Bohle A, Mackensen-Haen S, von Gise H
Institute of Pathology, University of Tübingen, FRG.
Am J Nephrol. 1987;7(6):421-33. doi: 10.1159/000167514.
This is an editorial review of investigations into the correlation of structure and function of the kidney in various inflammatory and noninflammatory glomerular diseases and in focal and diffuse interstitial nephritis. In detail these investigations produced the following results: (1) The excretory function of the glomeruli for substances usually eliminated with the urine is, in the case of inflammatory and noninflammatory glomerular diseases, detrimentally affected by tubulointerstitial changes, i.e. by processes accompanied by interstitial fibrosis and tubular atrophy. Likewise primary interstitial renal diseases when accompanied by interstitial fibrosis and tubular atrophy may lead to reduction in GFR. (2) Inflammatory and noninflammatory glomerular diseases, even when very severe, are not accompanied by a measurable reduction in GFR when the renal cortex interstitium shows no changes and the tubules exhibit no pathological findings. (3) The concentration ability of the kidney, too, depends primarily on tubulointerstitial changes and not primarily on a reduction of the glomerular filtration surface area. As interstitial fibrosis and tubular atrophy increase, the maximum concentration ability of the kidney decreases, even when the glomerular structure is preserved. (4) The decrease in GFR in the case of processes in the renal cortex accompanied by severe interstitial fibrosis is the result of the reduction of the number and of the area of the postglomerular vessels, i.e. the result of an impeded outflow from the glomeruli and of a concomitant slower circulation through the glomeruli. (5) In the case of inflammatory and noninflammatory glomerular and extraglomerular renal diseases accompanied by slight interstitial fibrosis and tubular atrophy, the GFR is detrimentally affected via a hormonally controlled self-regulating mechanism (Thurau-mechanism) in the form as modified by Baumbach and Skott and Leyssac. The glomerular function thereby adapts to an insufficient tubular function, without there necessarily being any structural changes in the glomeruli.
这是一篇关于各种炎症性和非炎症性肾小球疾病以及局灶性和弥漫性间质性肾炎中肾脏结构与功能相关性研究的编辑评论。具体而言,这些研究得出了以下结果:(1)在炎症性和非炎症性肾小球疾病中,肾小球对通常随尿液排出物质的排泄功能会受到肾小管间质变化的不利影响,即受到伴有间质纤维化和肾小管萎缩的过程的影响。同样,原发性间质性肾脏疾病伴有间质纤维化和肾小管萎缩时,可能导致肾小球滤过率降低。(2)当肾皮质间质无变化且肾小管无病理表现时,即使是非常严重的炎症性和非炎症性肾小球疾病,也不会伴有可测量的肾小球滤过率降低。(3)肾脏的浓缩能力也主要取决于肾小管间质变化,而不是主要取决于肾小球滤过表面积的减少。随着间质纤维化和肾小管萎缩的增加,即使肾小球结构保持完整,肾脏的最大浓缩能力也会降低。(4)肾皮质中伴有严重间质纤维化的过程导致肾小球滤过率降低,是肾小球后血管数量和面积减少的结果,即肾小球流出受阻以及随之而来的肾小球内循环减慢的结果。(5)在伴有轻微间质纤维化和肾小管萎缩的炎症性和非炎症性肾小球及肾小球外肾脏疾病中,肾小球滤过率会通过由鲍姆巴赫、斯科尔特和莱萨克修正的激素控制的自我调节机制(图劳机制)受到不利影响。由此,肾小球功能适应肾小管功能不足,而肾小球不一定有任何结构变化。