Bone J M, Sherman L A, Valdes A J, Lubowitz H
J Lab Clin Med. 1977 May;89(5):1043-52.
A model of antiglomerular basement membrane nephritis in the rat was used to elucidate the origin of urinary fibrin-fibrinogen-related antigen (FRA). The intrarenal distribution and excretion of 125I-rat fibrinogen was examined to determine whether there was increased filtration of bibrinogen or fibrin degradation products (FDP) or lysis of intraglomerular fibrin. 125I-protein appeared in the urine immediately after injection of 125I-fibrinogen and fell in parallel with the fall in plasma 125I-fibrinogen. Renal retention of 125I-fibrin averaged less than 0.2 percent of the administered dose of 125I-fibrinogen. The infusion of epsilon aminocaproic acid (EACA) had no significant effect on either FRA excretion or 125I-protein excretion. Plasma FDP levels and the elution patteren of 125I-protein from the urine were not significantly changed by EACA infusion. These observations support the view that ruinary FRA excretion in glomerulonephritis is derived predominantly from increased filtration of plasma fibrinogen rather than from breakdown of intraglomerular fibrin.
采用大鼠抗肾小球基底膜肾炎模型来阐明尿中纤维蛋白 - 纤维蛋白原相关抗原（FRA）的来源。检测了¹²⁵I - 大鼠纤维蛋白原在肾内的分布及排泄情况，以确定是否存在纤维蛋白原或纤维蛋白降解产物（FDP）滤过增加或肾小球内纤维蛋白溶解。注射¹²⁵I - 纤维蛋白原后，¹²⁵I - 蛋白立即出现在尿液中，并与血浆¹²⁵I - 纤维蛋白原水平下降呈平行关系。¹²⁵I - 纤维蛋白在肾内的潴留平均不到¹²⁵I - 纤维蛋白原给药剂量的0.2%。输注ε - 氨基己酸（EACA）对FRA排泄或¹²⁵I - 蛋白排泄均无显著影响。输注EACA后，血浆FDP水平及¹²⁵I - 蛋白从尿液中的洗脱模式均无明显变化。这些观察结果支持以下观点，即肾小球肾炎时尿中FRA排泄主要源于血浆纤维蛋白原滤过增加，而非肾小球内纤维蛋白的降解。
