Nephrology

Question 1

cRenal blood flow normally drains ___ of the cardiac output

Answer 1

~20%

Question 2

The most common clinical course of contrast nephropathy is characterized by a rise in SCr beginning ____ following exposure, peaking within ____ , and resolving within

Answer 2

24–48 h
3–5 days
1 week

Question 3

Definition of AKI

Answer 3

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.

Question 4

Diseases that may present with eosinophilluria (5)

Answer 4

Allergic interstitial nephritis
Atheroembolic dse
Pyelonephritis
Cystitis
Glomerulonephritis

Question 5

Diseases that may present with RBC casts (4)

Answer 5

Glomerulonephritis
Vasculitis
malignant Hypertension
Thrombotic Microangiopathy

Question 6

Diseases that may present with WBC casts (5)

Answer 6

Interstitial Nephritis
Glomerulonephritis
Plyelonephritis
Allograft Rejection
Malignant Infiltration of the kidney

Question 7

Diseases that may present with RTE casts (5)

Answer 7

ATN
Tubulointerstitial nephritis
Acute cellular allograft reaction
Myoglobulinuria
Hemoglobinuria

Question 8

Diseases that may present with granular casts (4)

Answer 8

ATN
GN
Vasculitis
TIN

Question 9

Diseases that may present with crystalluria

Answer 9

Acute uric acid nephropathy
Caox
Drugs or toxin (acyclovir, indinavir, sulfadiazin, amoxicillin)

Question 10

Fe Na of pre renal AKI

Answer 10

< 1%

Question 11

Dose for furosemide challenge

Answer 11

1-1.5 mg/kg

Question 12

UO of ________ after IV furosemide may identify patients at higher risk of progression to more severe AKI, and the need for renal replacement therapy

Answer 12

< 200 mL over 2 h a

Question 13

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

Answer 13

KIM-1

Question 14

_____ is highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2 h of cardiopulmonary bypass– associated

Answer 14

NGAL

Question 15

patients with AKI should achieve a total energy intake of ____ kcal/kg per day.

Answer 15

20–30 kcal/kg per day

Question 16

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

Answer 16

0.8–1.0 g/kg per day
1.0–1.5 g/kg
1.7 g/kg

Question 17

Alkali supplementation may attenuate the catabolic state and possibly slow CKD progression and is recommended when the serum bicarbonate concentration falls below ____ mmol/L.

Answer 17

20–23

Question 18

These PTH FGFR3 changes start to occur when the GFR falls below ___ mL/min.

Answer 18

60 mL/min

Question 19

_____ 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

Answer 19

Calciphylaxis

Question 20

Blood thinner that is considered a risk factor for calciphylaxis

Answer 20

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

Question 21

Target PTH level for CKD

Answer 21

150 and 300 pg/mL

Question 22

_______ is leading cause of morbidity and mortality in px at every stage of CKD

Answer 22

Cardiovascular disease

Question 23

First line therapy for CKD to reduce BP

Answer 23

Salt restriction

Question 24

In CKD patients with diabetes or proteinuria >1 g per 24 h, blood pressure should be reduced to ______ , if achievable without prohibitive adverse effects.

Answer 24

< 130/80 mmHg

Question 25

normocytic, normochromic anemia is observed as early as stage ___ CKD and is almost universal by stage __

Answer 25

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

Question 26

Target Hb for CKD

Answer 26

10-11.5 g/dl

Question 27

Peripheral neuropathy usually becomes clinically evident after the patient reaches stage __ CKD, although electrophysiologic and histologic evidence occurs earlier.

Answer 27

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

Question 28

Class of drugs that do not require dose reduction when EGFR is less than 50% of normal

Answer 28

SGLT 2 inhibitors

Question 29

A skin condition unique to CKD patients called _____ consists of progressive subcutaneous induration, especially on the arms and legs.

Answer 29

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

Question 30

Diseases where kidney size may be normal in the face of CKD (3)

Answer 30

diabetic nephropathy, amyloidosis, and HIV nephropathy

Question 31

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

Answer 31

> 1 cm

Question 32

The most important complication of arteriovenous grafts is _______

Answer 32

thrombosis of the graft and graft failure

due principally to intimal hyperplasia at the anastomosis between the graft and recipient vein

Question 33

_______ is the most common acute complication of hemodialysis, particularly among patients with diabetes mellitus.

Answer 33

Hypotension

Question 34

Peritonitis in peritoneal dialysis is defined as _____

Answer 34

elevated peritoneal fluid leukocyte count (100/mm3 , of which at least 50% are polymorphonuclear neutrophils

Question 35

_____ is the procedure of choice to rule out urinary obstruction or to confirm the presence of perirenal collections of urine, blood, or lymph.

