Suzuki S, Sato H, Shimada H, Takashima N, Kishimoto H, Ueno M, Nishi S, Wada K, Takahashi H, Shibata A
Department of Medicine, Niigata University School of Medicine, Japan.
Clin Nephrol. 1993 Nov;40(5):270-6.
To elucidate the relationship between glomerular deposition of plasmin-alpha 2-plasmin inhibitor complexes (PIC) and renal lesions or dysfunction, 25 patients with various glomerulopathies and various degrees of renal injuries were examined. Glomerular PIC deposition was found in eight patients (group A), and other 17 patients showed no deposition (group B). PIC was found mainly in the mesangium and along the capillary loops. Group A showed significantly more severe hematuria (p < 0.05) than group B. Group A showed a significant decrease in glomerular filtration rate (GFR; p < 0.05): the mean values being 60.8 +/- 39 in group A and 94.5 +/- 32 ml/min in group B. Group A showed a significant decrease in the phenolsulfonphthalein excretion test (p < 0.05). There was no significant difference in the mean values of plasma PIC, D-dimer, and thrombin-antithrombin III complexes (TAT) between two groups. Histologically, group A showed a significantly high incidence of adhesion (p < 0.05), crescentic formation (p < 0.05), endothelial swelling and/or detachment (p < 0.01), tubulointerstitial changes (p < 0.01), and glomerular deposition of platelet factor 4 (p < 0.01). The present study demonstrates that glomerular PIC deposition reflects the existence of activation of coagulation and fibrinolysis within the glomeruli and suggests that glomerular PIC deposition plays a part in the progression of renal injuries in various glomerulopathies.