Abstract
Lanthanum carbonate is a noncalcium phosphate binder used in advanced chronic kidney disease (CKD), especially in dialysis populations. Gastroduodenal lanthanum deposition is now a recognized histopathologic finding, but its clinical importance is heterogeneous. The central clinical question is not whether lanthanum can be found in the mucosa but when deposition should be interpreted as a possible contributor to mucosal injury and, otherwise, unexplained bleeding‐anemia phenotypes. Available evidence supports a spectrum from incidental histologic deposition to a smaller clinically meaningful subset associated with melena, occult or chronic upper gastrointestinal blood loss, iron deficiency, recurrent transfusion requirement, or erythropoiesis‐stimulating agent (ESA) hyporesponsiveness. Characteristic whitish lesions are useful endoscopic clues, but deposition can also occur in nonwhitish or minimally abnormal mucosa. Histopathology typically shows histiocyte‐rich accumulation of granular eosinophilic or light‐brown material, sometimes with a foreign‐body‐type reaction. A plausible subset‐specific pathway links mucosal deposition and macrophage activation to epithelial injury, chronic microbleeding, iron‐restricted erythropoiesis, and increased ESA requirements. Clinically meaningful disease is most plausible when exposure history, phenotype, mucosal context, biopsy findings, and—when observed—improvement after lanthanum withdrawal converge. Deposition alone does not establish causality, and the true prevalence of clinically meaningful disease remains unknown. Nevertheless, in selected patients with advanced CKD and refractory anemia, deliberate review of current and prior phosphate‐binder exposure, appropriate gastric biopsy even when endoscopy is nondiagnostic, and reassessment after discontinuation may reveal a potentially reversible diagnostic contributor.