Alterations Of Endothelial Function Indices In Chronic Renal Diseases And Their Clinical Significance

Different clinical and pathological changes occur in chronic renal diseases, and most of them accompany endothelial damage to various degree. Local endothelial damage could enhance blood clot and fibrin deposition, which play an important role in progressive renal diseases. There have been a number of reports about endothelial damage in renal diseases. However, the results were rather controversial and most of studies were limited to plasma. The renal diseases could directly affect the indices in urine. Therefore, we measured the concentrations of von Willebrand factor (vWF), 6-keto-PGFl a , tissue-type plaminogen (t-PA) and plasminogen activator inhibitor-1 (PAI-1) both in plasma and in urine. In addition, we studied the express of urine plasminogen activator receptor (u-PAR) in renal tissue by using the method of immunostaining.ELISA method was used to measure the plasma and urine levels of vWF, t-PA and PAI-1. Radioimmunoassay method was used to measure the plasma and urine levels of 6-keto-PGFl a . Streptavidin-Peroxidase method was used to measure u-PAR in the renal tissue with monoclonal antibodies SZ-99 (anti-uPAR). The plasma levels of vWF and t-PA in renal disease groups were higher in comparison with those in normal control groups (PO.05) . The urine levels of t-PA in CRF and NS groups werethan that in the control group (P<0.01) . The urine level of PAI-1 in renal disease groups was lower than that of control group (P<0.05) . The 6-keto-PGFl a levels of renal diseases patients were higher in plasma but lower in urine than those of normal individuals. ?PAR was only little expressed in normal kidney, but increasingly expressed in chronic glomerulonephritis patients' renal tissue. These indices in both blood and the urine were all altered in chronic renal diseases to various degree. Measurement of urine t-PA, PAI-1 and 6-keto-PGFl a would be useful to directly reflect the endothelial injury in kidney.There is no relativity in the alterations of these indices between plasma and urine, suggesting vascular endothelial damage in kidney itself, which is different from the reaction of the whole body. Our results suggest that the changes of indices in urine would be undependent of those in plasma. The indices in urine can more clearly reflect the endothelial damage in kidney than those in the plasma.