Cossio P M, Laguens R P, Pantin D J, de Bracco M M, Molinas F, Voyer L E, Arana R M
Clin Exp Immunol. 1977 Sep;29(3):361-8.
Immunopathological and ultrastructural studies were carried out on kidney biopsies of eight children with a persistent nephropathy (PN) following the haemolytic-uremic syndrome (HUS). Significant amounts of in vivo-bound immunoglobulins and C3 were demonstrated by immunofluorescence methods in the glomeruli of all the cases, with a nodular pattern along the capillary walls. In four cases studied, C1q and C4 were also demonstrated, with an identical distribution. Transmission electron-microscope studies revealed a marked thickening of the glomerular basement membrane, and the existence of an electron-dense material with an intramembranous and subepithelial localization. With the exception of one case, serum complement studies did not present major modifications. Coagulation studies reveal that alterations observed in acute HUS were not present in the PN. Results of the present study suggest that an immune mechanism of glomerular damage operates in the pathogenesis of the PN observed after HUS, leading to a normocomplementemic, chronic glomerulonephritis. Although a hypothetical antigen (or perhaps several antigens) remains to be demonstrated, immunofluorescence and electron-microscope studies suggest the deposition of immune complexes in the renal lesions.
对8例溶血尿毒综合征（HUS）后出现持续性肾病（PN）的儿童进行了肾脏活检的免疫病理学和超微结构研究。通过免疫荧光法在所有病例的肾小球中均证实有大量体内结合的免疫球蛋白和C3，沿毛细血管壁呈结节状分布。在4例研究病例中，还证实有C1q和C4，分布相同。透射电子显微镜研究显示肾小球基底膜明显增厚，存在电子致密物质，定位于膜内和上皮下。除1例病例外，血清补体研究未出现重大改变。凝血研究表明，急性HUS中观察到的改变在PN中不存在。本研究结果提示，在HUS后观察到的PN发病机制中存在肾小球损伤的免疫机制，导致补体正常的慢性肾小球肾炎。尽管仍有待证实一种假设的抗原（或可能几种抗原），但免疫荧光和电子显微镜研究提示免疫复合物在肾脏病变中沉积。
