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Sulfadiazine saw a resurgence in the 1980s, specifically in treating AIDS-associated CNS toxoplasmosis but its use brought on a renal risk. Its weak acid nature induces crystallization in acidic urine. Its crystals, resembling wheat sheaves, caused tubular and urinary tract obstruction, amplified by high drug doses, hypoalbuminemia, and volume depletion. Treatment revolves around urinary alkalinization and, in severe cases, hemodialysis. We report a modern-era case of AKI secondary to sulfadiazine crystal nephropathy.
Sulfadiazine was stopped given the strongly suspected crystal-related nephropathy. Intravenous bicarbonate-containing crystalloid solutions were started at a sufficient rate to both alkalinize the urine and maintain a high urinary flow rate. The patient improved clinically by the next day with serum creatinine returning to 0.9 mg/dl a week later at discharge. A kidney ultrasound done one-week post-discharge showed both kidneys to be normal in size and echogenicity, with no hydronephrosis or stones seen.
Sulfadiazine crystal nephropathy can develop when the drug is used for an extended period at high doses with the risk amplified by acidic urine, volume depletion, and hypoalbuminemia. Diagnosis is established by observing of positively birefringent fan-shaped (wheat sheaves) crystals on urine microscopy, abdominopelvic imaging, and stone composition analysis. Resolution of a sulfadiazine-induced crystal nephropathy hinges on stopping the medication, and intravenous volume expansion to achieve both urinary alkalinization and high urinary flow.