Board Review: Nephrology

Wednesday, August 19

Question 1
• A 60-year-old woman with a history of type 1 diabetes mellitus and stage 4 chronic kidney disease comes for a routine followup examination. • She asks about modalities of renal replacement therapy.

Which of the following is the best option for this patient? A. 0-Antigen-mismatched deceased donor kidney transplantation B. Peritoneal dialysis C. Hemodialysis D. Living donor kidney transplantation after a course of dialysis E. Preemptive living donor kidney transplantation

Which of the following is the best option for this patient? E. Preemptive living donor kidney transplantation .

. • Timely referral of patients with chronic kidney disease to a nephrologist facilitates preemptive transplantation. • The reasons for this fact are not entirely clear. but accelerated cardiovascular disease associated with dialysis therapy most likely accounts for a portion of the excess mortality seen in patients treated with dialysis before transplantation.• Preemptive kidney transplantation is associated with improved mortality compared with transplantation performed after a course of dialysis.

in whom peritoneal dialysis has been reportedly associated with a higher mortality rate in some centers. . • Mortality rates of patients treated with hemodialysis and peritoneal dialysis in the United States are roughly equivalent except for women with diabetes >65 years of age.• Outcomes of living donor renal transplantations are equivalent to or better than those of wellmatched deceased donor transplantations.

she received hydration with dextran 40. For the first 48 hours postoperatively. On physical examination. her creatinine level increased to 5. There is trace pretibial edema bilaterally. her creatinine level had been between 1. she began cefazolin therapy for wound prophylaxis.8 mg/dL (159. cerebrovascular disease.4 mg/dL (477. C3 and C4 levels are normal.or postoperative hypotension did not develop. Ultrasound shows symmetric echogenic kidneys without hydronephrosis. and C F).45%). Regular medications are ramipril.7 ° (98. intra.16 mol/L) over the past year. The operative site shows no erythema or drainage. temperature is 36. followed by half-normal saline (0. and chronic kidney disease develops nonoliguric acute renal failure after a left femoral– popliteal bypass.1 ° pulse rate is 86/min. and no cellular casts. which was discontinued 5 days preoperatively and has not been reinitiated. Complete blood count is normal without peripheral eosinophilia.Question 2 • A 62-year-old woman with type 2 diabetes mellitus. Preoperatively. Over the first 3 days of hospitalization. • • .47 mol/L) and 1. Urinalysis shows 1+ protein. and clopidogrel. many monomorphic erythrocytes. During the surgery.47 mol/L). The lungs are clear to auscultation. atenolol.6 mg/dL (141. blood pressure is 132/80 mm Hg. Cardiac examination is unremarkable except for a murmur of aortic sclerosis.

Thrombotic microangiopathy .Which of the following is the most likely diagnosis? A. Osmotic tubular injury B. Angiotensin-converting enzyme inhibitor–induced acute renal failure D. Ischemic tubular epithelial cell injury C.

Which of the following is the most likely diagnosis? A. Osmotic tubular injury .

This condition can present as oliguric or nonoliguric acute renal failure and also has been reported in patients treated with mannitol or sucrose-containing preparations of intravenous immune globulin. There are no clearly defined diagnostic urinary or laboratory findings associated with this condition. and renal biopsy is needed for definitive diagnosis. . • Patients with preexisting renal insufficiency are at increased risk for developing this disorder.• This patient has osmotic tubular injury due to dextran 40 use. • Treatment of osmotic tubular injury generally is supportive. but patients with oliguria and sustained increases in plasma osmolality may benefit from plasma exchange to remove retained dextran 40 and thereby limit further renal injury.

• Chronic angiotensin-converting enzyme inhibitor therapy is unlikely to cause acute renal failure. this diagnosis should be considered.• This patient's urinary sediment findings show no muddy brown casts to support a diagnosis of acute tubular necrosis. • Thrombotic microangiopathy is unlikely in the absence of thrombocytopenia and hemolytic anemia. Preliminary evidence shows that IgG inhibitors of the von Willebrand factor–cleaving protease ADAMTS13 mediate clopidogrel-induced thrombotic thrombocytopenic purpura. However. The absence of hypotension and tachycardia on physical examination and during the surgery is not consistent with prerenal azotemia. . because of this patient's recent use of clopidogrel therapy.