Answer 35

Diagnostic ultrasound

Question 36

The first rejection episode is usually treated with IV administration of

Answer 36

methylprednisolone, 500–1000 mg daily for 3 days.

Failure to respond is an indication for antibody therapy, usually with antithymocyte globulin.

Question 37

Greater than ____mg/day of albuminuria represents frank proteinuria and more advanced renal disease

Answer 37

300 mg/24 h

Question 38

___________ 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

Answer 38

PSGN

Question 39

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

Answer 39

90%

Question 40

Treatment for PSGN

Answer 40

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.

Question 41

Antibodies that that fix complement correlate best with the presence of renal disease in lupus nephritis

Answer 41

Anti-dsDNA

Hypocomplementemia is common in patients with acute lupus nephritis (70–90%) and declining complement levels may herald a flare.

Question 42

Class of Lupus nephritis that presents with mesangial hypercellularity with expansion of the mesangia matrix

Answer 42

Class II

Question 43

Class of Lupus nephritis that presents with focal endocapillary and extracapillary proliferation with focal subendothelial immune deposits and mild mesangial expansion

Answer 43

Class III

Question 44

Class of Lupus nephritis that presents with diffuse endocapillary and extracapillary proliferation with diffuse subendothelial immune deposits and mesangial alterations

Answer 44

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

Question 45

Class of Lupus nephritis that presents with thickened BM with diffuse subepithelial immune deposits

Answer 45

V

Patients with lupus nephritis class V, like patients with idiopathic membranous nephropathy (IMN), are predisposed to renal vein thrombosis and other thrombotic complications.

Question 46

Class of lupus nephritis with Global sclerosis of nearly all glomerular capillaries

Answer 46

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.

Question 47

Class of lupus nephritis with the most varied course

Answer 47

III

Question 48

Henoch-Schönlein purpura is distinguished clinically from IgA nephropathy by (4).

Answer 48

prominent systemic ssx, a younger age (<20 years old), preceding infection, and abdominal complaints

Question 49

Type I MPGN is associated with Hepatiti __ infection

Answer 49

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

Question 50

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.

Answer 50

<0.2 mg/24 h

Question 51

Response to steroids

Frequent relapsers have ____ relapses in ___ months following taper, and steroid-resistant patients fail to respond to steroid therapy.

Answer 51

two or more relapses in the 6 months

Question 52

Adults are not considered steroid-resistant until after ___ months of therapy.

Answer 52

4

Question 53

First line therapy for MCD

Answer 53

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

Question 54

Treatment of patients with primary FSGS should include

Answer 54

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

Question 55

The treatment of secondary FSGS typically involves

Answer 55

treating the underlying cause and controlling proteinuria.

Question 56

GN that has the highest reported incidences of renal vein thrombosis, pulmonary embolism, and deep-vein thrombosis.

Answer 56

MGN AKA membranous nephropathy

Prophylactic anticoagulation is controversial but has
been recommended for patients with hypoalbuminemia

Question 57

Therapy with immunosuppressive drugs is also recommended for patients with primary MGN and persistent proteinuria ____ g/day

Answer 57

(>3.0 g/24 h).

Question 58

What microscopic finding is a sensitive indicator for the presence of diabetes but correlates poorly with the presence or absence of clinically significant nephropathy.

Answer 58

Thickening of the GBM

Question 59

Microalbuminuria appears ____ years after the onset of diabetes.

Answer 59

5–10

Question 60

More than ___% of patients with type 1 diabetes and nephropathy have diabetic retinopathy

Answer 60

90%

so the absence of retinopathy in type 1 patients with proteinuria should prompt consideration of a diagnosis other than diabetic nephropathy

Question 61

There is a significant correlation between the presence of retinopathy and the presence of __________ nodules .

Answer 61

Kimmelstiel-Wilson

Question 62

Characteristic lesion of HIVAN

Answer 62

The lesion in HIVAN is FSGS, characteristically revealing a collapsing glomerulopathy

Question 63

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.

