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.
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Hoteit et al. (2024) studied this question.
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