S3910 Sevelamer in the Storm: A Silent Player in Ischemic Colitis?

Introduction: Sevelamer is a non-absorbable phosphate binder used in patients with end-stage renal disease (ESRD) to manage hyperphosphatemia. Although generally well tolerated, a rare complication is gastrointestinal mucosal injury due to sevelamer crystal deposition. These crystals can cause mechanical and vascular injury, leading to ulceration and bleeding that may mimic ischemic colitis. Case Description/Methods: A 63-year-old man with ESRD on hemodialysis, atrial fibrillation on apixaban, heart failure with reduced ejection fraction (15%–20%) with automatic implantable cardioverter-defibrillator, diabetes mellitus, and decompensated cirrhosis presented with abdominal pain and bright red blood per rectum following dialysis. He was afebrile with a blood pressure of 113/66 mmHg and heart rate of 78 bpm. Examination showed abdominal distension with bilateral lower quadrant tenderness. Rectal exam revealed scant brown stool with blood streaks. Computed tomography TA of the abdomen and pelvis showed concentric colonic thickening without mesenteric vascular occlusion. Colonoscopy demonstrated severe ischemia with suspected necrosis at the hepatic flexure. Biopsies revealed sevelamer crystal deposition, confirming drug-induced colitis. Surgery was consulted for possible colectomy, but the patient was not a candidate due to hypotension. Sevelamer was discontinued, and the patient was managed conservatively with bowel rest, serial abdominal exams, and supportive care. Bleeding resolved, diet was reintroduced, and the patient was discharged home. Discussion: Sevelamer-induced GI injury can range from mild discomfort to severe bleeding and ulceration. Lesions may appear endoscopically as erosions, ulcers, or pseudopolyps. In this patient, ischemic colitis was initially suspected due to multiple risk factors, but histology confirmed sevelamer crystal deposition. The condition can affect the entire GI tract, with over 25% of patients showing lesions in multiple segments. These crystals are typically non-polarizable and exhibit a “fish-scale” pattern under microscopy. This case highlights the diagnostic challenge in distinguishing ischemic colitis from drug-induced injury, especially when risk factors for both are present. Histological confirmation is crucial for diagnosis. Unlike ischemic colitis, sevelamer-induced colitis improves with discontinuation of the drug and supportive care, avoiding unnecessary surgery. Clinicians should consider this rare adverse effect in ESRD patients presenting with GI symptoms while on sevelamer.