Clinical and Experimental Studies on The Participation of The Blood Coagulation in The Development of Glomerular Injuries.

Research Project

Project/Area Number	60480227
Research Category	Grant-in-Aid for General Scientific Research (B)
Allocation Type	Single-year Grants
Research Field	Circulatory organs internal medicine
Research Institution	Gunma University
Principal Investigator	MARUSE Takuji Gunma University School of Medicine, 医学部, 助教授 (50010369)
Project Period (FY)	1985 – 1986
Project Status	Completed (Fiscal Year 1986)
Budget Amount *help	¥4,100,000 (Direct Cost: ¥4,100,000) Fiscal Year 1986: ¥600,000 (Direct Cost: ¥600,000) Fiscal Year 1985: ¥3,500,000 (Direct Cost: ¥3,500,000)
Keywords	Serotonin / Blood coagulation / Blood platelet / Thrombosis / 糸球体腎炎
Research Abstract	It has been suggested that the blood coagulation system plays an important role in the development and progression of some human glomerular diseases. Serotonin, a dense granule constituent is released during platelet activation. Plasma and platelet serotonin levels were measured in 40 patients with systemic erythematosus(SLE), 17 with IgA nephropathy, 44 with other miscellaneous diseases and 11 normal controls. Serotonin was assayed with high performance liquid chromatography coupled with fluorescence detection. Plasma levels of <beta> -thrombo-globulin( <beta> -TG) were also measured by radioimmunoassay using a commercially available kit(Amersham Co). Among the normal controls, platelet serotonin was 0.34 <+!-> 0.10 p-mole/ <10^5> platelets. SLE patients had significantly low mean serotonin level, 0.26 <+!-> 0.12 p-mole. In some SLE patients, the association between decreased platelet levels and clinical activities of the disease was observed. The platelet uptake of exogenous serotonin was not different in SLE patients from normal controls. On the other hand, patients with IgA nephropathy had significantly high mean platelet serotonin level , 0.44 <+!-> 0.17 p-mole. No correlation, however, could be demonstrated between platelet serotonin levels and clinical features of the patients. No abnormal platelet serotonin levels were found in patients with the other nephropathies or collagen diseases. Plasma serotonin concentrations were not significantly increased in all patients studied and plasma <beta> -TG levels did not correlate with magnitude of reduction in platelet serotonin. The mechanisms resulting in abnormal platelet serotonin levels with normal storage capacity for serotonin remain to be determined in SLE and IgA nephropathy.