% over the last 15 years due to glomerulosclerosis of nodules?
A. Mesangial necrosis and hemorrhage
B. Uniform thickening of the tubular membrane
C. Effacement of the foot processes
D. Eosinophilic PAS positive lesion
D. Eosinophilic PAS positive lesion
A 38-year-old male consulted your clinic 10 years ago for unexplained gross hematuria and proteinuria. His pertinent laboratory at that time were serum creatinine 201 umol/L, HBA1c 5.2, KUB ultrasound with normal appearing kidneys, ureter and bladder and no lithiasis noted. You advised him for biopsy but he was lost to follow up. He came again for consult at your clinic today complaining of generalized weakness, deafness and blurring of vision. His latest serum Creatinine is 408 umol/L. What is the likely underlying cause of his clinical condition?
A. Mutation in α5(IV) collagen chain on chromosome X
B. Autosomal dominant disorder in COL(IV) α3 locus
C. Haploinsufficiency for the transcription factor LMX1B
D. Risk allele associated with APOL1 gene
A. Mutation in α5(IV) collagen chain on chromosome X
What is the best therapy for Hepatorenal Syndrome?
A. Albumin infusion
B. Terlipressin
C. Midodrine with octreotide
D. Transplant
D. Transplant
A medical clerk asks you on the basic concepts of a patient with known heart failure that is now presenting with progressive renal dysfunction. The clerk asks you regarding the mechanism behind the possible cardiorenal syndrome. What will you tell the clerk?
A. Diuretics can further increase the serum creatinine inthe background of elevated right-sided filling pressure
B. The condition has a low mortality as long as the patientis adequately dialyzed
C. It is usually exacerbated by a “forward failure” resulting from decreased intraabdominal pressure
D. In late stages with low cardiac output state, noradrenalin will absolutely not improve renal function in selected individuals
A. Diuretics can further increase the serum creatinine inthe background of elevated right-sided filling pressure
A 43 year old male patient came to you for further workup and management of calcium oxalate crystals in his urinalysis. To objectively give a sound therapeutic recommendation, how will you instruct your patient in collecting urine samples for your baseline assessment?
A. Collect one early morning, clean catch urine sample without fasting
B. Collect two 24 hrs urine sample with usual diet
C. Collect two 24 hrs urine sample on a weekend with fluid restriction
D. Collect a random urine sample in the middle of the day and drink at least 2L of water 2 hrs prior
B. Collect two 24 hrs urine sample with usual diet
A 62 year old male complains of 3 months of recurrent flank pain and hematuria. He also mentioned increased thirst and frequent urination, which he attributes to drinking more fluids to alleviate his symptoms. He has been feeling fatigued and has experienced some weight loss over the past few months. Pertinent laboratory tests include serum calcium: 11.5 mg/dL (normal range: 8.5-10.5 mg/dL), Parathyroid hormone (PTH): 120pg/mL (normal range: 10-65pg/mL); Creatinine: 1.0mg/dL (normal range: 0.6-1.2mg/dL). What is a likely finding in the urinalysis?
A. Calcium phosphate
B. Calcium oxalate
C. Uric acid
D. Struvite
A. Calcium phosphate