Answer 63

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.

Question 64

Type of stone not influenced by pH

Answer 64

Calcium Oxalate

Question 65

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 _____ .

Answer 65

≤5.5 or lower

≥6.5or higher

Question 66

Size of stone with low probability of spontaneous passage

Answer 66

> = 6mm

Question 67

The “gold standard” diagnostic test is ____ for urolithiasis

Answer 67

helical CT without contrast.

Question 68

Urine volume needed to lessen risk of stone formation

Answer 68

> 2L/day

Question 69

______ 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.

Answer 69

Struvite stones

Question 70

Cystine stones may be treated with medication that covalently binds to cystine like ______ and a medication that raises urine pH.

Answer 70

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

Question 71

Preferred alkalinizing agent for cystine stones

Answer 71

The preferred alkalinizing agent to achieve a urine pH of 7.5 is potassium citrate or bicarbonate as sodium salts may increase cystine excretion

Question 72

Pentad for TTP

Answer 72

MAHA, thrombocytopenia, neurologic symptoms, fever, and renal failure.

Question 73

Which has deficiency of ADAMST13? HUS or TTP?

Answer 73

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.

Question 74

Antibody that may identify young patients at risk for scleroderma renal crisis

Answer 74

Anti-U3-RNP may identify young patients at risk for scleroderma renal crisis.

Question 75

Antibody that is a negative predictor of scleroderma renal crisis

Answer 75

Anticentromere antibody, in contrast, is a negative predictor of this disorder.

Question 76

First line therapy for scleroderma renal crisis

Answer 76

ACE-inhibition

Question 77

____ and _____ account for ~90% of cases of acute intrinsic renal failure

Answer 77

Ischemic and toxic Acute tubular necrosis (ATN)

Question 78

BUN: crea ratio of prerenal azotemia

Answer 78

> 20:1

Question 79

Fe Na of prerenal azotemia

Answer 79

< 1%

Question 80

Causes of hypercoagulable state in nephrotic syndrome

Answer 80

urinary losses of antithrombin III
reduced proteins S and C
hyperfibrinogenemia
enhanced platelet aggregation.

Question 81

Cause of hyperlipidemia in nephrotic syndrome

Answer 81

inc hepatic lipoprotein synthesis.

Question 82

Hematuria with dysmorphic RBCs, RBC casts, and protein excretion > ____mg/day is virtually diagnostic of glomerulonephritis.

Answer 82

> 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.

Question 83

1st test when evaluating polyruia

Answer 83

urine osmolality

Question 84

Recommended as the best method for distinguishing between central and nephrogenic diabetes insipidus.

Answer 84

plasma AVP level

Question 85

AVP secretion is stimulated as systemic osmolality increases above a threshold level of ____

Answer 85

~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

Question 86

Serum uric acid is often low (<_____) in patients with SIAD

Answer 86

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

Question 87

Most common malignancy associated with SIADH

Answer 87

small cell lung CA

Question 88

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.

Answer 88

> 8–10 mM in 24 h or 18 mM in 48 h

Question 89

_______ has long been a cornerstone of the therapy of chronic hyponatremia.

Answer 89

Water deprivation

chronic hyponat duration > 48h

Question 90

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 _____

Answer 90

(<500 mL/d)
500–700 mL/d
1 L/d

Question 91

________ 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

Answer 91

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.

Question 92

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

Answer 92

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.

Question 93

__________ is the most frequent manifestation of hypernatremia

Answer 93

Altered mental status

ranging from mild confusion and lethargy to deep coma.

Question 94

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

Answer 94

<50%
< 150 mOsm/kg

Question 95

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 _____

Answer 95

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).

Question 96

Class of diuretics that may reduce polyuria due to NDI, ostensibly by inducing hypovolemia and increasing proximal tubular water reabsorption.

Answer 96

Thiazides

Question 97

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.

