Oxalate and urolithiasis

Abstract

Calcium oxalate is the major component of 70�80 % of renal calculi. Both of these components have both dietary and endogenous sources. Oxalate is found in many plant foods but is particularly rich in certain foods such as spinach, certain nuts, green leafy vegetables, and fruits. Hyperoxaluria occurs in 18 % of kidney stone patients, and treatment has been to reduce intake of oxalate-containing foods or co-ingesting calcium-containing foods or supplements in an attempt to have calcium and oxalate bind together to stay in the gastrointestinal tract. Oxalate absorption occurs all along the intestinal tract and recently shown to be transported from the bloodstream into the lumen of the gastrointestinal tract (i.e., secreted). Small intestine and proximal colon are thought to be the secretory portion, and the distal colon is thought to absorb oxalate into the body. This may prove to be an important mechanism to reduce systemic levels of oxalate in future studies. The intestinal bacterium, Oxalobacter formigenes, has been shown to degrade oxalate from dietary foodstuffs and is found less commonly in stoneforming patients. There are any other oxalate-degrading bacteria, but many of these do not rely solely on oxalate as their main food source. There is much room for investigation in this area as only a small amount of the complete intestinal fl ora can be identi fi ed using traditional microbiologic techniques. Probiotic preparations involving many different types of bacteria have met with limited success in clinical trials to reduce hyperoxaluria. There are many subtypes of O. formigenes and it is unknown which would be the best to recolonize kidney stone patients. Enteric hyperoxaluria increases the bioavailability of oxalate in patients with extensive small-bowel resection or enteric bypass surgery for obesity. Primary hyperoxaluria is a rare genetic disorder whereby the defective liver enzyme peroxisomal AGT1 results in a failure to convert glyoxylate to glycine or glycolate resulting in an increased conversion to oxalate. Treatment is challenging and typically requires a combined hepatic and renal transplantation.