Oxalosis and chronic renal failure after intestinal bypass.

A 45-year-old man underwent a jejunoileal shunt procedure for obesity. Twenty months later he developed severe oxalosis and chronic renal failure, which required maintenance hemodialysis. The sequential observation of two biopsy specimens and the necropsy (over a span of 39 months) suggests that oxalate deposition caused tubular obstruction and destruction with subsequent atrophy of nephrons. This indicates that patients undergoing intestinal bypass are at risk for developing irreversible renal failure due to enteric hyperoxaluria.

Effect of diuretics on intestinal transport of electrolytes, glucose, and amino acid.

The jejunal mucosal membrane of albino mice was used to study the electrical properties and ion transport. The membrane was bathed in Krebs-Ringer solution with or without glucose. When ethacrynic acid (EA), furosemide, or amiloride was added to the bathing fluid of both sides, a transient increase followed by a decrease of both potential difference (PD) and short circuit current (Isc) were observed. In glucose-containing bathing medium, EA inhibited both net Na and Cl flux and residual flux; however, EA had little effect on both Na and Cl flux in glucose-free bathing medium. Studies using everted intestinal sac technique showed that EA inhibited both glucose and L-tyrosine across the mucosal membrane against concentration gradients. Furosemide and amiloride were less potent than EA in inhibiting the Na and Cl flux when the bathing solution contained glucose. But these two compounds had no effect on glucose and L-tyrosine transport across the intestinal mucosa. Furthermore, they did inhibit Cl flux even in the condition of glucose-free bathing medium. It is postulated that all three diuretics act on the brush-border membrane of the intestine. EA probably inhibits the Na-glucose cotransporting system; furosemide and amiloride inhibit the simple diffusion process of Na entry of Cl exit by decreasing the conductance of the membrane.