Answer 97

> 50

Question 98

Critical diagnostic test in Giterlman vs Barter syndrome

Answer 98

urinary calcium excretion

Patients with GS are uniformly hypomagnesemic and exhibit marked hypocalciuria (hece hypercalcemic), rather than the hypercalciuria typically seen in BS

Question 99

ECG findings are most marked when serum K+ is <_____

Answer 99

2.7mmol/L

Question 100

Urine K value that will differentiate extrarenal from renal losses

Answer 100

< 15 mmol / day for extrarenal losses

Question 101

TTKG in hypokalemia level that connotes inc K secretion

Answer 101

> 4

Question 102

TTKG level in hypokalemia that connotes INCREASED tubular flow

Answer 102

< 2

2bular

Question 103

Urine calcium/crea for Barters

Answer 103

> 0.20

B for bente

Question 104

Urine calcium/crea for Gitelman

Answer 104

< 0.15

Question 105

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 ( )

Answer 105

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)

Question 106

Electrolyte imblances that may potentiate digoxin

Answer 106

Hypokalemia and hypercalcemia

Question 107

In hyperkalemic patients with glucose concentrations of ≥ _____mg/dL, insulin should be administered without glucose, again with close monitoring of glucose concentrations

Answer 107

200–250

Question 108

TTKG level in hyperkalemia that connotes reduced tubular flow

Answer 108

> 8

Question 109

TTKG level in hyperkalemia that connotes decreased distal K secretion

Answer 109

< 5

Question 110

Drug that you should give if TTKG < 5 in hyperkalemia to test for tubular resistance

Answer 110

Fludrocortisone

F-ive, F-ludrocortisone

Question 111

Hypercalcemia associated with granulomatous disease (e.g., sarcoidosis) or lymphomas is caused by ___________

Answer 111

enhanced conversion of 25(OH)D to the potent 1,25(OH)2 D.

Question 112

The first step in the diagnostic evaluation of hyper- or hypocalcemia is to ensure that ____________

Answer 112

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

Question 113

Chronic hypercalcemia is most commonly caused by __________ , as opposed to the second most common etiology of hypercalcemia, an underlying ______.

Answer 113

primary hyperparathyroidism
malignancy

Question 114

Initial therapy of significant hypercalcemia begins with ________

Answer 114

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

Question 115

In patients with 1,25(OH)2 D-mediated hypercalcemia, ______ are the preferred therapy, as they decrease 1,25(OH)2 D production.

Answer 115

glucocorticoids

Question 116

Formula for plasma osmolality

Answer 116

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

Question 117

Type of RTA that is most often due to generalized proximal tubular dysfunction manifested by glycosuria, generalized aminoaciduria, and phosphaturia

Answer 117

Proximal RTA (type 2 RTA)

Question 118

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).

Answer 118

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)

Question 119

Type of RTA in which hyperkalemia is disproportionate to the reduction in (GFR) because of coexisting dysfunction of potassium and acid secretion.

Answer 119

distal RTA (type 4 RTA)

Question 120

______ syndrome results from an inherited gain of function mutation of genes that regulate the collecting duct Na+ channel (ENaC).

Answer 120

Liddle’s

Question 121

most common acid-base disturbance in critically ill patients and, when severe, portends a poor prognosis

Answer 121

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

Question 122

the most common cause of drug-induced respiratory alkalosis as a result of direct stimulation of the medullary chemoreceptor

Answer 122

Salicylates

Question 123

mechanism that predominantly
mediates potassium balance in CKD

Answer 123

Aldosterone dependent secretion in the
distal nephron

Question 124

complication is prevented by
supplemental bicarbonate in CKD

Answer 124

protein catabolism

Question 125

Target blood pressure for
patients with CKD and concomitant proteinuria?

Answer 125

<130/80

Question 126

most common organisms implicated in peritonitis in px undergoing peritoneal dialysis

Answer 126

G+ cocci

Question 127

main feature distinguishing
pyelonephritis from cystitis?

Answer 127

fever

Question 128

What is the threshold for diagnosing asymptomatic bacteriuria in urine culture expressed in bacterial CFU/mL?

Answer 128

10^5

Question 129

type of AKI caused by cyclosporine

Answer 129

pre-renal

Question 130

portion of the kidney is particularly
susceptible to ischemic damage?

