Several cases of acute renal failure following cocaine abuse, all associated with rhabdomyolysis, have been reported [1, 2]. We report a case of acute renal failure occurring secondary to cocaine abuse but without evidence of rhabdomyolysis.

A 16-year-old girl with no contributory medical history except for oral contraceptive use was transferred to our hospital for acute renal failure in November 1993. She admitted having inhaled cocaine 3 days before admission. Findings from her physical examination were unremarkable. Her blood pressure was 110/60 mm Hg without orthostatic change, her pulse rate was 72 beats per minute, and she was afebrile. Her urine output remained at 1 to 1.5 L/d with a sodium fractional excretion greater than 1%. Her weight was stable during hospitalization. Complete blood count and routine coagulation test results were normal. Her serum biochemistry results are summarized in Table 1.

Serum levels of complement, antistreptolysin, and antinuclear antibodies were all within normal limits, and a test result for hepatitis B surface antigen was negative. Urinalysis showed a pH of 5.0, positivity for blood, and traces of protein. Microscopic examination showed 3 to 4 erythrocytes, 4 to 6 leukocytes, and 1 granular cast per high-power field. Her kidneys appeared normal in size and slightly hyperechogenic on ultrasound examination. A kidney biopsy specimen obtained on day 2 showed 10 glomeruli of normal appearance. Vessels, interstitium, and tubules were unremarkable except for rare dilatations of tubular lumens, in which a few granular casts were seen. Immunofluorescence staining was nonspecific. The patient recovered renal function spontaneously.

In this case, cocaine was strongly suspected as the only cause of the acute renal failure. To our knowledge, however, all previously reported cases of cocaine-associated acute renal failure were related to an induced rhabdomyolysis. Because the half-life of serum creatine kinase is 17 hours in normal persons and is prolonged in patients with renal insufficiency [3], it seems improbable that rhabdomyolysis was the initiating event of acute renal failure in this patient. Of note, however, the vasoconstrictive properties of cocaine have been previously implicated in cardiovascular toxicity [4]. Vasoconstriction caused by cocaine relates to the blockade of norepinephrine reuptake and to the release of adrenal catecholamines [5]. Ischemia caused by intense intrarenal vasoconstriction may have resulted in medullary hypoxia and tubular dysfunction in our patient. We suggest that acute renal failure following cocaine abuse can supervene in the absence of concomitant rhabdomyolysis.