Enteric hyperoxaluria: an important cause of end-stage kidney disease

Abstract

Hyperoxaluria is a frequent complication of inflammatory bowel diseases, ileal resection and Roux-en-Y gastric bypass and is well-known to cause nephrolithiasis and nephrocalcinosis. The associated prevalence of chronic kidney disease and end-stage kidney disease (ESKD) is less clear but may be more consequential than recognized. In this review, we highlight three cases of ESKD due to enteric hyperoxaluria following small bowel resections. We review current information on the pathophysiology, complications and treatment of this complex disease.

Keywords: inflammatory bowel disease; kidney stones; oxalate; transplantation; urolithiasis.

FIGURE 1:

Pathophysiology of enteric hyperoxaluria. Fat malabsorption increases (1) oxalate solubility in the intestinal lumen and (2) bowel permeability to oxalate. Malabsorption also causes deficiency of pyridoxine or vitamin B6 leading to the accumulation of peroxisomal glyoxylate that is eventually oxidized to oxalate in the liver. High levels of oxalate excreted in the urine can lead to nephrocalcinosis and calcium oxalate kidney stones.