Answer 130

outer medulla

Question 131

PSGN usually develops
After _____ weeks post impetigo/skin infection
After _____weeks post strep pharyngitis

Answer 131

2-6 weeks
1-3 weeks

Question 132

Most common cause of nephrotic syndrome in the elderly

Answer 132

MGN

Biopsy: uniform thickening of the basement
membrane along the peripheral capillary loops on light microscopy, diffuse granular deposits of IgG and C3 on IF and subepithelial electron-dense deposits on EM

Question 133

urine osmolality of pre renal AKI

Answer 133

> 500

Question 134

urine crea/ plasma crea ratio of pre renal AKI

Answer 134

> 40

Question 135

Vomiting, nausea, confusion, and seizures, usually at plasma Na+ concentration _____

Answer 135

<125 mM

Question 136

The ultimate “gold standard” for the diagnosis of hypovolemic hyponatremia is __________

Answer 136

the demonstration that plasma Na+ concentration corrects after hydration with normal saline

Question 137

Causes of low FeNa aside from pre-renal AKI

Answer 137

Rhabdomyolysis
Sepsis
Hemolysis
CIN

-sis + CIN

Question 138

Myeloma light chains can also cause AKI
by

Answer 138

Binding to Tamm-Horsfall protein to form obstructing intratubular
casts

Question 139

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?

Answer 139

Acute nephritis

Question 140

If BM thickening is a sensitive indicator of DM but does not corrrelate with nephropathy, what histologic finding correlates well with DM nephropathy?

Answer 140

Mesangial expansion

Question 141

Peripheral neuropathy usually becomes clinically evident after the patient reaches Stage ___ CKD

Answer 141

4

P-eripheral neuropathy P-or

Question 142

Formula for corrected anion gap

Answer 142

CorrectedAnionGap=MeasuredAnionGap+2.5×(4.0−SerumAlbumin(g/dL))

*some sources use 4.5 as normal value for albumin

Question 143

In IgA nephropathy what provides the greatest predictive power for adverse renal outcomes

Answer 143

Monitoring of persistent proteinuria

Question 144

The primary mechanism mediating potassium balance in a patient with chronic kidney disease is ___

Answer 144

aldosterone-dependent secretion in the distal nephron

Question 145

What possible complication is prevented by bicarbonate supplementation in CKD

Answer 145

Protein catabolism

Question 146

What is the mechanism of Vancomycin in causing acute kidney injury?

Answer 146

Intratubular obstruction

** same with acyclovir

Question 147

What is the osmotic threshold for AVP release?

Answer 147

More than 285 mOsm/kg

Question 148

In a patient with milk alkali syndrome, what is the likely mechanism for metabolic alkalosis?

Answer 148

exogenous bicarb loads

Question 149

What is the mechanism of hypokalemia in magnesium deficiency?

Answer 149

Intracellular block of K efflux through the secretory K channel

Question 150

how do you treat PSGN?

Answer 150

Treatment is mainly supportive, and directed towards control of hypertension, oedema, and dialysis, if necessary.

Question 151

Vitamin C supplementation increases risk for what kind of stone formation

Answer 151

CaOx

Question 152

What is the recommended urine pH for uric acid stones

Answer 152

6.5

Question 153

Most common cause of nephrotic syndrome in the elderly

Answer 153

Mebranous nepropathy/ MGN

Question 154

What are the containdications to kidney biopsy?

Answer 154

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

Question 155

A urine osmolality <___mOsm/kg is suggestive of polydipsia

Answer 155

100

Question 156

from the earliest stages of microalbuminuria, it usually takes ___ years to reach ESRD.

Answer 156

10–20

Question 157

GNs that presents with hypocomplementenemia (3)

Answer 157

MPGN
Lupus nephritis
PSGN

Question 158

Type of cast seen in pre renal AKI

Answer 158

granular/hyaline

Question 159

Most common type of stone

Answer 159

Calcium oxalate

Question 160

The majority of calcium oxalate stones grow on calcium phosphate at the tip of the renal papilla AKA

Answer 160

(Randall’s plaque).

Question 161

Effect of pH on citrate reabsorption

Answer 161

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.

Question 162

When is urologic intervention warranted for px with urolithiasis?

Answer 162

Urologic intervention should be postponed unless there is evidence of UTI, a low probability of spontaneous stone passage (e.g.,
a stone measuring ≥6 mm or an anatomic abnormality), or intractable pain

Question 163

This test serves as the cornerstone on which therapeutic recommendations are based for px with urolithiasis

Answer 163

The results from 24-h urine collections serve as the cornerstone on which therapeutic recommendations are based.

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.

