Urinary plasminogen activator activity in progressive renal failure.

Abstract

The purpose of this study was to discover how functional nephrons produce the plasminogen activator as renal function progresses to renal failure. Urine Plasminogen activator (U-PA) activity was measured by the fibrin plate method in 73 patients with various degrees of renal function deterioration from various underlying diseases and in one healthy individual in order to evaluate the plasminogen activator activity of remanant nephrons. The plasminogen activator activity of the 12 consecutive urine samples from the healthy individual showed that is varied according to the time of day, but there was no circadian rhythm. The urine plasminogen activator activity correlated with the osmolality (r = 0.51, P<0.001) and creatinine (r = 0.56, P<0.001) of the urine, suggesting that it is concentrated at distal nephrons. The fractional sodium excretion rate (FeNa) increased abruptly when GFR decreased below 25 L/day. This pattern was very similar with the relation between total U-PA activity/GFR and GFR. The correlation between total U-PA activity and FeNa was not significant, but there was a significant direct correlation between total U-PA activity/GFR and FeNa (r = 0.775, P<0.0001). There was no relationship between the 24-hour urine protein and total U-PA activity or total U-PA activity/GFR. The total urine plaminogen activator activity correlated with the 24-hour urine Na (r = 0.3, P<0.0001) and volume (r = 0.434, P<0.0001) but not with total U-PA activity/GFR. The total U-PA activity correlated with GFR (r = 0.41, P<0.0001) but the total U-PA activity/GFR correlated inversely with the GFR (r = 0.552, P<0.0001). Our result suggests that as the renal mass decreases, the total urine plasminogen activator activity decline, but remnant nephrons produce larger amounts of plasminogen activator activity than do normal nephrons.