.Question 3 • A 60-year-old man with a 10-year history of hypertension is hospitalized for shortness of breath. Two weeks before admission.5 mg/dL (132. Laboratory studies at that time showed a potassium level of 4.2 mmol/L) and a creatinine level of 1. he developed headache and dyspnea on exertion. • Physical examination on admission reveals a blood pressure of 180/120 mm Hg.2 meq/L (4.63 mol/L). Medications include metoprolol and hydrochlorothiazide.

Question 3 • Over the next 2 weeks. Funduscopic examination shows arteriolar tortuosity. 5 mg once daily. • On follow-up examination. Distal pulses are 1+ bilaterally. . He has a right femoral systolic bruit. the blood pressure gradually normalizes after enalapril. 5 mg once daily. his blood pressure is 132/76 mm Hg. The point of maximal impulse is laterally displaced. are added to his regimen. and there is no peripheral edema. and amlodipine.

several hyaline casts/hpf .5 mg/dL (309.1 mmol/L) 105 meq/L (105 mmol/L) 20 meq/L (20 mmol/L) Trace protein.07 mmol/L) 3.47 mol/L) 140 meq/L (140 mmol/L) 5.Laboratory Studies Blood urea nitrogen Creatinine Sodium Potassium Chloride Bicarbonate Urinalysis 45 mg/dL (16.1 meq/L (5.

Decrease the enalapril dose to 2.5 mg/d C. Discontinue enalapril E. Switch enalapril to losartan . Perform magnetic resonance angiography of the renal arteries D.Which of the following is the most appropriate initial step in this patient's management? A. Perform renal biopsy B.

Discontinue enalapril .Which of the following is the most appropriate initial step in this patient's management? D.

• This patient most likely has angiotensin-converting enzyme (ACE) inhibitor–induced prerenal acute renal failure. Therefore. • Generally. Therefore. . A recent study demonstrated that continued ACE inhibitor therapy was associated with sustained renoprotective benefit in patients with stage III and IV chronic kidney disease. the most appropriate initial step in this patient's management is discontinuing enalapril. disease. continuation of ACE inhibitor therapy in patients with chronic kidney disease is indicated when possible. an increase in the creatinine level up to 30% is acceptable after initiation of ACE inhibitors or angiotensin receptor blockers.

this patient demonstrated a >100% increase in the creatinine level. which should raise suspicion for bilateral renal artery stenosis or advanced intrarenal small-vessel disease. as is measurement of the potassium and creatinine levels 7 to 10 days after initiation of therapy and then every 2 to 3 months. • The glomerular filtration rate (GFR) in patients with bilateral renal artery stenosis is maintained to a great extent by an angiotensin II– induced vasoconstriction at the efferent arteriole. • However. . Both ACE inhibitors and angiotensin receptor blockers cause loss of efferent arteriolar vasoconstriction with a resultant decrease in the glomerular capillary pressure and GFR.• Once-daily administration of lower doses of these agents is initially indicated.

• This patient's urine sediment is not sufficiently active to warrant a renal biopsy. • Prospective randomized clinical trials have yet to definitively establish indications for intervening to preserve renal function or decrease cardiovascular complications. percutaneous angioplasty for renal artery stenosis generally is reserved for patients who remain hypertensive despite aggressive pharmacologic therapy. an angiotensin receptor antagonist. Losartan. • Magnetic resonance angiography of the renal arteries would document the status of the renal arteries after discontinuing enalapril. would be as likely as enalapril to cause a decrease in GFR. However. . • Discontinuation of enalapril would be favored over a dose reduction because of this patient's marked decline in GFR and the risk for subsequent ischemic renal injury.

Three months ago. he began treatment with an angiotensin-converting enzyme inhibitor to decrease his proteinuria. The lungs are clear to auscultation and percussion.42 mol/L) and 24hour urinary protein excretion was 3 g/24 h. • • . Ophthalmologic examination reveals hypertensive retinopathy.Question 4 • A 75-year-old man with a 6-month history of the nephrotic syndrome is evaluated for the sudden onset of flank pain and hematuria of 18 hours' duration. On physical examination. At that time. The abdomen is soft with no masses. Cardiac examination reveals an S4 and a normal S1 to S2 with a systolic murmur at the base. His loop diuretic dose also was increased to treat worsening peripheral edema. his blood pressure is 170/90 mm Hg with no orthostatic drop. his creatinine level was 1 mg/dL (88.

