D'Agati V, Chander P, Nash M, Mancilla-Jimenez R
Am J Kidney Dis. 1986 Jan;7(1):95-110. doi: 10.1016/s0272-6386(86)80062-2.
Although the glomerulonephritis (GN) and renal vasculitis in polyarteritis nodosa (PAN) are generally considered to be immune-mediated, the pathogenesis of the renal injury and the role of immune complex (IC) deposition are unclear. To better define the nature of the glomerular and vascular injury in PAN, we performed a detailed ultrastructural study of 27 renal biopsies from 20 patients with histologically confirmed PAN of the microscopic or overlap (microscopic/macroscopic) type. A total of 48 arteries and arterioles were studied ultrastructurally, including 20 vessels with recognizable vasculitis in 1 micron-thick survey sections. By immunofluorescence, glomerular and vascular immunoglobulin deposits were generally scanty, primarily located in areas of necrosis or sclerosis. Fibrinogen, C3 and C1 were more commonly detected, often in the absence of demonstrable immunoglobulin. By electron microscopy, discrete electron-dense deposits of probable immune-type were found in the glomeruli of five initial biopsies. No electron-dense deposits were identified in any of the arteries or arterioles studied. In both glomeruli and vessels, endothelial injury and subendothelial fibrin deposition were the earliest detectable ultrastructural changes. The pathogenetic implications of these findings are discussed.
尽管结节性多动脉炎（PAN）中的肾小球肾炎（GN）和肾血管炎通常被认为是免疫介导的，但肾损伤的发病机制以及免疫复合物（IC）沉积的作用尚不清楚。为了更好地界定PAN中肾小球和血管损伤的性质，我们对20例经组织学确诊为显微镜下型或重叠型（显微镜下/肉眼可见型）PAN患者的27份肾活检标本进行了详细的超微结构研究。共对48条动脉和小动脉进行了超微结构研究，其中包括在1微米厚的观察切片中20条可识别血管炎的血管。通过免疫荧光检查，肾小球和血管免疫球蛋白沉积物通常较少，主要位于坏死或硬化区域。纤维蛋白原、C3和C1更常被检测到，且往往在无明显免疫球蛋白的情况下出现。通过电子显微镜检查，在最初的5份活检标本的肾小球中发现了可能为免疫类型的离散电子致密沉积物。在所研究的任何动脉或小动脉中均未发现电子致密沉积物。在肾小球和血管中，内皮损伤和内皮下纤维蛋白沉积是最早可检测到的超微结构变化。本文讨论了这些发现的发病机制意义。
