A 65-year-old man is being evaluated in the hospital. The patient was admitted 5 days ago for increasing lower extremity edema and dyspnea. Medical history is significant for obesity hypoventilation syndrome, pulmonary hypertension, and chronic lower extremity edema. Current temperature is 37.2 C (99 F), blood pressure is 110/70 mm Hg, pulse is 90/min, and respirations are 16/min. BMI is 50 kg/m². Laboratory results are as follows: Which of the following is the most likely cause of the laboratory abnormalities in this patient?

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11ec160b_3b59_6b82_9249_b340a72273e2_MD0001_00 This patient has volume overload due to right-sided heart failure from pulmonary hypertension; he was most likely treated with diuretics to improve his volume status. However, laboratory results on day 5 demonstrate an abrupt decrease in renal function with low urine sodium and an elevated BUN/creatinine ratio (prerenal azotemia). In association with a normal urinalysis, this presentation suggests volume depletion from the excessive use of diuretics. Excessive diuresis can cause renal hypoperfusion and activation of the renin-angiotensin-aldosterone system (RAAS), which increases solute and water reabsorption by the kidney in an attempt to restore intravascular volume. As a result, laboratory studies will show low urine sodium (<20 mEq/L) and low fractional excretion of sodium (FENa <1%). Urea reabsorption is also increased in the collecting ducts, resulting in an increased BUN/creatinine ratio (>20:1). Elevated urine osmolality (>450 mOsm/kg) and urine specific gravity (>1.015) reflect concentrated urine. Evidence of hemoconcentration (eg, increased hemoglobin, albumin, uric acid levels) is also common in volume depleted patients. (Choice B) Interstitial nephritis is characterized by acute kidney injury following exposure to a new medication. Diuretics are a common cause of interstitial nephritis, but urinalysis typically shows pyuria, white blood cell casts, and eosinophils. (Choice C) Osmotic diuresis can cause hypovolemia with low urine sodium but most commonly occurs due to hyperglycemia (eg, uncontrolled diabetes). This patient's blood glucose is normal. (Choice D) Renal artery stenosis causes chronic activation of the RAAS. Patients can develop prerenal failure, but this typically occurs after initiation of an ACE inhibitor rather than a diuretic, and patients are typically hypertensive at baseline. (Choice E) Acute tubular necrosis can be seen in patients with renal ischemia, which can occur in severe hypovolemia; however, muddy brown casts are seen on urinalysis. Laboratory results also demonstrate an intrinsic renal injury pattern (ie, BUN/creatinine ratio ~10:1, FENa >2%) due to impaired tubular function. (Choice F) Ureteral compression can cause unilateral renal obstruction, but AKI typically develops only with bilateral ureteral or bladder outflow obstruction (eg, prostatic hypertrophy). Patients develop significant oliguria or anuria, and pain or a sensation of incomplete voiding is common. Urine studies (ie, sodium, FENa, osmolality) are variable. Educational objective: Hypovolemia (eg, excessive diuresis) can cause acute kidney injury due to reduced renal blood flow (prerenal azotemia). Urine sodium and fractional excretion of sodium levels are low, and the BUN/creatinine ratio is elevated. In severe cases, acute tubular necrosis can occur and cause an intrinsic renal injury pattern (ie, high urine sodium, normal BUN/creatinine ratio) with muddy brown casts on urinalysis. __________ References: Analysis of the prerenal contributions to acute kidney injury. (http://www.ncbi.nlm.nih.gov/pubmed/21921604)

A 65-Year-Old Man Is Being Evaluated in the Hospital