Petrucco O M, Thomson N M, Lawrence J R, Weldon M W
Br Med J. 1974 Mar 16;1(5906):473-6. doi: 10.1136/bmj.1.5906.473.
Renal biopsies were performed on 11 patients considered clinically and histologically to have pre-eclampsia. Immunofluorescent studies with fluorescein-labelled anti-IgG, IgA, IgM, and IgE complement, albumin, fibrin, and fibrinogen were carried out on the tissue obtained. Significant correlation was obtained between the clinical severity of the disease and the density and pattern of IgM and IgG deposition. Complement was found in glomeruli in severe cases, while complement deposition in the walls of afferent and efferent arterioles was a constant finding. These findings support the concept that an immunological mechanism may be responsible for the renal lesions in pre-eclampsia. If immunity does play a part in the pathogenesis of pre-eclampsia, possible mechanisms include the involvement of histocompatibility antigens and cross-reactivity of fetal and maternal tissues. Renal fibrin deposition in pre-eclampsia may be secondary to an immune process, an occurrence well-described in other forms of glomerulonephritis in man and other species.
对11例临床和组织学诊断为子痫前期的患者进行了肾活检。对所取组织进行了用荧光素标记的抗IgG、IgA、IgM、IgE、补体、白蛋白、纤维蛋白和纤维蛋白原的免疫荧光研究。疾病的临床严重程度与IgM和IgG沉积的密度及模式之间存在显著相关性。在重症病例的肾小球中发现了补体，而在入球小动脉和出球小动脉壁中的补体沉积则是一个恒定的发现。这些发现支持了免疫机制可能是子痫前期肾损害原因的观点。如果免疫在子痫前期的发病机制中确实起作用，可能的机制包括组织相容性抗原的参与以及胎儿和母体组织的交叉反应。子痫前期肾内纤维蛋白沉积可能继发于免疫过程，这在人类和其他物种的其他形式的肾小球肾炎中已有充分描述。