Question 164

Risk factors for caox stones

Answer 164

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

Question 165

Mediation used to tx hypertension that can decrease Caox recurrence

Answer 165

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%.

Question 166

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.

Answer 166

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.

Question 167

T/F
Partial bilateral UTO often results in acquired distal renal tubular acidosis, hypokalemia, and renal salt wasting

Answer 167

False
Partial bilateral UTO often results in acquired distal renal tubular acidosis, HYPERkalemia, and renal salt wasting

Question 168

Fluid of choice for post obstructive diuresis

Answer 168

. Often replacement with 0.45% saline is required

Question 169

Management of cardiorenal syndrome

Answer 169

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

Question 170

Difference between Type 1 vs Type 2 HRS

Answer 170

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

Question 171

Management of HRS

Answer 171

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.

Question 171

The most important complication of arteriovenous grafts is

Answer 171

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

Question 172

Hypotension is the most common acute complication of hemodialysis, particularly among patients with _______

Answer 172

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

Question 173

Difference between two dialyzer reaction types

Answer 173

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

Question 174

Difference between CAPD vs CCPD peritoneal dialysis

Answer 174

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.”

Question 175

formal evaluation of peritoneal membrane characteristics that measures the transfer rates of creatinine and glucose across the peritoneal membrane

Answer 175

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

Question 176

major complications of peritoneal dialysis p

Answer 176

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).

Question 177

How do you differentiate pre renal from renal cause of AKI based on FeNa, U/P ratio and urine osmolality

Answer 177

Question 178

How do you differentiate PSGN vs Iga nephropathy with regard to timing of pharyngitis?

Answer 178

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

Question 179

Acute allergic or immune interstitial nephritis (AIN) usually occurs __________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

Answer 179

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.

Question 180

most common cause of chronic interstitial nephritis

Answer 180

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

Question 181

3 defining features of nephrotic syndrome

Answer 181

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.

Question 182

A characteristic finding of rapid-onset hypoalbuminemia in NS is horizontal linear white lines in the nail bed, known as

Answer 182

A characteristic finding of rapid-onset hypoalbuminemia in NS is horizontal linear white lines in the nail bed, known as Muehrcke’s line

Question 183

Exception to the low sodium excretion in prerenal AKI

Answer 183

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

Question 184

Stage of CKD in which the patient should be prepared and educated about transplant and dialysis

Answer 184

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

Question 185

Based on CPG 2018, Among CKD 5 patients on low-flux hemodialysis, ___ times a week hemodialysis may be recommended.

Answer 185

3 (4 hrs each session)

same with hi flux

Question 186

Based on CPG 2018, Initiation of hemodialysis at eGFR greater than ___ ml/min is not recommended among asymptomatic patients with CKD 5.

Answer 186

Initiation of hemodialysis at eGFR greater than 10 ml/min is not recommended among asymptomatic patients with CKD 5.

Question 187

Based on CPG 2018, Among CKD 5 patients with CHF, initiating hemodialysis at eGFR <__ml/min may be recommended.

Answer 187

15

Question 188

T/F
The mean GFR is lower in women than in men

Answer 188

True

Question 189

Diagnostic test for monitoring albuminuria

Answer 189

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.

Question 190

Leading causes of CKD

Answer 190

Diabetic nephropathy
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

Question 191

T/F thiazide diuretics may be used across all stages of CKD

Answer 191

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

Question 192

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.

Answer 192

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.

Question 193

CXR findings of low pressure pulmonary edema from CKD

Answer 193

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

Question 194

Causes of anemia in CKD

Answer 194

Question 195

Subtle clinical manifestations of uremic neuromuscular disease usually become evident at stage ___ CKD

Answer 195

3

Question 196

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

Answer 196

40

Question 197

Most useful imaging study for CKD

Answer 197

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

Question 198

Which CCB has superior antiproteinuric and renoprotective effects

Answer 198

Among the calcium channel blockers, diltiazem and verapamil may exhibit superior antiproteinuric and renoprotective effects compared to the dihydropyridines.

Question 199

AKI staging

Answer 199

Question 200

Even in healthy adults, renal autoregulation usually fails once the systolic blood pressure falls below ____ mmHg

Answer 200

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

Question 201

most common causes of intrinsic AKI

Answer 201

The most common causes of intrinsic AKI are sepsis, ischemia, and nephrotoxins, both endogenous and exogenous

Question 202

markedly elevated intraabdominal pressures, usually >__ mmHg, lead to renal vein compression and reduced GFR

Answer 202

20

Question 203

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.

