Nephrology/Urology Flashcards
Which glomerular disease is represented by this clinical presentation:
Proteinuria 150mg - 3 g/day
Hematuria > 2 RBCs/high power field in spun urine
Asymptomatic glomerular disease
Which glomerular disease is represented by this clinical presentation:
Brown/red painless hematuria (no clots); typically coincides with intercurrent infection
Macroscopic hematuria
Which glomerular disease is represented by this clinical presentation:
Proteinuria: adult > 3.5 g/day; child > 40mg/hr/m^2
Hypoalbuminemia (
Nephrotic syndrome
Which glomerular disease is represented by this clinical presentation:
Oliguria
Hematuria: may see casts
Proteinuria (usually
Nephritic syndrome
Which glomerular disease is represented by this clinical presentation:
Renal failure over days/weeks
Proteinuria (usually
Rapidly progressive glomerulonephritis
Which glomerular disease is represented by this clinical presentation:
Hypertension
Renal insufficiency
Proteinuria (> 3g/day)
Shrunken, smooth kidneys
Chronic glomerulonephritis
What urine protein measurement could be indicative of glomerular disease?
Spot urine protein:creatinine >200mg
Spot urine albumin:creatinine >30mg
What are some clinical features seen with heavy proteinuria and nephrotic syndrome?
Most cases are primary renal disease
Leg and facial edema
Xanthelasma
Five Primary renal diseases discussed:
1) Minimal change disease
2) Focal segmental glomerular sclerosis
3) Membranous nephropathy
4) Membranoproliferative GN
5) Mesangial GN
What is the standard for diagnosing primary renal diseases?
Renal biopsy
Which primary renal disease involves diffuse fusion of foot processes of podocytes, doesn’t normally progress to renal failure, and usually responds to steroids (prednisone)?
Minimal change disease
What is the ddx for MCD?
NSAIDs, Hodgkin’s lymphoma
What are the most common causes of nephrotic syndrome in adults?
Focal Segmental Glomerular Sclerosis
and
Membranous Nephropathy
Secondary causes of FSGS?
HIV, IVDA, ureteral reflux, morbid obesity, unilateral agenesis of kidney
How is FSGS treated? How is that different than MCD?
FSGS is treated with Prednisone for longer than MCD and is more resistant to steroid tx.
If FSGS patient exhibits minimal to no response to steroids, what comes next?
Cyclosporine or cytoxan
Which antibodies are seen in 80% of cases of membranous nephropathy?
Phospholipase A2 receptor antibodies
What is seen histologically with membranous nephropathy?
Thickened basement membranes with subepithelial immune deposits
What is the typical natural history of membranous nephropathy? (3)
1/3 remission
1/3 same
1/3 worse
How is membranous nephropathy treated?
Steroids with either cytoxan or cyclosproine
What medications may act as secondary causes of membranous GN?
Gold, D-penicillaminne, NSAIDs, captopril
What infections commonly act as secondary causes of membranous GN?
Hep B, syphilis, schistosomiasis, malaria, Hep C
What consistency of malignancy is commonly associated as a secondary cause of membranous GN?
Solid tumors
Which autoimmune diseases can be secondary causes of membranous GN?
SLE, RA, thyroiditis
Which is the least common primary glomerular disease?
Membranoproliferative GN
Histologically, MPGN presents with:
Thick glomerular BM due to immune complex deposition and mesangial cell interposition
Increased mesangial and endocapillary cellularity
MPGN can be mediated two different ways:
Immune complexes or complement
MPGN is less commonly caused by the alternative complement pathway, but if glomerulus only stains for complement, one should consider
congenital or acquired defects in complement cascade.
Examples of chronic immune complex diseases associated with MPGN in the following categories:
Autoimmune, infections, thrombotic microangiopathy, other
Autimmune: SLE, sjogren’s, RA, compelement deficiency
Infection: Hep C, SBE, chronic visceral abscess, Hep B
Thrombotic microangiopathy: renal transplant glomerulopathy, antiphospholipid antibody syndrome, TTP/HUS, scleroderma
Other: CLL, melanoma, non-Hodgkins lymphoma, renal cell Ca, a-1-antitrypsin deficiency, partiel lipodystrophy
Which serologies are tested during work up for glomerular disease?
ANA ASO C3, C4 Hep B and C SPEP or UPEP Cryglobulin, HIV, rheumatoid factor, ANCA, anti-GBM
Which glomerular disease presents with:
Preceded by a latent period of 1 - 2 weeks with pharyngitis or 3 - 6 weeks with skin infection.
Then: Edema, hematuria, back pain, oliguria, HTN, may progress to RPGN.
