Test yourself: Acute renal failure
From the March ACP Hospitalist, copyright © 2007 by the American College of Physicians.
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Sidebar: Key Points |
The following four cases and commentary deal with evaluation of acute renal failure. They are excerpted from ACP's Medical Knowledge Self-Assessment Program (MKSAP14). View correct answers now.
Case 1
A 62-year-old woman with type 2 diabetes mellitus, cerebrovascular disease and chronic kidney disease develops nonoliguric acute renal failure after a left femoral–popliteal bypass. During the surgery, intra- or postoperative hypotension did not develop. Preoperatively, she began cefazolin therapy for wound prophylaxis. For the first 48 hours postoperatively, she received hydration with dextran 40, followed by normal saline (0.45%). Over the first 3 days of hospitalization, her creatinine level increased to 5.4 mg/dL (477.47 µmol/L); her creatinine level had been between 1.6 mg/dL (141.47 µmol/L) and 1.8 mg/dL (159.16 µmol/L) over the past year. Regular medications are ramipril; atenolol; and clopidogrel, which was discontinued 5 days preoperatively and has not been reinitiated.
On physical examination, temperature is 36.7 °C (98.1 °F), pulse rate is 86 beats/min and blood pressure is 132/80 mm Hg. Cardiac examination is unremarkable except for a murmur of aortic sclerosis. The lungs are clear to auscultation. There is trace pretibial edema bilaterally. The operative site shows no erythema or drainage.
Complete blood count is normal without peripheral eosinophilia. C3 and C4 levels are normal. Urinalysis shows 1+ protein, many monomorphic erythrocytes and no cellular casts. Ultrasound shows symmetric echogenic kidneys without hydronephrosis.
Which of the following is the most likely diagnosis?
- Osmotic tubular injury
- Ischemic tubular epithelial cell injury
- Angiotensin-converting enzyme (ACE) inhibitor–induced acute renal failure
- Thrombotic microangiopathy
Case 2
A 38-year-old man with advanced AIDS is hospitalized for respiratory distress, fever and hypoxemia. Community-acquired pneumonia is diagnosed, and the patient initially improves after initiation of levofloxacin therapy. Over the next 2 weeks, his creatinine level progressively increases from 0.8 mg/dL (70.74 µmol/L) to 3.7 mg/dL (327.15 µmol/L). Over the past 3 days, his urine output has decreased to 500 mL/24 h. He has previously been treated for pulmonary tuberculosis and polysubstance abuse.
On physical examination, temperature is 37.8 °C (100.1 °F), pulse rate is 110 beats/min and blood pressure is 110/60 mm Hg. He is thin and in mild respiratory distress. There are scattered petechiae and ecchymoses across his skin, and he has spontaneous gingival bleeding. Pulmonary examination reveals crackles at the right base. The PMI is laterally displaced. The abdomen is soft without organomegaly. There is no edema. On neurologic examination, he is lethargic and able to answer only simple questions.
Laboratory findings are as follows: hemoglobin level, 7.6 g/dL (76 g/L); leukocyte count, 9400 cells/µL (9.4 × 109 cells/L); platelet count, 18,000 cells/µL (18 × 109 cells/L); blood urea nitrogen level, 75 mg/dL (26.78 mmol/L); creatinine level, 3.5 mg/dL (309.47 µmol/L); sodium level, 129 mEq/L (129 mmol/L); potassium level, 3.2 mEq/L (3.2 mmol/L); chloride level, 88 mEq/L (88 mmol/L); bicarbonate level, 30 mEq/L (30 mmol/L); lactate dehydrogenase level, 7483 U/L (124.74 µkat/L); and urinalysis results of 1+ leukocyte esterase, 1+ protein, trace blood and 5 to 10 dysmorphic erythrocytes per high-power field.
A peripheral blood smear is shown here.
Which of the following is the most appropriate next step in this patient's management?
A. Cryoprecipitate infusions
B. Renal biopsy
C. Plasmapheresis and antiretroviral therapy
D. Oral corticosteroids
Case 3
A 60-year-old man with a 10-year history of hypertension is hospitalized for shortness of breath. Two weeks before admission, he developed headache and dyspnea on exertion. Medications include metoprolol and hydrochlorothiazide. Physical examination on admission reveals a blood pressure of 180/120 mm Hg. Laboratory studies at that time showed a potassium level of 4.2 mEq/L (4.2 mmol/L) and a creatinine level of 1.5 mg/dL (132.63 µmol/L).
