Crystal-induced acute kidney injury (AKI) is caused by the intratubular precipitation of crystals, which results in obstruction. Crystal-induced AKI mostly occurs as a result of acute uric acid nephropathy and following the administration of drugs or toxins that are poorly soluble. A 23-year-old man presented with AIDS and 1 week history of right sided weakness. Brain MRI showed bilateral ring enhancing lesions. Patient was empirically started on pyrimethamine, sulfadiazine and leucovorin. Brain biopsy confirmed the diagnosis of toxoplasmosis. Hospital course was complicated by AKI and labs showed serum creatinine 2.0 mg/dL (baseline 0.8 mg/dL). Urinalysis showed no hematuria or pyuria with urine pH of 6. Examination of urine sediments under polarized light revealed multiple yellow brown asymmetric rosette shaped crystals (sulfonamide crystals). Sulfadiazine was discontinued and patient was switched to clindamycin. Patient was treated with IV fluids (sodium bicarbonate) for urinary alkalinization. The patient’s serum creatinine returned to baseline within 8 days. Sulfadiazine induced crystalluria is a serious complication in patients with AIDS who are treated for toxoplasmosis. Predisposing factors include high dose of sulfadiazine and volume depletion. It usually presents with AKI within 3 weeks of starting the medication. Treatment requires stopping the offending agent, aggressive IV hydration (urine output at least 1.5 L/day) and bicarbonate infusion for urinary alkalinization (goal pH > 7). This case highlights sulfadiazine-induced crystal nephropathy as a reversible cause of AKI. Early drug withdrawal, aggressive hydration, and urinary alkalinization are crucial for recovery. Preventive measures, especially hydration and urine pH monitoring, can significantly reduce risk.
Alahmadi et al. (Fri,) studied this question.