Post streptococcal GN
What are the 4 S’s of GN associated with low complement?
The other two?
SLE SBE (Post) Strep Shunt nephritis \+MPGN and cryoglobulinemia
Which GN presents with:
Hematuria, proteinuria, ARF, nephrotic syndrome, RPGN, diffuse mesangial deposits of IgA and may progress to ESRD in 20 - 30% of patients over years?
IgA nephropathy/Berger’s disease
For IgA nephropathy, what is the interval between the synpharyngitic flare and the gross hematuria? How is this different from Post strep GN?
24 - 48 hours. In post strep, latent period is 1 - 2 weeks. Also, C3 and C4 are normal in IgA GN.
How is IgA GN treated?
Prednisone (with fish oil if proteinuria >1g)
Three types of kidney disease associated with SLE:
- Lupus GN/Lupus nephritis
- Tubulointerstitial nephritis
- Antiphospholipid antibody syndrome
Lupus nephritis classes with good prognosis include:
Class I (normal) and class II (mesangial GN)
Lupus nephritis classes with poor prognosis in any form:
Class IV (Diffuse and membrano- proliferative GN, >50% glomerular involvement with capillary hypercellularity)
Class VI (sclerosis, >90%, progresses to ESRD)
Lupus nephritis classes with poor prognosis if severe form:
Class III (focal,
Three classes of lupus nephritis require aggressive treatment
Severe Class III (focal proliferation)
All Class IV (diffuse prolif)
Some Class V (membranous)
What treatment options are available for cases of lupus nephritis that require aggressive therapy?
Steroids (prednisone) plus cytoxan in monthly pulses for 3 - 6 mos
Cellcept! and low dose steroids
Rituximab
Systemic vasculitis involving granulomatous inflammation of the respiratory tract and necrotizing vasculitis of small and medium vessels
Wegener’s/granulomatosis with polyangiitis (GPA)
Systemic vasculitis involving eosinophil rich and granulomatous inflammation of respiratory tract with necrotizing vasculitis of small and medium vessels, associated with asthma and blood eosinophilia.
Churg-Strauss/Eosinophilic granulomatosis with polyangiitis (EGPA)
Systemic vasculitis involving necrotizing vasculitis with few or no immune deposits affecting small vessels. Necrotizing arteritis may also be present.
Microscopic polyangiitis (MPA)
Systemic vasculitis involving IgA dominant immune deposits in small blood vessels
Henoch-Schonlein Purpura
Systemic vasculitis involving proteins that precipitate in the cold
Cryoglobulinemia
Organ system manifestations consistent with which vasculitis?
Cutaneous, Renal, Musculoskeleta, GI
HSP
Organ system manifestations consistent with which vasculitis?
Cutaneous, Renal, Musculoskeletal
Cryoglobulinemia
Organ system manifestations consistent with which vasculitis?
Renal, pulmonary, ENT, musculoskeletal, neurologic/GI, least often cutaneous
Wegener granulomatosis (GPA)
Organ system manifestations consistent with which vasculitis?
Renal, musculoskeletal, pulmonary/GI, least often cutaneous
Microscopia polyangiitis
Organ system manifestations consistent with which vasculitis?
Pulmonary, neurologic, cutaneous, ENT/MS/GI
Churg-Strauss syndrome
What complication can develop within 5 years of the onset of Scleroderma?
Scleroderma renal crisis
What is the DOC for treating scleroderma renal crisis?
ACE inhibitors, though a significant number of pts require dialysis
What disorders result in deposits of abnormal proteins?
Amyloid, myeloma, light chain nephropathy, fibrillary GN, immunotactoid glomerulopathy
What pathological pattern is seen with amyloid deposition in the kidney?
Fibrils of beta pleated sheets
What symptoms are specific to amyloid disease? What’s seen on U/A? Renal ultrasound?
Anorexia, orthostasis, edema, purpura…
U/A: benign
Ultrasound: large kidneys
How is amyloid visualized upon biopsy?
Congo red stain: apple-green birefringence with polarized light
How is amyloid disease of the kidney treated?
Prednisone, melfalan.
Colchicine may be used for 2ndary amyloid.
What is the distribution of TBW between ICF, ECF and intravascular space?
ICF = 2/3 ECF = 1/3 intravascular = 1/4 ECF
Addition of a normal saline solution will add to which portion of TBW?
ECF
What is the normal range of serum sodium?
135 mEq/L - 145 mEq/L
Equation for plasma osmolality:
Posm = 2[Na+] +
Posm = 2[Na+] + (BUN/2.8) + (Glucose/18)
What types of hyponatremia result from drawing water out of cells into the blood and what substances may cause this? Is the osmolality considered normal?
