Gaber L W, Spargo B H, Lindheimer M D
Baillieres Clin Obstet Gynaecol. 1987 Dec;1(4):971-95. doi: 10.1016/s0950-3552(87)80045-7.
Pre-eclampsia affects the kidney both functionally and morphologically. Renal haemodynamics decrease and urinary protein excretion increases, in part due to lesions affecting the glomerulus, where a combination of changes produces a characteristic appearance and permits differentiation of pre-eclamptic nephropathy from other glomerular alterations associated with hypertension in pregnancy. In pre-eclampsia the glomerulus is diffusely enlarged and bloodless, due not to proliferation, but to hypertrophy of the intracapillary cells. These alterations, best described ultrastructurally, include hypertrophy of the cytoplasmic organelles in endothelial and occasionally mesangial cells, particularly the lysosomes, which undergo marked enlargement and vacuolization (due to accumulation of free neutral lipids). These reactive changes have been termed 'glomerular capillary endotheliosis'. Other lesions, observed occasionally, include subendothelial and mesangial electron-dense deposits, as well as interposition of mesangial cell cytoplasm or mesangial matrix along an otherwise normal basement membrane. Some investigators have described immunohistologic findings (presence of IgM, IgG and fibrin) which they believe specific for pre-eclampsia, and others have claimed the disease may cause focal segmental glomerulosclerosis (FSGS). We believe the immunohistologic findings are non-specific and insudative, and that FSGS when present predates the pre-eclamptic complication. Finally, the renal lesions appear fully reversible and the disease has no remote cardiorenal effects on its patients.
子痫前期在功能和形态上都会影响肾脏。肾脏血流动力学降低，尿蛋白排泄增加，部分原因是影响肾小球的病变，多种变化的组合产生了特征性表现，使得子痫前期肾病能够与妊娠高血压相关的其他肾小球病变相鉴别。子痫前期时，肾小球弥漫性增大且无血供，这并非由于增殖，而是由于毛细血管内细胞肥大。这些改变在超微结构下描述最为清晰，包括内皮细胞和偶尔的系膜细胞内细胞器肥大，尤其是溶酶体，其会显著增大并空泡化（由于游离中性脂质的积累）。这些反应性改变被称为“肾小球毛细血管内皮病变”。偶尔观察到的其他病变包括内皮下和系膜区电子致密沉积物，以及系膜细胞胞质或系膜基质在原本正常的基底膜处插入。一些研究者描述了免疫组织学发现（IgM、IgG和纤维蛋白的存在），他们认为这些发现是子痫前期特有的，还有一些研究者声称该疾病可能导致局灶节段性肾小球硬化（FSGS）。我们认为免疫组织学发现是非特异性的且为渗出性的，并且当存在FSGS时，它早于子痫前期并发症出现。最后，肾脏病变似乎完全可逆，并且该疾病对患者没有远期心肾影响。
