What causes hyperoxaluria?
- Approximately 14% of urinary oxalate comes from dietary absorption and the remainder from metabolism of glyoxylate and ascorbic acid.
- Increased oxidation of glyoxylate to oxalate occurs in the rare autosomal recessive hereditary hyperoxaluria.
- The clinically more important enteric hyperoxaluria occurs with small bowel resection, bypass, or inflammation.
- Small bowel disease may cause bile salt and fat malabsorption, resulting in increased delivery of bile salts and fats to the colon.
- Bile salts damage colonic mucosa, increasing colonic permeability and oxalate absorption. Intestinal fatty acids are negatively charged and bind calcium and magnesium, decreasing the amounts of calcium and magnesium available for binding intestinal oxalate and leaving more oxalate free for intestinal absorption.
- Low-calcium diets do the same. Excess oxalate is primarily absorbed in the bile salt-damaged colon. Thus, patients with small bowel disease and an ileostomy do not hyperabsorb oxalate.
- Excessive dietary oxalate or ascorbic acid (> 2 g/day) also leads to hyperoxaluria.
- Oxalobacter formigenes metabolizes oxalate in the intestinal tract; reductions in these bacteria may also increase oxalate absorption.
- Recent evidence suggests that a healthy microbiome including the gram-negative bacteria O. formigenes may be important in reducing gut absorption of oxalate and urinary oxalate excretion.