Translocational hyponatremia; caused by addition of glucose, mannitol, glycine, or maltose
Pseudohyponatremia; caused by elevated proteins or lipids
Plasma osmolality may be normal or elevated
What states may cause a hyponatremia with a low plasma osmolality and normally dilute urine? What is the osmolarity of normally dilute urine?
Psychogenic polydipsia
Infants fed dilute formula
Low solute intake
Normal:
What state may result in a hyponatremic patient with low plasma osmolality and a concentrated urine?
Elevated vasopressin (results in hypovolemia with decreased TBW and severely decreased TB Na+)
Uosm: >100 mOsm/kg
What disorders should one consider with a hypovolemia patient that has a decreased TBW, an even more decreased TB sodium, and urine sodium >20mEq/L?
Renal losses:
diuretic excess mineralcorticoid deficiency salt-losing deficiency bicarbonaturia ketonuria osmotic diuresis cerebral salt wasting
What disorders should one consider with a hypovolemia patient that has a decreased TBW, an even more decreased TB sodium, and urine sodium
Extra renal losses:
vomiting or diarrhea third spacing of fluids burns pancreatitis trauma
What might cause a patient with euvolemia to have hyponatremia with a urine sodium >20 mEq/L?
Glucocorticoid deficiency Hypothyroidism Stress Drugs SIADH Aging
What classes of drugs may cause hyponatremia?
Vasopressin analogs (DDAVP, oxytocin, chlorpropamide, carbamazepine, nicotine, narcotics, antidepressants)
Renal vasopressin potentiators (chlorpropamide, cyclophosphamide, NSAIDs, acetaminophen)
Unknown mechanisms (haloperidol, fluphenazine, amitriptyline, thioradazine, fluoxetine, MDMA, sertraline)
What are the clinical features of SIADH?
Euvolemic, Uosm > 100 mOsm/kg, urine sodium = intake, low BUN and low uric acid
What is the time frame for acute hyponatremia? What is a possible immediate result? Symptoms?
What are risk factors for neurologic complications from acute hyponatremia?
Post-op menstruant females, psychiatric polydipsic patients, marathon runners, elderly women on thiazides, children, hypoxemic pts
Which are more sensitive to correction rate: chronic or acute hyponatremic patients?
Chronic patients are more sensitive to correction rate. Acute hyponatremia can be rapidly corrected.
What are symptoms of chronic hyponatremia?
Nausea, vomiting, cramps and weakness, ataxia, confusion and mental status change, seizures
How should acute symptomatic hyponatremia be treated?
Intubate if O2 desaturating
Hypertonic saline (3%) or mannitol
Furosemide
Goal: 2 mEq/L/hr
What patients are at risk for ODS?
Chronic hyponatremia alcoholism malnutrition liver disease burns hypokalemia
How should chronic symptomatic hyponatremia be treated?
Furosemide
Replace Na and K
No more than 1.5/mM/L/hr or 12mM in 24 hours
What might be some reasons for impaired thirst or osmoreceptor lesions?
Tumor Granulomatous diseases Ischemia Primary hyperaldosteronism Age
Three types of renal water losing disorders:
Neurogenic DI (decreased vasopressin secretion) Gestational DI (increased degradation) Nephrogenic DI (renal resistance to vasopressin)
Autosomal recessive DI normally involves mutations in the region coding for what protein? What syndrome is this most commonly a part of?
Mutation in region coding for neurophysin II.
Part of Wolfram syndrome (DIDMOAD)
How does one treat neurogenic DI?
DDAVP nasal or oral
How does one treat partial neurogenic DI?
Chlorpropamide or carbamezapine
How does one treat gestational DI?
DDAVP nasal
How does one treat nephrogenic DI?
HCTZ and low Na diet to reduce GFR and lower ECFV
or
NSAID to decrease GFR
Water deficit =
Water deficit = 0.6 x body weight x [(SNa/140)-1]
What is a normal range of TBK?
50(m) - 40(f) mEq/kg
What factors increase K+ uptake in cells?
Insulin
B-catecholamines
Alkalosis
What factors decrease uptake or increase efflux of K+ in cells?
a-catecholamines
acidosis
Hyperosmolarity (efflux)
What are common etiologies for renal K+ loss?
Diuretics
Magnesium deficiency
ATN
What might be some consequences of hypokalemia?
HTN Arrhythmias Muscle weakness Metabolic alkalosis Insulin resistance AKI, ESRD Polydipsia, polyuria
What are the clinical manifestations of hypokalemia?
Muscle weakness Arrhythmias Resp failure Ileus Hypokalemic nephropathy Increased ammonia formation
In treating hypokalemia, what is the first step?