Answer 203

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.

Question 204

How does aminoglycosides and amp B cause intrinsic AKI?

Answer 204

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.

Question 205

Electrolyte abnormalities associated with ifosfamide

Answer 205

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

Question 206

MOA of AKI from ethylene glycol

Answer 206

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

Question 207

AKI accompanied by palpable purpura, pulmonary hemorrhage, or sinusitis raises the possibility of ______1-

Answer 207

systemic vasculitis with glomerulonephritis

Question 208

Treatment for rhabdomyolysis

Answer 208

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

Question 209

Metabolic acidosis is generally not treated unless severe (pH <____ AND serum bicarbonate <___ mmol/L).

Answer 209

Metabolic acidosis is generally not treated unless severe (pH <7.20 and serum bicarbonate <15 mmol/L).

Question 210

T/F Anemia in AKI can be tx by erythropoiesis-stimulating agents

Answer 210

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

Question 211

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)

Answer 211

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)

Question 212

first step in the diagnostic evaluation of hyper- or hypocalcemia is

Answer 212

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.

Question 213

e/serum creatinine) of <____ is suggestive of FHH, particularly when there is a family history of mild, asymptomatic hypercalcemia.

Answer 213

0.01

Question 214

Although there are many potential causes of hypocalcemia, _____________ are the most common etiologies

Answer 214

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)

Question 215

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).

Answer 215

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).

Question 216

The MDRD equation is better correlated with true GFR when the GFR is <____ mL/min per 1.73 m2 .

Answer 216

The MDRD equation is better correlated with true GFR when the GFR is <60 mL/min per 1.73 m2 .

Question 217

Lab findings between prerenal AKI vs oliguric AKI

Answer 217

Question 218

Patients with atheroembolic acute renal failure often have a normal urinalysis, but the urine may contain

Answer 218

eosinophils and casts

Question 219

Next step when px with hematuria presents with proteinuria

Answer 219

Question 220

The dipstick measurement detects only albumin and gives false-positive results at pH

Answer 220

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.

Question 221

Hematuria is defined as ______ RBCs per high-power field (HPF) and can be detected by dipstick

Answer 221

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

Question 222

1st diagnostic test when px presents with polyuria

Answer 222

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

Question 223

Winter’s equation

Answer 223

Paco2 = (1.5 × [HCO3 −]) + 8 ± 2 (Winter’s equation)

Question 224

Cause of HAGMA

Answer 224

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).

Question 225

Formula for corrected anion gap

Answer 225

For example, for each g/dL of serum albumin below the normal value (4.5 g/dL), 2.5 mmol/L should be added to the reported (uncorrected) AG.

Question 226

Indications for bicarbonate therapy in DKA

Answer 226

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.

Question 226

4 principal causes of HAGMA

Answer 226

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

Question 227

2 types of lactic acidosis

Answer 227

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)

Question 228

Treatment for ethylene glycol toxicity

Answer 228

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

Question 229

Difference between isopropyl alcohol intoxication vs ethanol and methanol intoxication

Answer 229

The characteristic features differ significantly from EG and methanol intoxication in that the parent compound, not the metabolites, causes toxicity, and a high-AG acidosis is not present because acetone is rapidly excreted

Isopropanol alcohol toxicity is treated by supportive therapy, IV fluids, pressors, ventilatory support if needed, and acute hemodialysis for prolonged coma, hemodynamic instability, or levels >400 mg/dL

Question 230

Treatment for metab acidosis in CKD

Answer 230

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

Question 231

How do you differentiate NAGMA from RTA vs diarrhea?

Answer 231

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

Question 232

Fanconi syndrome is associated with what type of RTA?

Answer 232

Proximal RTA (type 2 RTA) is most often due to generalized proximal tubular dysfunction manifested by glycosuria, generalized aminoaciduria, and phosphaturia (Fanconi syndrome).

Question 233

Type of RTA associated with nephrolithiasis and nephrocalcinosis

Answer 233

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

Question 234

Type of RTA associated with hyperkalemia

Answer 234

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

Question 235

How do you correct potassium in Type 2 RTA

Answer 235

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).

