S4695 Lanthanum Carbonate-Induced Gastritis Presenting With Melena in a Patient With End Stage Renal Disease

Introduction: We present a rare case of upper gastrointestinal (GI) bleeding in a patient with end-stage renal disease (ESRD), where lanthanum carbonate therapy leads to histologic gastritis and melena, highlighting an underrecognized complication of phosphate binder use. Case Description/Methods: A 63-year-old man with ESRD on hemodialysis, secondary hyperparathyroidism, iron deficiency anemia, anal fissure, and remote tobacco and alcohol use, presents with black stools and is referred for gastroenterology evaluation. He reports black stools with every bowel movement for the past 4–5 months, which temporarily resolve when he runs out of his phosphate binder (lanthanum carbonate). He denies abdominal pain, hematochezia, dizziness, cramping, bloating, appetite changes, or weight loss. A trial of omeprazole twice daily provides no relief. Labs reveal Hgb 10.5 g/dL (baseline 10–11) and Plt 180 × 10⁹/L. Esophagogastroduodenoscopy (EGD) shows a normal esophagus, stomach, and duodenum. Colonoscopy reveals a 6 mm cecal polyp, diffuse diverticulosis, and non-bleeding internal hemorrhoids. Gastric biopsies show mild chronic inflammation and foveolar hyperplasia, with negative H. pylori immunostaining. Notably, granular brown-red amorphous deposits are seen in the superficial lamina propria, consistent with lanthanum carbonate deposition. Lanthanum carbonate is discontinued, and an alternative phosphate binder is initiated. At his follow-up visit, he reports normal-colored stools and no further melena. Discussion: Lanthanum carbonate is a phosphate binder commonly prescribed to manage hyperphosphatemia in patients with end-stage renal disease. Recent literature demonstrates that lanthanum carbonate can deposit in the GI mucosa, particularly in the stomach and duodenum. Many cases of lanthanum carbonate deposition are asymptomatic and discovered incidentally during endoscopy. However, some patients present with symptoms such as nausea, vomiting, and abdominal pain. The mechanism of injury is not fully understood, but it may involve foreign body-type granulomatous reactions, oxidative stress, or direct cytotoxicity from lanthanum. Histology typically shows granular eosinophilic material in the lamina propria, foveolar hyperplasia, and macrophage infiltration. In patients with unexplained upper gastrointestinal symptoms or melena on lanthanum therapy, it is important to consider biopsy even in the setting of normal endoscopy. Discontinuation of lanthanum carbonate and switching to alternative binders often leads to symptom resolution.