Ratschek M, Ratschek E, Bohle A
Clin Nephrol. 1986 May;25(5):221-6.
Using semiquantitative morphometric methods, the clinical picture of decompensated benign nephrosclerosis is distinguished from that of secondary malignant nephrosclerosis, designated as the consequence of high pressure. It is shown that hypertensive glomerulopathy triggered by high pressure and postglomerular interstitial fibrosis with tubular atrophy are in the foreground of pathologic changes in decompensated benign nephrosclerosis, whereas the preglomerular vessel network is most often affected in secondary malignant nephrosclerosis. The preglomerular vascular lesions in secondary malignant nephrosclerosis lead to such heavy stenosis of the afferent vessels that the clinical picture of hypertensive glomerulopathy is rarely observed, while that of ischemic glomerular capillary collapse is frequent. The preferred affliction of the glomeruli and the postglomerular vessel network leads in decompensated benign nephrosclerosis to severe interstitial fibrosis, which has a pyramidal form, decreasing from the base of the pyramid at the corticomedullary boundary to the outer renal cortex. In secondary malignant nephrosclerosis fibrosis of the renal cortical interstitium is homogeneous in all layers of the renal cortex. Clinically, decompensated benign nephrosclerosis and secondary malignant nephrosclerosis, which occur predominantly in young to middle-aged males, manifest malignant hypertension. They are also accompanied by progressive renal insufficiency.
运用半定量形态测量方法，可将失代偿性良性肾硬化的临床表现与继发性恶性肾硬化相区分，后者被认为是高血压的后果。研究表明，高压引发的高血压性肾小球病以及伴有肾小管萎缩的肾小球后间质纤维化是失代偿性良性肾硬化病理变化的主要特征，而继发性恶性肾硬化中最常受累的是肾小球前血管网络。继发性恶性肾硬化中的肾小球前血管病变导致入球小动脉严重狭窄，以至于很少观察到高血压性肾小球病的临床表现，而缺血性肾小球毛细血管塌陷则较为常见。在失代偿性良性肾硬化中，肾小球和肾小球后血管网络的优先受累会导致严重的间质纤维化，这种纤维化呈锥体状，从皮质髓质交界处的锥体底部向肾外皮质递减。在继发性恶性肾硬化中，肾皮质间质的纤维化在肾皮质的所有层面都是均匀的。临床上，失代偿性良性肾硬化和继发性恶性肾硬化主要发生在青年至中年男性，表现为恶性高血压。它们还伴有进行性肾功能不全。