Over the next 2 weeks, the blood pressure gradually normalizes after enalapril, 5 mg once daily, and amlodipine, 5 mg once daily, are added to his regimen. On follow-up examination, his blood pressure is 132/76 mm Hg. Funduscopic examination shows arteriolar tortuosity. The PMI is laterally displaced. Cardiac examination reveals a right femoral systolic bruit. Distal pulses are 1+ bilaterally, and there is no peripheral edema.
Laboratory findings are as follows: blood urea nitrogen level, 45 mg/dL (16.07 mmol/L); creatinine level, 3.5 mg/dL (309.47 µmol/L); sodium level, 140 mEq/L (140 mmol/L); potassium level, 5.1 mEq/L (5.1 mmol/L); chloride level, 105 mEq/L (105 mmol/L); bicarbonate level, 20 mEq/L (20 mmol/L); and urinalysis results of trace protein and several hyaline casts per high-power field.
Which of the following is the most appropriate initial step in this patient's management?
A. Perform renal biopsy
B. Decrease the enalapril dose to 2.5 mg/d
C. Perform magnetic resonance angiography of the renal arteries
D. Discontinue enalapril
E. Switch enalapril to losartan
Case 4
A 49-year-old woman with end-stage renal disease is evaluated for painful ulcers involving both legs. Approximately 6 months ago, she noted nodular lesions on the right thigh and then the left. These lesions became progressively more painful and developed into ulcerative lesions over several months. She also has type 2 diabetes mellitus, atrial fibrillation and hypertension. She has been maintained on long-term in-center hemodialysis for the past 6 years. Medications are warfarin; aspirin, 81 mg/d; enalapril; metoprolol; atorvastatin; calcium carbonate; calcitriol; and erythropoietin.
On physical examination, pulse rate is 86 beats/min and irregular and blood pressure is 140/90 mm Hg. She is obese. There are necrotic ulcers covering most of the thighs bilaterally. Cardiac examination shows an irregularly irregular rhythm. The lungs are clear to auscultation. Abdominal examination is unremarkable. There is no peripheral edema.
Laboratory findings are as follows: hemoglobin level, 11.6 g/dL (7.2 mmol/L); leukocyte count, 15,000 cells/µL (15 × 109 cells/L); platelet count, 326,000 cells/µL (326 × 109 cells/L); international normalized ratio, 2.6; sodium level, 136 mEq/L (136 mmol/L); potassium level, 5.3 mEq/L (5.3 mmol/L); chloride level, 105 mEq/L (105 mmol/L); bicarbonate level, 19 mEq/L (19 mmol/L); calcium level, 10.1 mg/dL (2.52 mmol/L); and phosphorus level, 8.8 mg/dL (2.84 mmol/L).
Which one of the following is the most likely diagnosis?
A. Calcinosis cutis
B. Necrobiosis lipoidica diabeticorum
C. Calcific uremic arteriolopathy
D. Venous stasis ulcers
E. Warfarin-induced skin necrosis
Answers and commentary
Case 1
Correct answer: A
This patient has osmotic tubular injury due to dextran 40 use. 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. Patients with preexisting renal insufficiency are at increased risk for developing this disorder. There are no clearly defined diagnostic urinary or laboratory findings associated with this condition, and renal biopsy is needed for definitive diagnosis. 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.
This patient's urinary sediment findings show no muddy brown casts to support a diagnosis of acute tubular necrosis. The absence of hypotension and tachycardia on physical examination and during the surgery is not consistent with prerenal azotemia. Long-term ACE inhibitor therapy is unlikely to cause acute renal failure. Thrombotic microangiopathy is unlikely in the absence of thrombocytopenia and hemolytic anemia. However, because of this patient's recent use of clopidogrel therapy, this diagnosis should be considered. Preliminary evidence shows that IgG inhibitors of the von Willebrand factor–cleaving protease ADAMTS13 mediate clopidogrel-induced thrombotic thrombocytopenic purpura.
Case 2
Correct answer: C
The most appropriate next step in this patient's management is plasmapheresis and antiretroviral therapy. This patient presents with the classic pentad of thrombocytopenia, anemia, neurologic symptoms, renal dysfunction and fever characteristic of thrombotic thrombocytopenic purpura. The peripheral blood smear shows schistocytes that indicate an underlying thrombotic microangiopathy.
A deficiency or decreased activity of the von Willebrand factor–cleaving protease ADAMTS13 plays an important role in the pathogenesis of thrombotic thrombocytopenic purpura–hemolytic uremic syndrome. Decreased cleavage of large multimers of von Willebrand factor by ADAMTS13 synthesized in endothelial cells leads to the persistence of unusually large multimers of von Willebrand factor, which results in platelet activation and endocapillary thrombosis.
