10/20/2026

A 47-year-old man with dark-colored urine and weakness

A 47-year-old man presents to the emergency department because of dark-colored urine and profound weakness that developed over the past 24 hours. Three days ago, he completed an intensive 14-mile backcountry trail repair shift during unseasonably humid weather. His medical history is notable for hyperlipidemia treated with atorvastatin. Over the last 2 days, he has taken several doses of over-the-counter ibuprofen for diffuse muscle soreness. Temperature is 37.1 C (98.8 F), blood pressure is 118/74 mm Hg, pulse is 88/min, and respirations are 16/min. Cardiopulmonary examination is normal. The abdomen is soft and non-tender without suprapubic fullness. He has diffuse tenderness to palpation over both quadriceps and calves without swelling or induration. Laboratory studies reveal: Serum sodium: 138 mEq/L; Serum potassium: 5.3 mEq/L; Serum chloride: 103 mEq/L; Serum bicarbonate: 19 mEq/L; Blood urea nitrogen: 38 mg/dL; Serum creatinine: 3.2 mg/dL (baseline was 0.9 mg/dL 4 months ago); Serum calcium: 8.1 mg/dL; Serum phosphorus: 5.4 mg/dL; Serum uric acid: 9.8 mg/dL. Urinalysis shows reddish-brown urine with specific gravity 1.018, large blood on dipstick, trace protein, and negative leukocyte esterase and nitrites. Microscopic sediment examination demonstrates 0 to 1 red blood cells per high-power field and numerous pigmented granular casts. Which of the following is the most appropriate initial treatment?

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The Correct Answer

D


Explanation

Clinical Pearl:
The diagnostic hallmark of myoglobinuric renal injury is urine dipstick positivity for blood in the absence of red blood cells on microscopy, accompanied by hyperphosphatemia, hyperuricemia, and early hypocalcemia. Prompt intravenous volume expansion with isotonic crystalloid is standard initial therapy, whereas routine bicarbonate administration lacks proven clinical benefit and risks worsening hypocalcemia.


Explanation:
This patient has rhabdomyolysis with pigment-induced acute tubular injury, confirmed by marked discordance between large blood on urine dipstick and minimal red blood cells on microscopic sediment examination, accompanied by pigmented granular casts, muscle tenderness after heavy exertion while taking a statin, and the classic cellular release pattern of hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. Prompt intravenous administration of isotonic saline is the standard of care to restore intravascular volume, enhance tubular flow, dilute intratubular heme pigments, and counteract pigment-mediated vasoconstriction. Routine urinary alkalinization with sodium bicarbonate has not demonstrated superiority over isotonic fluid resuscitation in randomized or observational studies and carries substantial risk of worsening this patient's existing hypocalcemia by promoting calcium phosphate precipitation. Oral prednisone is appropriate for drug-induced acute interstitial nephritis, but that condition is excluded by the absent sterile pyuria or white cell casts and the presence of heme-pigment cast nephropathy. Loop diuretics such as furosemide do not improve outcomes in pigment nephropathy and risk exacerbating hypovolemia in the absence of clinical volume overload. Urgent hemodialysis catheter placement is unwarranted because this patient has no refractory hyperkalemia, severe metabolic acidosis, uremic symptoms, or intractable pulmonary edema.

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