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近年来已有证据表明血浆凝血因子Ⅷ(AHF,抗血友病因子)很可能是在血管壁内皮细胞中合成的。肾小球肾炎时,肾小球血管内皮因补体沉淀及其后的炎症反应而受损,继之血小板聚集和局部血管内凝血引起肾小球中纤维素沉淀。因子Ⅷ可刺激血小板聚集/粘附,从而加重肾炎中的纤维素沉淀。作者推测肾炎中最初的血管内皮损害可能与继而发生的肾小球受损的严重性密切相关,因而研究了85例入院时有早期肾炎的患者的因子Ⅷ活性及其相关抗原。其中经肾活检确诊的70例肾炎随访测定了4年。以血清肌酐、24小时内生肌酐清除率(部分病例还包括~(51)铬-EDTA清除率)判断肾功能,入院时有64例肾功能正常,6例中度损害。该70例又以随访结束时
In recent years, there is evidence that plasma coagulation factor Ⅷ (AHF, anti-hemophilia factor) is likely to be synthesized in the vascular wall endothelial cells. Glomerular nephritis, glomerular endothelial endothelium due to complement deposition and subsequent inflammatory response and damage, followed by platelet aggregation and local intravascular coagulation caused glomerular cellulose precipitation. Factor VIII stimulates platelet aggregation / adhesion, thereby exacerbating cellulose deposition in nephritis. The authors hypothesize that the initial endothelial damage in nephritis may be closely related to the subsequent severity of glomerular damage, thus investigating the activity of the factor VIII and its associated antigens in 85 patients with early nephritis on admission. Among them, 70 cases of nephritis confirmed by renal biopsy were followed up for 4 years. Serum creatinine, 24-hour endogenous creatinine clearance (in some cases also includes ~ (51) chromium-EDTA clearance) to determine renal function, 64 cases of normal renal function, 6 cases of moderate damage. The 70 cases were at the end of follow-up