Decreased ADAMTS13 activity has been demonstrated in patients with HIV infection who have thrombotic thrombocytopenic purpura, possibly because endothelial production of ADAMTS13 by HIV-infected endothelial cells is decreased or because these patients produce an IgG inhibitor of ADAMTS13 activity. Plasmapheresis has been shown to effectively ameliorate thrombotic thrombocytopenic purpura in this setting, and highly active antiretroviral therapy reduces the incidence of relapses. If plasmapheresis is not available, infusions of cryoprecipitate-free fresh frozen plasma may be helpful until plasma exchange can be performed. However, this intervention is not the preferred initial therapy.
Infusions of cryoprecipitate are contraindicated in this setting, because this fraction of plasma is enriched with von Willebrand factor. Platelet transfusions may worsen renal and neurologic complications and therefore generally are avoided. Renal biopsy is indicated for selected patients with atypical features in whom the diagnosis remains uncertain when thrombocytopenia is not a limiting factor; however, a clinical diagnosis can be established in this patient. Oral corticosteroids may be beneficial but are insufficient as the sole intervention.
Case 3
Correct answer: D
This patient most likely has ACE inhibitor–induced prerenal acute renal failure. Therefore, the most appropriate initial step in this patient's management is discontinuing enalapril.
Generally, an increase in the creatinine level up to 30% is acceptable after initiation of ACE inhibitors or angiotensin-receptor blockers. 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. Therefore, continuation of ACE inhibitor therapy in patients with chronic kidney disease is indicated when possible. Once-daily administration of lower doses of these agents is initially indicated, as is measurement of the potassium and creatinine levels 7 to 10 days after initiation of therapy and then every 2 to 3 months. However, this patient demonstrated a more than 100% increase in the creatinine level, which should raise suspicion for bilateral renal artery stenosis or advanced intrarenal small-vessel disease.
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. Both ACE inhibitors and angiotensin-receptor blockers cause loss of efferent arteriolar vasoconstriction with a resultant decrease in the glomerular capillary pressure and GFR.
This patient's urine sediment is not sufficiently active to warrant a renal biopsy.
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. Magnetic resonance angiography of the renal arteries would document the status of the renal arteries after discontinuing enalapril. However, percutaneous angioplasty for renal artery stenosis generally is reserved for patients who remain hypertensive despite aggressive pharmacologic therapy. Prospective randomized clinical trials have yet to definitively establish indications for intervening to preserve renal function or decrease cardiovascular complications. Losartan, an angiotensin-receptor antagonist, would be as likely as enalapril to cause a decrease in GFR.
Case 4
Correct answer: C
The location and clinical presentation of this patient's lesions are most characteristic of calcific uremic arteriolopathy, often termed "calciphylaxis." These lesions typically present as painful violaceous nodules on the trunk, proximal extremities and buttocks. Risk factors for development of this syndrome include use of warfarin, vitamin D analogues and calcium-based phosphate binders; an elevated calcium–phosphorus product; protein S or C deficiency; obesity; and female sex.
Calcinosis cutis presents with painless calcified subcutaneous nodules that do not ulcerate. Necrobiosis lipoidica 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. Venous stasis ulcers are shallow, red-based ulcers typically located medially in the lower leg. Warfarin-induced skin necrosis typically occurs early in the course of warfarin therapy, and lesions associated with this condition present as erythematous macules but progress to ulcers within hours.
The role of parathyroid hormone in the pathogenesis of calcific uremic arteriolopathy remains uncertain. Therapy for this condition includes avoidance of vitamin D analogues and calcium-based phosphate binders, control of the phosphorus level with non–calcium-based phosphate binders, aggressive wound care and treatment of secondary infection. Parathyroidectomy is reserved for affected patients whose serum calcium and phosphorous levels cannot be controlled with phosphate binders and other medical interventions such as cinacalcet.
Key Points
Case 1:
- Patients with chronic kidney disease have increased risk for acute renal failure because of their use of osmotic agents such as dextran 40, mannitol and sucrose-containing preparations of intravenous immune globulin.
Case 2:
- Antiretroviral therapy and plasmapheresis are indicated for patients with HIV infection and thrombotic thrombocytopenic purpura.
Case 3:
- Angiotensin-converting enzyme inhibitor therapy is warranted in patients with stage III and stage IV chronic kidney disease unless the creatinine level rises more than 30% after initiation of therapy.
- Once-daily dosing of ACE inhibitors can decrease the risk for hyperkalemia.
Case 4:
- Calcific uremic arteriolopathy typically presents with painful violaceous nodules on the trunk, proximal extremities and buttocks.
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