Enteric (secondary) hyperoxaluria can occur as a result of the following, except:a. Insufficient dietary calcium intake
Hyperoxaluria may be classified as primary, enteric or idiopathic. Primary hyperoxaluria (Types I and II) is inherited as an autosomal recessive condition that causes defective metabolism of glyoxalate in the liver and excess levels of endogenous oxalate. Enteric hyperoxaluria may occur in patients with functionally or anatomically abnormal small bowel. Oxalate normally complexes with calcium to form an insoluble salt that is excreted in the faeces. However, in conditions such as inflammatory bowel disease or after small bowel resection, the malabsorption of fatty acids leads to the saponification of calcium resulting in increased oxalate absorption from the colon. Similarly, a low-calcium diet encourages the absorption of oxalate from the bowel and should not be recommended to patients who form calcium oxalate stones.
Ethylene glycol (anti-freeze) induces hyperoxaluria and is commonly used in experimental animal studies to investigate calcium oxalate urolithiasis. Ascorbic acid (vitamin C) is converted to oxalate in the liver and may cause hyperoxaluria.
Oxalobacter formigenes is an anaerobic bacterium which colonises the large intestine of humans and causes the degradation of oxalate. It is important in the metabolism of calcium oxalate and its absence in the intestine following treatment with broad spectrum antibiotics such as quinolones may increase the risk of calcium stone formation.