0 mg/dL (176.76 mmol/L) 5 erythrocytes and numerous oval fat bodies/hpf.Laboratory Studies Blood urea nitrogen Creatinine Cholesterol Urinalysis 38 mg/dL (13.57 mmol/L) 2.84 mol/L) 300 mg/dL (7. no leukocytes 15 g /24 h 24-Hour urinary protein excretion .

Renal vein thrombosis D. Overaggressive diuresis B. Kidney stones .Which of the following most likely precipitated this patient's renal insufficiency? A. Renal artery stenosis C.

Which of the following most likely precipitated this patient's renal insufficiency? C. Renal vein thrombosis .

• The loss of several inhibitors of the clotting system.• In the setting of the nephrotic syndrome. deteriorating renal function and a urinary protein excretion that markedly increases over the course of 6 months accompanied by worsening peripheral edema raises the suspicion for renal vein thrombosis. such as angiotensin III. into the urine predisposes patients with the nephrotic syndrome to the development of deep venous and renal vein thrombosis. .

• Overaggressive diuresis can cause kidney dysfunction. • Renal stones can cause flank pain. but this presentation would be accompanied by findings associated with volume depletion. In addition. . this condition does not cause an increase in proteinuria. However. not an increase in proteinuria. a rise in the creatinine level indicates the presence of bilateral obstructive stones. including elevated total bicarbonate and blood urea nitrogen levels. which would present with leukocyturia.

Cardiac examination reveals a grade 2/6 systolic ejection murmur. pulse rate is 74/min and blood pressure is 148/86 mm Hg. 25 mg/d. Medications are lisinopril. . • On physical examination. Therapy with over-the-counter ibuprofen was unsuccessful. and hydrochlorothiazide. and new-onset dyspnea on exertion. 20 mg/d. and she discontinued its use. She has a history of hypertension and was diagnosed with type 2 diabetes mellitus that is controlled by diet 2 years ago. decreased exercise tolerance of 1 month's duration. The conjunctivae are pale.Question 5 • A 66-year-old woman is evaluated for fatigue. There is 1+ lower-extremity edema.

1+ protein.Laboratory Studies Hemoglobin Leukocyte count Platelet count Blood urea nitrogen Creatinine Sodium Potassium Chloride Bicarbonate Glucose Albumin Calcium Phosphorus Urinalysis Urinary protein–creatinine ratio 7. no blood.5 mg/g . 5–10 leukocytes/hpf 2.015.0. specific gravity 1.000/ L 64 mg/dL 5.0 mg/dL 5.2 g/dL 7100/ L 125.1 meq/L 110 meq/L 19 meq/L 142 mg/dL 4.4 mg/dL pH 5.0 mg/dL 11.2 mg/dL 133 meq/L 4.

Myeloma kidney E. Acute interstitial nephritis D. Hypertensive nephrosclerosis C.Which of the following is the most likely cause of this patient's renal failure? A. Diabetic nephropathy . Chronic interstitial nephritis B.

Myeloma kidney .Which of the following is the most likely cause of this patient's renal failure? D.

• In addition. and a low anion gap due to an increase in unmeasured cations such as calcium and immunoglobulins in the setting of kidney disease should raise suspicion for myeloma-related kidney disease. Urine protein electrophoresis also confirms the presence and type of light chains excreted in the urine. and nearly 50% of patients with this condition have an elevated creatinine level at the time of diagnosis. Abnormalities in renal function are common in multiple myeloma. severe anemia. including light chains. the addition of sulfosalicylic acid to the urine specimen precipitates all proteins. . However. hypercalcemia. • Myeloma kidney is characterized by an intratubular obstruction with light-chain casts that results in kidney failure. • Classically.• Myeloma kidney is most likely causing this patient's renal failure. myeloma kidney is associated with a discrepancy in proteinuria detection between the dipstick urinalysis and timed urine collection in which dipstick urinalysis reveals only albumin and not light chains.

