Fibrotic diseases of the genitourinary tract are devastating and incompletely understood pathologies. These diseases include urethral and ureteral strictures, retroperitoneal fibrosis, and Peyronie’s disease. They can contribute to obstructive uropathy and sexual dysfunction. Poor understanding of the pathophysiology of these diseases severely limits our ability to prevent and treat them. Genitourinary fibrotic diseases likely represent related pathologies that share common underlying mechanisms involving wound healing in response to injury. These diseases share the common feature of extracellular matrix abnormalities—such as collagen deposition, transforming growth factor-β accumulation, and dysregulation of collagen maturation—leading to abnormal tissue stiffness. Given the association of many of these diseases with autoimmunity, a systemic pro-inflammatory state likely contributes to their associated fibrogenesis. Herein, we explore the immunologic contribution to fibrogenesis in several fibrotic diseases of the genitourinary system. Better understanding how the immune system contributes to fibrosis in these diseases may improve prevention and therapeutic strategies and elucidate the functions of immunologic contributors to fibrosis in general.

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Although rare, sulfamethoxazole-induced urolithiasis has been reported in patients taking trimethoprim-sulfamethoxazole (TMP/SMX). We present the case of a 79-year-old female who formed sulfamethoxazole stones in the setting of chronic indwelling catheterization with recurrent urinary tract infections (UTIs). The patient was a recurrent stone former with five prior stone composition analyses over a 10-year period varying from calcium phosphate to calcium oxalate, to struvite. We highlight the need for further investigation of this phenomenon given the frequent use of TMP/SMX in stone formers with recurrent infections.