Question
A 71-year-old, hospitalized man develops abnormal laboratory studies 4 days after starting treatment for exacerbation of congestive heart failure. He also has a history of osteoarthritis and benign prostatic hyperplasia. He recently completed a course of amikacin for bacterial prostatitis. Before hospitalization, his medications included simvastatin and ibuprofen. Blood pressure is 111/76 mm Hg. Serum studies show a creatinine of 2.3 mg/dL (previously normal) and a BUN of 48 mg/dL. Urinalysis shows a urine osmolality of 600 mOsm/kg and urine sodium of 10 mEq/L. Which of the following is the most likely explanation for this patient’s renal insufficiency?
| A. |
Volume depletion
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| B. |
Glomerulonephritis
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| C. |
Renal tubular obstruction
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| D. |
Bladder outlet obstruction
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Show Answer
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Correct Answer � A
Explanation
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Answer A. Volume depletion
This patient’s rise in creatinine (2.3 mg/dL) with a BUN:Cr ratio of > 20:1 indicates prerenal acute kidney injury (AKI).
Volume depletion
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This patient has likely developed AKI due to volume depletion secondary to loop diuretic use (e.g., furosemide), which is an important part of pharmacotherapy for decompensated congestive heart failure (CHF).
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This patient probably already had reduced renal blood flow due to systolic heart failure. Excess diuresis (e.g., with loop diuretics) with subsequent volume depletion further reduces renal blood flow, which stimulates the activation of RAAS.
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Aldosterone causes Na+ and water retention in an attempt to maintain GFR and systemic blood pressure, which in turn, also increases urea reabsorption (BUN:Cr ratio > 20:1).
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The increased Na+ and water retention causes elevated urine osmolarity.
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Because of this potential adverse effect on the kidney, it is important to monitor renal laboratory values in patients with CHF who are being treated with loop diuretics.
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This patient likely also has reduced urine output.
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