Pauci-immune crescentic glomerulonephritis associated with use of trimethoprim-sulfamethoxazole

Abstract

Drug-induced pauci-immune crescentic glomerulonephritis has been described with several agents, including propylthiouracil, minocycline, D-penicillamine, and hydralazine. We present the case of a 60-year-old man who presented with rapidly progressive glomerulonephritis in the setting of recent use of trimethoprim-sulfamethoxazole complicated by the development of the Stevens-Johnson syndrome, and was found to have biopsy-proven pauci-immune crescentic glomerulonephritis and undetectable anti-neutrophilic cytoplasmic antibodies. We review the existing literature on the potential association between sulfonamides and hypersensitivity polyangiitis.

Keywords: Pauci-immune crescentic glomerulonephritis; Rapidly progressive glomerulonephritis; Trimethoprim–sulfamethoxazole.

Fig. 1

Kidney biopsy findings of pauci-immune crescentic glomerulonephritis and time course of disease. a Top right and bottom left glomeruli contain small cellular crescents with fibrinoid necrosis. Tubules reveal evidence of acute injury with distention by red blood cells and cellular debris (PAS stain, ×100). b A cellular crescent with fibrinoid exudate in the extracapillary space and compression of the glomerular tuft (PAS stain, ×400). c No significant reactivity for immunoglobulin G is seen on direct immunofluorescence microscopy (×400). d Time course of the serum creatinine and daily urine output over the course of the hospitalization. Solid line indicates the serum creatinine (mg/dL), and hatched line indicates the daily urine output