EP1035 - Watch Out For Phosphate Binders: Colonic Necrosis In A 58-Year-Old Female With Newly Diagnosed End-Stage Renal Disease

Purpose/Background: Medication-induced gastrointestinal injury can cause significant morbidity and mortality in high-risk patients. Sevelamer carbonate, a non-absorbable phosphate binder commonly prescribed for advanced kidney disease, is generally considered safe. However, reports have increasingly linked sevelamer crystal deposition to gastrointestinal (GI) injury, including ulceration, ischemia, and, in rare cases, full-thickness necrosis. Unlike potassium binders, which carry black box warnings for colonic necrosis, phosphate binders are widely used in end-stage renal disease (ESRD) without such recognized risk. While mucosal injury and bleeding have been described, there are few reports of frank colonic necrosis. This report describes a case of extensive colonic necrosis associated with sevelamer initiation in a patient with newly diagnosed ESRD.

Methods/Interventions: A 58-year-old female with a history of daily tobacco and methamphetamine use and untreated atrial fibrillation presented with weakness, dyspnea, and chronic cough. She developed an acute kidney injury requiring dialysis and was started on 1.6 g of sevelamer via nasogastric tube. By hospital day eight, she developed abdominal distension and leukocytosis (34,000/mm³). While emergency department CT showed no signs of bowel compromise, subsequent CT imaging after initiation of sevelamer revealed transmural thickening, edema, and hypo-enhancement of the sigmoid and descending colon, along with new splenic infarcts compared with admission imaging. Exploratory laparotomy demonstrated full-thickness necrosis extending from the rectosigmoid to the splenic flexure, requiring en bloc resection. A second-look operation confirmed no additional necrosis, and an end colostomy was created. Histopathology showed ischemic necrosis with characteristic sevelamer crystal deposition. The patient recovered, regained renal function, and was discharged after 27 days.

Results/Outcomes: This case illustrates severe sevelamer-associated colonic necrosis in a critically ill dialysis-dependent patient. Although rare, sevelamer-related GI injury can mimic ischemic colitis from other causes such as hypoperfusion, embolism, or infection. Definitive diagnosis relies on histopathology, as sevelamer crystals display a distinctive "fish-scale" appearance on microscopy. The proposed mechanism involves direct mucosal injury and potentiation of ischemia. Clinicians should suspect sevelamer-induced injury when unexplained colitis occurs in patients receiving this medication, as prompt recognition and surgical intervention are critical to survival.

Conclusion/Discussion: Colonic necrosis due to sevelamer is an uncommon but potentially fatal complication. This case emphasizes the need for vigilance among clinicians, thorough evaluation of GI symptoms in patients prescribed sevelamer, and the importance of early pathological confirmation to guide timely management.

Sevelamer crystals present within the colonic tissue demonstrating the fish scale appearance
This image visualizes the sevelamer crystals that were deposited into the lining of the colon leading to transmural colonic necrosis.
Ischemic necrosis of the colon
This image depicts the pathological changes within the colonic tissue depicting full thickness colonic wall necrosis.