. However. • Acute interstitial nephritis due to nonsteroidal antiinflammatory drug use has developed in patients with minimal exposure to these agents. sterile pyuria. or peripheral eosinophilia. Diabetes mellitus also would not cause this patient's low anion gap or hypercalcemia.• Chronic tubulointerstitial disease secondary to analgesic use is unlikely in a patient with no history of chronic analgesic use. • Diabetic nephropathy is the most common cause of chronic kidney disease but is unlikely to cause a discrepancy concerning the presence of proteinuria between the urinalysis and the timed urine collection. this condition is uncommon in the absence of skin rash.

benazepril. simvastatin. 30 mg/d. pioglitazone. and chronic kidney disease comes for a routine office visit. She follows a renal diet. . • Medications are glipizide. 80 mg/d. obesity.Question 6 • A 60-year-old woman with hypertension. type 2 diabetes mellitus. 81 mg/d. 100 mg/d. 40 mg twice daily. 40 mg/d. atenolol. 10 mg twice daily. furosemide. and aspirin.

0 meq/L 106 meq/L 23 meq/L 9.Laboratory Studies Creatinine Sodium Potassium Chloride Bicarbonate Calcium Phosphorus Albumin 2.9 mg/dL 4 g/dL .3 mg/dL 140 meq/L 5.7 mg/dL 6.

Sevelamer C. Aluminum hydroxide B.Which of the following should be started to most appropriately treat this patient? A. Vitamin D D. Hemodialysis .

Which of the following should be started to most appropriately treat this patient? B. Sevelamer .

. Hyperphosphatemia contributes to renal osteodystrophy by stimulating parathyroid hormone secretion and may be an important cardiovascular risk factor in patients with chronic kidney disease. • Oral calcium-free phosphate binders such as sevelamer or calcium-containing phosphate binders should be used to lower phosphorus levels and decrease parathyroid hormone secretion in chronic kidney disease.• Sevelamer should be added to this patient's regimen.

• Aluminum hydroxide is the most potent phosphate binder available. 1. Calcitriol or newer generations of vitamin D analogs should be considered in chronic kidney disease to prevent renal osteodystrophy but only after hyperphosphatemia is controlled. which results in increased parathyroid hormone secretion by removing the direct inhibitory effect of calcitriol on the parathyroid gland and by decreasing the serum calcium level. . the active metabolite of vitamin D) decreases. However. and severe osteomalacia.25-dihydroxyvitamin D synthesis (calcitriol. • With a progressive decrease in the glomerular filtration rate. this agent is not recommended because its chronic use is associated with aluminum retention and erythropoietin-resistant microscopic anemia. dementia.

• She also has type 2 diabetes mellitus. 81 mg/d. These lesions became progressively more painful and developed into ulcerative lesions over several months. She has been maintained on chronic in-center hemodialysis for the past 6 years. atrial fibrillation. aspirin. metoprolol. • Medications are warfarin. and erythropoietin. atorvastatin. and hypertension. she noted nodular lesions on the right thigh and then the left. calcium carbonate. calcitriol.Question 7 • A 49-year-old woman with end-stage renal disease is evaluated for painful ulcers involving both legs. . enalapril. • Approximately 6 months ago.

Abdominal examination is unremarkable. There is no peripheral edema. pulse rate is 86/min and irregular and blood pressure is 140/90 mm Hg. She is obese. • There are necrotic ulcers covering most of the thighs bilaterally. .Question 7 • On physical examination. • Cardiac examination shows an irregularly irregular rhythm. The lungs are clear to auscultation.

6 136 meq/L 5.8 mg/dL .1 mg/dL 8.3 meq/L 105 meq/L 19 meq/L 10.Laboratory Studies Hemoglobin Leukocyte count Platelet count INR Sodium Potassium Chloride Bicarbonate Calcium Phosphorus 11.000/µL 2.6 g/dL 15.000/µL 326.

Warfarin-induced skin necrosis . Venous stasis ulcers E. Necrobiosis lipoidica diabetoricum C.Which of the following is the most likely diagnosis? A. Calcific uremic arteriolopathy D. Calcinosis cutis B.