Replete magnesium
What conditions make patients high risk with hypokalemia (at
Severe hepatic disease
HF
Ischemic HD or MI
On digoxin or antiarrhythmics
What might cause pseudohyperkalemia?
Leukocytosis > 50k wbc
Thrombocytosis >1m plts
Hemolysis
Prolonged tourniquet
What are four causes of true hyperkalemia?
Impaired renal excretion
Excessive intake
Cellular shift
tissue destruction
What can be given to move K+ into cells with hyperkalemic patients?
Glucose & insulin
NaHCO3 for acidemic pts
Beta agonists
What can be given to oppose the electrical abnormalities in a hyperkalemic patient?
Ca2+ gluconate
What can be given to remove excess K+ from a hyperkalemic patient?
Kayexalate
Diuretics
Florinef
Dialysis
What are some clues with hematuria that it might be a UTI?
Dysuria and/or pyuria
What clue with hematuria suggests that it might be glomerulonephritis?
A recent URI
What might lead one to think that hematuria is a result of hereditary nephritis or PKD?
Positive family hx of renal disease
What might lead to the diagnosis of a kidney stone (calculus) with hematuria?
Unilateral flank pain with radiation
What symptoms accompanying hematuria might suggest BPH?
Hesitancy and dribbling
What are some other possible causes of hematuria?
Malignancy, recent vigorous exercise or trauma, endometriosis, medications, sickle cell, TB
What is a normal excretion of albumin?
Up to 30mg/day
What are ways to measure protein excretion?
24 hour urine collection
Random urine protein:creatinine
normal: 0.1 - 0.15
What are possible etiologies of transient proteinuria?
Fever Exercise UTI Malignant HTN CHF
Acute kidney injury is defined as a reduction in kidney function that occurs in a period less than ___ hours, consists of:
Absolute increase in serum creatinine of >/= ___mg/dl
Percentage increase in serum creatinine >/= ____ %
Reduction in urine output of __ hours.
> 48 hours
Serum creatinine increase >/= 0.3 mg/dl
Percentage serum creatinine increase >/= 50%
Reduction in urine output 6 hours
The RIFLE criteria defines degree of kidney disease based on GFR and urine output. RIFLE:
Risk Injury Failure Loss ESKD
According to the RIFLE criteria, Injury is defined as:
SCreat =
GFR =
SCreat = x2 GFR = decrease > 50%
According to the RIFLE criteria, Risk is defined as:
SCreat =
GFR =
SCreat = x1.5 GFR = decrease > 25%
According to the RIFLE criteria, Failure is defined as:
SCreat =
GFR =
SCreat = x3 or >/= 4mg/dl GFR = decrease > 75%
According to the RIFLE criteria, Loss is defined as:
Persistent ARF with complete loss of kidney function >4 weeks
According to the RIFLE criteria, ESKD is diagnosed after __ months
> 3 months
Anuria is UO of
Oliguria is UO of
100 - 400cc/24 hrs
Polyuria is UO of >
> 3000cc/24 hrs
How much of ARF is iatrogenic?
50%
Symptoms common with uremic milieu of AKI:
General, fluid, CV, pulm, abd, neuro, heme
- Nausea, vomiting, malaise, altered taste and sensorium
- Fluid imbalance (hypo or hypervolemia)
- Pericardial effusion, tamponade
- Rales with hypervolemia
- Diffuse abd pain and ileus
- Encephalopathic changes (asterixis), confusion, seizures, hiccups
- Platelet dysfx
A sudden and severe drop in BP or interruption of blood flow to kidneys from severe injury or illness is which type of etiology for ARF?
Pre-renal
Direct damage to the kidneys by inflammation, toxins, drugs, infection or reduced blood supply is which type of etiology for ARF?
Intrarenal
Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury represents which type of etiology for ARF?
