Renal and urinary glycosaminoglycans in an experimental model of chronic renal failure in rats.

The present paper reports the glomerular and renal individual glycosaminoglycan levels in an experimental model of chronic renal failure (CRF) that was induced in Wistar rats by five-sixths mass ablation. Glycemia, body weight, blood systolic pressure and urinary excretions of creatinine, albumin and glycosaminoglycans were measured for 12 weeks. At the end of the experiment, the weight and the glycosaminoglycan composition of the kidneys were determined. In control rats, heparan sulfate was the main glycosaminoglycan found both in whole kidney and isolated glomeruli, with trace amounts of dermatan sulfate. Isolated glomeruli presented higher heparan sulfate concentrations than whole kidney (expressed as mg/g dry weight). In CRF rats, albuminuria appeared from the 2 week on, and dermatan sulfate and chondroitin sulfate contents of the kidney increased, whereas heparan sulfate levels remained unaltered. Changes in urine glycosaminoglycans (heparan sulfate, chondroitin sulfate and dermatan sulfate) were not statistically significant. The increase in glomerular dermatan sulfate and chondroitin sulfate observed in this experimental model could be related to the mechanisms involved in the glomerulosclerosis and proteinuria that occur in CRF.

Possible role for chondroitin sulfate in urolithiasis: in vivo studies in an experimental model.

The effect of chondroitin sulfate upon the growth of calcium oxalate crystals was measured in vivo by using an experimental model in rats. Adult male Wistar rats were treated by chronic i.p. injections of chondroitin sulfate solutions (1, 5 or 10 mg in 0.3 ml of saline, every 2 days). This treatment led to a dose-dependent increase in the urinary chondroitin sulfate concentration. Urolithiasis was induced by the introduction of a calcium oxalate seed into the bladder of the animals. Urine samples were collected and the calculi formed were removed after 42 days. The chondroitin sulfate concentration have decreased in the lithiasic urines, as compared to controls and higher chondroitin sulfate doses correlated with larger calculi. The presence of chondroitin sulfate in the matrices of stones obtained from chondroitin sulfate-treated animals suggested that there was some adsorption of chondroitin sulfate on to the growth sites of the calcium oxalate crystals. In contrast to the chondroitin sulfate effect observed in vitro, which inhibits the growth of calcium oxalate crystals, our results suggest that in vivo chondroitin sulfate promotes the growth of stones in the urinary tract.