Calcific uremic arteriolopathy .Which of the following is the most likely diagnosis? C.

an elevated calcium–phosphorus product. and female sex. • Risk factors for development of this syndrome include use of warfarin. obesity. vitamin D analogues.” • These lesions typically present as painful violaceous nodules on the trunk.• The location and clinical presentation of this patient's esions are most characteristic of calcific uremic arteriolopathy. . protein S or C deficiency. and buttocks. and calcium-based phosphate binders. proximal extremities. often termed “calciphylaxis.

• Necrobiosis lipidoca diabeticorum usually is asymptomatic. and the lesions associated with this condition typically appear as oval to irregularly shaped plaques on the shins of patients with diabetes. . red-based ulcers typically located medially in the lower leg. Warfarininduced skin necrosis typically occurs early in the course of warfarin therapy.• Calcinosis cutis presents with painless calcified subcutaneous nodules that do not ulcerate. • Venous stasis ulcers are shallow. and lesions associated with this condition present as erythematous macules but progress to ulcers within hours.

aggressive wound care. • Therapy for this condition includes avoidance of vitamin D analogues and calcium-based phosphate binders. • Parathyroidectomy is reserved for affected patients whose serum calcium and phosphorus levels cannot be controlled with phosphate binders and other medical interventions such as cinacalcet. . and treatment of secondary infection. control of the phosphorus level with non–calcium-based phosphate binders.• The role of parathyroid hormone in the pathogenesis of calcific uremic arteriolopathy remains uncertain.

He has felt well recently and is currently on the liver transplant list.Question 8 • A 44-year-old man diagnosed with cryptogenic cirrhosis 2 years ago is hospitalized for a fractured left hip sustained after a car accident. lactulose. He smokes 1 pack of cigarettes daily and does not drink alcoholic beverages or use illicit drugs. . • He is asymptomatic except for pain in his hip. 20 mg twice daily. 30 mL twice daily. • Medications are spironolactone. 50 mg twice daily. oral propranolol. and furosemide. 20 mg twice daily.

respiratory rate is 18/min. and no asterixis is noted. • He has normal mentation. • Cardiac examination reveals no murmurs or rubs. The abdomen is distended but nontender. temperature is 36 ° pulse C. . He is cachectic. and blood pressure is 98/55 mm Hg. There is 2+ peripheral edema and palmar erythema.Question 8 • On physical examination. and his lungs are clear to auscultation. rate is 72/min. There is scleral icterus.

9 mg/dL 130 meq/L 3.Laboratory Studies Glucose Blood urea nitrogen Creatinine Sodium Potassium Chloride Bicarbonate Albumin Arterial blood gas studies pH PCO PO 2 2 88 mg/dL 14 mg/dL 0.3 meq/L 107 meq/L 18 meq/L 2.6 g/dL 7.48 25 mm Hg 92 mm Hg .

Lactulose-induced diarrhea D.Which of the following is the most likely cause of this patient's acid–base disorder? A. Renal tubular acidosis B. Increased minute ventilation . Impaired hepatic conversion of lactate C. Reduced acid buffering capacity of the blood E.

Which of the following is the most likely cause of this patient's acid–base disorder?

E. Increased minute ventilation

• Increased minute ventilation is the most likely cause of this patient's acid–base disorder. • The acid–base disturbance in this patient is a respiratory alkalosis, which commonly develops in end-stage liver disease. • If the serum pH is not measured, this disturbance can be misdiagnosed as metabolic acidosis in patients with end-stage liver disease. • The liver helps to metabolize circulating steroid hormones. Elevated levels of progestins in end-stage liver disease lead to stimulation of the respiratory drive, which causes a primary respiratory alkalosis. • In severe liver disease, decreased clearance of lactate from the circulation can lead to lactic acidosis. However, the absence of an anion gap in this patient excludes this condition.

