Gastrointestinal Mucosal Cell Injury Caused by Sevelamer Crystals: Case Series and Literature Review

In end-stage kidney disease (ESKD), hyperphosphatemia occurs secondary to decreased renal elimination with continued intestinal absorption of dietary phosphate. Even in chronic kidney disease, glomerular filtration rate lower than 30 mL/min markedly decreases the filtration of inorganic phosphate and increases its serum level. Sevelamer, a noncalcium phosphate binder, is commonly used to control hyperphosphatemia. Available in 2 forms, sevelamer hydrochloride and sevelamer carbonate, it absorbs phosphate in the gastrointestinal tract and is known to have minimal adverse effects. These are limited to nausea, vomiting, flatulence, and metabolic acidosis, with infrequent significant adverse outcomes. We present a series of 2 patients with ESKD on sevelamer, with lower gastrointestinal bleeding and endoscopic findings of colonic mucosal injuries with histopathological findings of sevelamer crystals deposition. Although reported in gastrology literature, nephrology reports show a paucity of discussion around this increasingly common adverse effect and the need for vigilance in ESKD.