Post-renal
Prerenal ARF resulting from intravascular volume depletion can be associated with:
Dehydration, hemorrhage, renal fluid loss (diuresis), skin loss, third space loss (cirrhosis, CHF, nephrotic syndrome)
Prerenal ARF resulting from inadequate cardiac output can be associated with:
Cardiogenic shock, CHF, pericardial effusion with tamponade, massive PE
Prerenal ARF resulting from systemic vasodilation can be associated with:
Sepsis syndrome
Prerenal ARF resulting from renal vasoconstriction can be associated with:
PG inhibitors, aspirin, NSAIDs, cyclosporine, tacrolimus, radiocontrast
Intrarenal causes for ARF can be divided into (4) causes
Vascular, glomerular, interstitial, and tubular causes
Intrarenal ARF resulting from vascular disease can be associated with:
Bilateral renal artery stenosis/thrombosis/embolism
Bilateral renal vein thrombosis
Small vessel disease: thrombotic microangiopathy (HUS/TTP, scleroderma, malignant HTN, HELLP syndrome), atheroembolic disease
Atheroembolism may cause ARF by:
cholesterol emboli following a procedure or anticoagulation that presents as pt with blue toes and levido reticularis, eosinophilia/eosinophiluria, low C3 and C4
Rapidly Progressive glomerulonephritis histologically looks like:
Crescentic GN
RPGN is classified with ________ on biopsy
Immunofluorescence
RPGN can be attributed to:
Immune complex deposition (linear or granular), Pauci-immune diseases
RPGN associated with Linear immune complex deposition includes two diseases:
Good pasture’s
Anti-GBM renal limited disease
RPGN associated with granular immune complex deposition includes 6 diseases:
Post-infectious GN Infective endocarditis Lupus nephritis IgA nephropathy Henoch-Schonlein purpura Membranoproliferative GN
RPGN associated with no immune deposits (Pauci-immune) includes two diseases:
C-ANCA disease (Wegener’s granulomatosis)
P-ANCA diseases (Churgg-Strauss, polyarteritis nodosa)
RPGN immune complex GN with Low C3/C4
SLE, SBE, MPGN, PIGN, cryo, shunt nephritis, heavy chain dz, HBV
RPGN immune complex GN with normal C3/C4
IgA nephropathy
Intrarenal ARF resulting from interstitial diseases such as:
Bacterial pyelonephritis
Drug induced acute allergic
What is the classic triad of drug-induced acute allergic interstitial nephritis?
Fever, rash, urine eosinophilia
What drugs are common etiologies of drug induced AIN?
Abx, anti-TB meds, diuretics, NSAIDs, anticonvulsants, allopurinol, many more
Intrarenal ARF resulting from tubular diseases such as:
Renal ischemia, exogenous toxins and drugs, endogenous toxins
Common exogenous agents that can cause ATN:
- Amphotericin B (direct nephrotoxic fx)
- Aminoglycosides (proximal tubule damage, hypomagnesemia)
- Cisplatin (magnesuria and hypomagnesemia)
- Radiocontrast
- Ethylene glycol
How does one prevent ATN associated with contrast dye?
Volume loading with NSS before and after study, oral acetylcystine before and after, stop diuretics/ACEI/ARB/NSAIDs 24 - 28 hrs before, iso-osmolar contrast agents
How quickly does ATN associated with contrast dye occur?
Within 12 hours of study
Post-renal etiologies for ARF are divided into three locations:
Intraureteral
Extraureteral
Urether and bladder outlet
Intraureteral causes of ARF include:
Stones, blood clots, papillary necrosis, vesicoureteral reflux, stricture
Extraureteral causes of ARF include:
Cancer, retroperitoneal fibrosis, pregnant uterus
Urethral and bladder outlet causes of ARF include:
Phimosis, stricture, BPH, neurogenic bladder, calculi, trauma, blood clot, spasm, malignancy of prostate/bladder/cervix/colon
Post-renal etiologies of ARF present with symptoms such as:
Suprapubic or flank pain, decreased UO, oliguria and polyuria, hesitancy, intermittency, dribbling, nocturia, frequency
Post-renal etiologies of ARF may be associated wiith:
Hx of UTI
Indwelling catheter
Anticholinergics or alpha antagonists
Autonomic dysfx
Findings upon physical exam with post-renal causes of ARF may include:
Enlarged kidneys Palpable bladder Abd mass, distension Pelvic mass BPH, prostatic induration Aortic dilitation Edema
Post-renal ARF should be expected if
bladder or prostate are enlarged or there is evidence of tumor or UA is non-diagnostic
What is the first step if ARF is suspected to be obstruction-related?
Bladder scan for post-void residual (normal
Urine eosinophilia is associated with which two nephritic conditions?
Allergic interstitial nephritis
Atheroembolism
What is the FeNa?
Fractionoal Excretion of Sodium
FeNa = [(U/P Na)/(U/P Cr)] x 100
Measures resorption activity of tubules
Chronic kidney disease is defined as presence of damage or decreased function for:
three months or more, regardless of cause
CKD staging based on GFR stages ranges from G1, corresponding to a GFR of ___ and G5, corresponding to a GFR of ___.
G1; GFR = > 90 mL/min/1.73m^2 (normal)
G5; GFR =
CKD staging based on albuminuria stages ranges from A1, corresponding to AER of ___, to A3, corresponding to ___.
