Enteric hyperoxaluria

Contraindications Primary or secondary hyperparathyroidism, including hypercalci-uria (renal calcium leak), hypomagnesemic states (serum magnesium less than 1.5 mg/dl), bone disease (osteoporosis, osteomalacia, osteitis), hypocalcemic states (e.g., hypoparathyroidism, intestinal malabsorption), normal or low intestinal absorption and renal excretion of calcium, enteric hyperoxaluria, and patients with high fasting urinary calcium or hypophosphatemia. 

The terminology used to describe conditions associated with prominent renal calcium deposits dismisses the importance of the phosphate anion. Renal parenchymal injury with prominent calcium oxalate deposition is referred to as oxalate nephropathy. Oxalate nephropathy is seen in the setting of primary hyperoxaluria or enteric hyperoxaluria secondary to fat malabsorption. Renal parenchymal injury with abundant calcium phosphate deposits is referred to as... 

Enteric hyperoxaluria refers to a state in which oxalate is over-absorbed in the bowel because of a defect in absorption of fat and bile adds. In those patients, suffering from Crohn s disease or patients with jejunoileal bypass [14, 15], Ca is complexated to fatty (bile) acids by which Ca-oxalate is no longer formed making oxalate available for intestinal absorption. Daily oxalate excretion is in between that of healthy volunteers and... 

Secondary-enteric-hyperoxaluria is a typical complication in patients with diseases involving fat malabsorption, e.g., cystic fibrosis, chronic inflammatory bowel diseases (Crohn s disease), and short-bowel syndrome (Hoppe et al. 1998 Karlowicz and Adelman 1998 SiDHuetal. 1998). Normally, oxalate is intestinally bound to calcium to form insoluble calcium oxalate, which is not absorbed. In patients with enteric hyperoxaluria, calcium instead binds to fatty acids, so more soluble oxalate is absorbed (Williams and Wandzilak 1989). Secondly, patients with cystic fibrosis lack intestinal oxalatedegrading bacteria, Oxalobacter formigenes, which will increase free and absorbable intestinal oxalate (SiDHU et al. 1998). Up to 50% of our patients with cystic fibrosis have hyperoxaluria and nearly 15% develop urolithiasis or NC (Hoppe et al. 2005). Enteric hyperoxaluria may also lead to progressive NC and/or recurrent urolithiasis (Neuhaus et al. 2000). 

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