Effects of the antiplatelet agents, dipyridamole and dilazep dihydrochloride, on in vivo platelet function and proteinuria

• Published in: Nihon Jinzo Gakkai shi Vol. 27; no. 9; pp. 1261 - 1270
• Main Authors: INAGE, HIROMI, KOYAMA, AKIO, NARITA, MITSUHARU, TOJO, SHIZUO
• Format: Journal Article
• Language: English
• Published: Japan Japanese Society of Nephrology 1985
• Subjects: Adolescent; Adult; Azepines - therapeutic use; Blood Platelets - physiology; Dilazep - therapeutic use; Dilazep dihydrochloride; Dipyridamole; Dipyridamole - therapeutic use; Female; Humans; Male; Middle Aged; Platelet function; Proteinuria; Proteinuria - blood; Proteinuria - drug therapy; Serotonin
• ISSN: 0385-2385; 1884-0728
• DOI: 10.14842/jpnjnephrol1959.27.1261

We examined the effects of antiplatelet agents on in vivo platelet function in relation to reduction of proteinuria. Forty-seven patients with glomerulonephritis were studied, of whom 26 were treated with dipyridamole (225-300 mg/day) and 21 were treated with dilazep dihydrochloride (300-450 mg/day, dilazep). Reduction in proteinuria was observed in 8 of the patients treated with dipyridamole (31%), and in 9 of the patients treated with dilazep (43%). In the patients with reduced proteinuria, the concentration of intraplatelet serotonin were increased significantly and the levels of plasma serotonin were decreased significantly by the therapy. The number of patients who became ameliorated in intraplatelet serotonin and plasma serotonin was significantly higher in the patients with reduced proteinuria than in those whose proteinuria unchanged. The plasma β-TG and PF4 levels appeared not to correlate with the reduction in proteinuria. It is concluded that chemical mediators released from platelets, as represented by serotonin, play an important role in the induction of proteinuria. The antiplatelet agents, dipyridamole and dilazep, reduce proteinuria by inhibiting the process involving the release reaction from platelets.