A1; AER = 300 mg/day (severely increased)
CKD staging w/r/t comorbidities: Stage I:
Treat comorbidities. Goal is to slow progression of disease. Reduce CV risk.
CKD staging wrt comorbidities: Stage II:
Determining prognosis. Keep an eye on PTH.
CKD staging wrt comorbidities: Stage III:
Focus is treating complications like hypocalcemia and anemia and malnutrition.
CKD staging wrt comorbidities: Stage IV:
Preparing pt for transplant. Monitoring phosphate in blood. Managing metabolic acidosis. Managing hyperkalemia.
CKD staging wrt comorbidities: Stage V:
Transplant is goal. Managing uremia.
The normal GFR for women and men is ___ and ___ respectively.
Women: 120 mL/min/1.73m^2
Men: 130 mL/min/1.73m^2
Problem with using serum creatinine to estimate GFR?
Can only rely upon in in individuals with stable kidney function.
Creatinine is ____ filtered and not metabolized, but it is ____ in the proximal tubule.
Freely filtered, secreted in proximal tubule.
The Cockcroft-Gault equation results in how much of an overestimate of creatinine clearance?
10 - 40 percent.
The equation used to estimate kidney function in patients with CKD
MDRD equation
The equation used to estimate GFR that is best used with normal or mildly reduced GFR (>60mL/etc)
CKD-EPI
Other conditions commonly associated with CKD (5):
Anemia HTN CVD Mineral bone disease Hyperkalemia
Uremic cardiomyopathy in patients with advanced CKD is characterized by:
diastolic dysfunction, heart failure, and LVH
Dipstick values for albuminuria corresponding to: \+1 \+2 \+3 \+4
\+1 = 30 mg/dl \+2 = 100 mg/dl \+3 = 300 mg/dl \+4 = >1000 mg/dl
Two erythropoiesis-stimulating agents that can be given to predialysis patients with anemia:
Procrit
Arenesp
Target Hg levels for patients with CRF:
10 - 11 g/dL
Metabolic acidosis resulting from CKD becomes overt when GFR reaches:
Metabolic acidosis with CKD results in what response on the PTH-calcium axis? Muscle?
Bone buffering and skeletal muscle break down
Patients who are oliguric with CKD will develop problems with elevated _____ in the blood.
Potassium
Sodium and intravascular volume balance is maintained in patients with CKD until GFR reaches
The target serum PTH in patients with CKD ranges from ___ in stage II to ____ in stage V
Stage II: 35 - 70 pg/ml
Stage V: 150 - 300 pg/ml
Four things to manage in slowing the progression of CKD:
Blood pressure
Protein restriction
Glycemic control in DM
Dyslipidemia
The AEIOU of indications for dialysis:
Acidosis Electrolytes Ingestions/Intoxications Overload of volume Uremia
Uremia signs and symptoms
Fatigue, weakness, decreased appetite, weight gain, nausea, vomiting, bizarre dreams, altered mental status, seizures
Hiccups, diffuse pruritis, twitching
Complications of uremia:
Pericarditis, pleuritis, encephalopathy, bleeding diathesis, nausea, vomiting, malnutrition, hiccups, pruritis
Anion gap equation
Anion gap = Na - (HCO3 + Cl)
[Normal = 10 - 12]
In respiratory compensation for metabolic acidosis, for every Mmole of bicarb BELOW normal ,the PCO2 falls ___ and H+ increases about ___
PCO2 falls 1.2
H+ increases 1
In respiratory compensation for metabolic alkalosis, for every bicarb ABOVE normal, PCO2 increases ____ and H+ decreases ____
PCO2 inc 0.7 Mmole
H+ dec 0.5 Mmole
In renal compensation for acute respiratory _______, H+ increaeses by 0.8 nmole for each mmHg pCO2
Acidosis
In renal compensation for chronic respiratory ______, HCO3 decreases by 5 for a pCO2 decrease of 10 and H+ decreases by 0.25 nMole for each mmHg pCO2
Alkalosis
Winter’s formula
Evaluates respiratory compensation
pCO2 = 1.5 x HCO3 + 8 +/- 2
Distal RTA Type 1 is a dysfunction of ______ cells
Intercalated
In Distal RTA type 1, urine pH is _____, blood potassium is _____ and urine calcium is _____
Alkaline
Low
High
Distal RTA type 1 is diagnosed with:
Tests of H+ excretion (NH4):
Urinary AG
Urinary OG
Blood pCO2
Proximal RTA type 2 is characterized by: HCO3 wasting for TCO2 \_\_\_\_\_ HCO3 in urine that \_\_\_\_ with TCO2 K+ is \_\_\_\_ Urine pH is \_\_\_\_ Other things in urine (3):
> 17mEq/L
inc/dec
K+ = Low
Urine pH = low
Phosphaturia, glycosuria, proteinuria?