Question 236

In Type 1 RTA, which should be corrected first, hypokalemia or acidosis?

Answer 236

. 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

Question 237

how does hypokalemia cause alkalosis?

Answer 237

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.

Question 238

How do you correct metabolic alkalosis due to ECV contraction

Answer 238

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.

Question 239

Vasopressin secretion, water ingestion, and renal water transport collaborate to maintain human body fluid osmolality between 280 and 295 mOsm/kg

Answer 239

Vasopressin secretion, water ingestion, and renal water transport collaborate to maintain human body fluid osmolality between 280 and 295 mOsm/kg

Question 240

More reliable signs of hypovolemia on physical examination

Answer 240

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).

Question 241

two key effectors in the defense of serum osmolality

Answer 241

Water intake and circulating AVP constitute the two key effectors in the defense of serum osmolality

Question 242

Causes of euvolemic hyponatremia

Answer 242

if UNa >20, renal losses

Question 243

Causes of hypervolemic hyponatremia

Answer 243

if UNa >20, renal losses

Question 244

T/F
The degree of hyponatremia provides an indirect index of the associated neurohumoral activation and is an important prognostic indicator in hypervolemic hyponatremia.

Answer 244

True

Question 245

Formula for corrected sodium in hyperglycemia

Answer 245

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

Question 246

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.

Answer 246

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.

Question 247

subset of px with highest risk of developing hypernatremia

Answer 247

Elderly individuals with reduced thirst and/or diminished access to fluids are at the highest risk of developing hypernatremia.

Question 248

Rate of correction of hypernatremia in adults

Answer 248

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

Question 249

Majority of potassium is excreted via

Answer 249

urine (90%)

Question 250

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.

Answer 250

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.

Question 251

What beta lactams are associated with hypokaleia

Answer 251

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

Question 252

T/F licorice is associated with hyperkalemia

Answer 252

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.

Question 253

Loss of the transport functions of the TALH and DCT nephron segments causes hereditary hypokalemic alkalosis and ______ and _______ respectively

Answer 253

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

Question 254

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

Answer 254

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

Question 255

most important infectious cause of adrenal insufficiency

Answer 255

HIV has surpassed tuberculosis as the most important infectious cause of adrenal insufficiency

Question 256

How does brugada type 1 pattern from hyperkalemia differ from genetic brugada syndrome based on ecg?

Answer 256

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.

Question 257

Effect of hyperkalemia on pH

Answer 257

Hyperkalemia can cause metabolic acidosis

Question 258

First step in managing px with severe hyperkalemia

Answer 258

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.

Question 259

What could be given to reduce hyperkalemia by means of Rapid reduction in plasma K+ concentration by redistribution into cells.

Answer 259

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.

Question 260

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 .

Answer 260

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.

Question 261

Treatment for endocarditis associated GN

Answer 261

Primary treatment is eradication of the infection with 4–6 weeks of antibiotics, and if accomplished expeditiously, the prognosis for renal recovery is good

Question 262

Pathophysiology of Goodpasture syndrome

Answer 262

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.

Question 263

Treatment for Goodpasture syndrome

Answer 263

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.

Question 264

Scoring system with predictive value for IgA Nephropathy

Answer 264

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

Question 265

Treatment for IgA Nephropathy

Answer 265

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.

Question 266

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.

Answer 266

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

Question 267

small-vessel vasculitis that is associated with peripheral eosinophilia, cutaneous purpura, mononeuritis, asthma, and allergic rhinitis

Answer 267

EGPA

previously known as Churg Strauss

Question 268

Treatment for MPGN

Answer 268

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

Question 269

most common cause of nephrotic
syndrome in the elderly.

Answer 269

membranous nephropathy/ MGN

Uniform thickening of the basement membrane along the peripheral capillary loops is seen by light microscopy on renal biopsy

Question 270

Treatment for membranous nephropathy

Answer 270

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.

Question 271

When do you test for albuminuria in px with T1DM and T2DM

Answer 271

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.

Question 272

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

Answer 272

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).

Question 273

Presentation of Alport’s syndrome

Answer 273

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.

Question 274

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

Answer 274

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

Question 275

How does HIVAN differ from other causes of nephrotic syndrome?

Answer 275

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

Question 276

Scistosoma species associated with renal dse

Answer 276

Schistosoma mansoni is most commonly associated with clinical renal disease