• Renal tubular acidosis would lead to a metabolic acidosis. However, this patient's pH is alkaline, indicating that an alkalosis is the primary disorder or that another acid–base disorder is present. • Reduced conversion of lactate would be associated with an anion gap metabolic acidosis (lactic acidosis), which is not present in this patient. • Diarrhea would cause a metabolic acidosis, not respiratory alkalosis. • Cirrhosis is not associated with a decreased buffering capacity of the blood.

the protein/creatinine ratio was 1 mg/g. . He strictly maintains a sodium-restricted diet. the blood pressure is 138/85 mm Hg. The cardiac. There is no peripheral edema or rash. pulmonary. • One year ago. • On physical examination. • His only medication is the maximal dose of an angiotensin-converting enzyme inhibitor.Question 9 • A 29-year-old man with a 10-year history of IgA glomerulonephritis is evaluated for persistent microscopic hematuria. and abdominal examinations are unremarkable.

8 g/dL 2 mg/g .Laboratory Studies Creatinine Albumin Urinary protein– creatinine ratio 1 mg/dL 3.

Which of the following is the most appropriate next step in the management of this patient's IgA glomerulonephritis? A. An angiotensin receptor blocker E. A calcium-channel blocker . Tonsillectomy B. Oral corticosteroids D. A diuretic C.

A diuretic C.Which of the following is the most appropriate next step in the management of this patient's IgA glomerulonephritis? A. Tonsillectomy B. An angiotensin receptor blocker E. Oral corticosteroids D. A calcium-channel blocker .

. Therefore. which included many patients with IgA glomerulonephritis. This patient's protein excretion has doubled over the course of a year. combination therapy with an angiotensin-converting enzyme inhibitor and an angiotensin receptor blocker was associated with a decrease in proteinuria. and his blood pressure is not optimally controlled at a level <130/80 mm Hg despite using a maximal dose of an angiotensin-converting enzyme inhibitor. • In the Combination Treatment of Angiotensin-II Receptor Blocker and Angiotensin-Converting Enzyme Inhibitor in Nondiabetic Renal Disease (COOPERATE) trial. the addition of another antihypertensive agent is indicated.• The most appropriate next step for this patient is the addition of angiotensin receptor blocker therapy.

. the addition of a calcium-channel blocker or diuretics in a patient with IgA glomerulonephritis using an angiotensin-converting enzyme inhibitor has been shown to be less useful compared with the addition of an angiotensin receptor blocker. therapy with corticosteroids alone has not been shown to be useful. • Finally. However. • Corticosteroid therapy has been shown to be effective in IgA glomerulonephritis when used with pulse methylprednisolone.• There are no prospective data showing that tonsillectomy decreases morbidity in adult patients in this setting.

The remainder of the examination is normal.Question 10 • A 34-year-old asymptomatic black man is evaluated for peripheral edema of several months' duration. Medical history is unremarkable. pulse rate is 79/min and blood pressure is 140/90 mm Hg. He is in excellent health and appears muscular. • On physical examination. . There is 2+ lower-extremity edema.

0 g/dL (30 g/L) 3+ proteinuria.82 mmol/L) 1.16 mol/L) 3.8 mg/dL (159.1 mg/dL (1. several oval fat bodies/hpf Urinary protein–creatinine ratio 3 mg/g .Laboratory Studies Blood urea nitrogen Creatinine Albumin Urinalysis 5.

Membranoproliferative glomerulonephritis E.Which of the following is the most likely diagnosis? A. Focal segmental glomerulosclerosis C. Focal proliferative lupus nephritis . Membranous nephropathy B. Minimal change disease D.

Focal segmental glomerulosclerosis .Which of the following is the most likely diagnosis? B.

particularly those of younger age. .• This patient most likely has focal segmental glomerulosclerosis. are much less likely. whereas membranous nephropathy usually affects older white patients. membranous nephropathy and minimal change disease. This condition is the most common cause of the nephrotic syndrome in black patients. • Minimal change disease primarily occurs in children. • Two other possible causes of the nephrotic syndrome.

of which this patient shows no signs. . • Moreover. hematuria. • Although this patient has hypertension and renal insufficiency.• Membranoproliferative glomerulonephritis and focal proliferative lupus nephritis are both examples of the nephritic syndrome characterized by hypertension. the absence of hematuria makes any form of the nephritic syndrome less likely. membranoproliferative glomerulonephritis typically is associated with infectious diseases or systemic lupus erythematosus. and renal insufficiency.