RTA type IV involves low levels of
Renin and aldosterone
Four principal cell disorders:
Liddle’s
Pseudohypoaldo I
Pseudohypoaldo II
Hyporenin/hypoaldo
Liddle’s syndrome mimics primary hypoaldosteronism but with increased volume and is caused by:
Open Na+ channel in principal cells and low renin
Pseudohypoaldosteronism I presents with increased K+, Na+ wasting, RTA and is caused by
closed Na+ channels in principal cells
Pseudohypoaldosteronism II (Gordon’s syndrome) presents with increased K+, increased Na+ reabsorption, RTA, and is caused by
Increased Chloride shunt
Hyporenin/hypoaldo presents with
Hyperkalemia, Na+ wasting, RTA
Bartter’s acid base disorder has a _____ effect
Loop-diuretic-like effect
NaCl wasting, K+ wasting, hypercalciuria, hypomangesuria
Gitelman’s acid base disorder has a _______ defect
Thiazide-like defect
NaCl wasting, K+ wasting, hypocalciuria, hypermagnesuria
UTI is defined by the presence of a pure growth of more than _____ colony forming units of bacteria per ml
10^5 CFUs
MC UTI:
e. coli
Recurrent UTI tests get a urologic work up that consists of:
Unspun urine Urinalysis Culture KUB U/S
Bacteriuria CFU/mL for acute cystitis
> 10^3
Bacteriuria CFU/mL for acute pyelonephritis
> 10^4
Bacteriuria CFU/mL for UTI in men
> 10^4
Bacteriuria CFU/mL asymptomatic
> 10^5 x 2
Microalbuminuria is defined as ____mg / day albumin
30 - 300 mg / day
Macroalbuminuria is defined as ____mg / day albumin
> 300 mg / day albumin
Of the 10% of T1DM patients that develop diabetic nephropathy, __% of them develop ESRD within 30 years if untreated
75%
Stage 1 of diabetic nephropathy
Rernal hypertrophy and hyperfunction: GFR increases, risk stratification difficult
Stage 2 of diabetic nephropathy
Latency: detectable glomerular lesions but urinary albumin and bp are normal
Stage 3 of diabetic nephropathy
Microalbuminuria: usually 5+ years after disease onset, declining GFR, HTN mor prevalent, vascular complications (retinopathy, neuropathy, PVD, CAD, CVA)
Stage 4 of diabetic nephropathy
Macroalbuminuria: GFR declines monthly (1.2mL/min), ESRD in 5 - 15 years, 3/4 with HTN
Stage 5 of diabetic nephropathy
Progression to ESRD
In type 1 diabetics, _______ universally precedes nephropathy
Retinopathy
Why might one with stage 1 diabetic nephropathy have increased GFR?
Increased activation of renin-angiotensin-aldosterone system, resulting in elevated pressure that eventually damages glomerulus
_____ bind cell surfaces and induce cytokine release, oxidative stress, and free radical formation in diabetic nephropathy
Advanced Glycation End products
In diabetic nephropathy, increased activity of ________ results in increased sorbitol which induces free radicals and ECM synthesis
Aldose reductase
In diabetic nephropathy, ______ is increased, resulting in free radicals and hydrogen peroxide
Nitric oxide synthase
In diabetic nephropathy, mesangial cell nuclei form palisades around masses of mesangial matrix and glomerular capillaries form microaneurysms in a presentation known as _____
Kimmelstein-Wilson nodules (Nodular Glomerulosclerosis)
Immunofluorescence staining for diabetic nephropathy has a _____ pattern for the GBM, TBM, and Bowman’s capsule for Ig_
Linear, IgG
_____ is the earliest clinical finding of diabetic nephropathy
Increased urinary protein excretion
In patients with the microalbuminuria stage of diabetic nephropathy, __% will remain microalbuminuric and ______% will progress to frank proteinuria after ten years
40% remain, 20 - 45% progress
What is the gold standard test for proteinuria?
24 hour collection of urine for albumin
How often should a diabetic patient have a urinalysis?
Yearly starting 5 years after diagnosis/onset
The most important points of control in preventing diabetic nephropathy are:
Glycemic and blood pressure, especially blood pressure!
The drug class(es) used to treat diabetic nephropathy:
ACEIs and ARBs, low does aspirin
ACEIs and ARBs promote dilation of ____ arterioles more than ____ arterioles.
Efferent > afferent
Treatment options for a patient with diabetic nephropathy that develops ESRD:
Hemodialysis
Peritoneal dialysis
Transplant
Examples of endogenous antigens involved in AIN
TBM glycoproteins (3M-1, TIN1)
Tamm-Horsfall tubular protein
Immune complexes
Before antibiotics, AIN was mainly induced by:
scarlet fever, diphtheria
Medications commonly implicated in AIN
Methicillin, Rifampin, Allopurinol, NSAIDs, COX2I, PPI, HAART
AIN manifests clinically after a few days to weeks and presents with:
ARF, mild proteinuria, hematuria, pyuria, leukocyte casts, possible flank pain, fever, maculopapular rash, and arthralgia
For best prognosis with drug-induced AIN, treatment should start with:
Removing aggravating agent
Poor prognostic findings for drug-induced AIN are associated with:
Delayed improvement (1 week) Prolonged exposure (>2 - 3 weeks) Pre-existing CKD Biopsy findings of diffuse interstitial infiltrates, granulomas, fibrosis, or tubular atrophy
Systemic diseases associated with AIN:
Sarcoidosis
SLE
Sjogren’s
Malignancies associated with AIN:
Lymphoma, leukemia
Possible general causes of chronic interstitial nephritis:
Toxins, drugs, crystals, infections, obstructions, immunologic mechanisms, ischemia
Histology findings for CIN:
Tubular dilation, hypercellularity, noncaseating granulomas, crystals
CIN clinical manifestation:
Loss of GFR over time, mild proteinuria, proximal and distal tubular dysfx, concentrating defect, salt wasting
Mechanism for Lithium-induced diabetes insipidus:
Inhibits ADH signaling and decreases expression of AQP2 in collecting ducts
Treatment for Lithium renal toxicity:
Discontinue cautiously, K-sparing diuretics (amilioride, triamterene), possibly hemodialysis
Analgesic nephropathy may be caused by prolonged use of ______ and ______ and is a result of:
Aspirin and acetaminophen, result of decreased BF to renal medulla
MC complications of analgesic nephropathy:
Renal papillary necrosis
Papillary necrosis is associated with (6) conditions and will present on CT with ______ or _____
Analgesic nephropathy, diabetic nephropathy, APN, sickle cell, UT obstruction, renal TB
Bumpy contours or papillary calcifications
In rhabdomyolytic nephrotoxic injury, muscle destruction releases ______ and ______ which cause injury via:
Myoglobin: vasoconstriction, NO scavenging, oxidative injury
Hemoprotein: direct tubular cytotoxicity
With rhabdomyolysis and ATN will see upon UA:
Muddy brown casts, granular casts but no RBCs
Renal perfusion autoregulation mechanisms impaired when .. BP? drops below
80?
ATN phases involve:
Ischemic injury, disruption of polarity and sloughing of cells causing _______ ____________ , then maintenance of injury followed by recovery which often presents with initial post-ATN _______
tubular obstruction, diuresis
By definition, a complicated UTI involves:
a structural or functional impairment that reduces efficacy of antimicrobial therapy
Most common urinary pathogen in community UTI:
E. coli
Nosocomial UTI often caused by:
Proteus
Klebsiella
Enterococcus
S. saprophyticus
Hematogenous spread of infection to UT usually associated with
s. aureus or candidal fungemia
What bacterial virulence factor seems to be instrumental in pathogenesis of bacterial cystitis by attaching to vaginal and bladder mucosae?
Type 1 pili
Risk factors for UTI in young women include
Frequency of sexual intercourse Previous UTI Condom Diaphragm Abx 2 - 4 weeks earlier
A UTI may be complicated by pre-existing conditions such as:
DM
Transplant
Granulocytopenia
HIV/AIDS
Treating a mild infectious pyelonephritis with a compliant patient:
7 - 14 days
12 - 24 hr observation
Quinolone, TMP/SMZ
Gram positive cocci: amox or amox/clav
Treating moderate to severe infectious pyelonephritis or non-compliant pt:
Parenteral:
Quinolone
Aminoglycoside +/- ampicillin
Extended spectrum cephalosporin +/- aminoglycoside
MC instrumental complication for UTI in men:
Foley catheter
Treatment duration for uncomplicated UTI in women
Cystitis: 3 days
APN: 7 days
Treatment duration for complicated UTI in women
Cystitis: 7 - 10 days
APN: >2 weeks
Post-menopausal women have a decrease in _____ and an increase in ______ in their vaginal flora, associate with:
Lactobacilli, e.coli
Decreased estrogen
Mechanism of cranberry juice in managing a UTI
Proanthocyandins inhibit bacterial adherence to epithelial cells
What antibiotic is preferred DOC for treating gram negative infections with ESBL?
Carbapenem
