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肾血管病变中慢性肾功能不全的发病机制。

The pathogenesis of chronic renal insufficiency in renal vasculopathies.

作者信息

Bohle A, Mackensen-Haen S, Wehrmann M, Xiao T C

机构信息

Institute of Pathology, University of Tübingen, Germany.

出版信息

Pol Arch Med Wewn. 1994;92 Spec No:92-100.

PMID:7731905
Abstract

Comparative clinical and morphological investigations on the pathogenesis of chronic renal insufficiency in various types of renal vasculopathy revealed the following: 1) Compensated benign nephrosclerosis, with hyalinosis of the walls of the afferent vessels, does not lead to renal insufficiency, since relatively few glomeruli, mostly subcapsular, become obliterated in this disease. 2) In decompensated benign nephrosclerosis, in which not only the afferent vessels but also the glomeruli and the cortical interstitium are involved, there is a significant positive correlation between the relative width of the renal cortical interstitium and the serum creatinine concentration and a significant negative correlation between the relative volume of the postglomerular capillaries and the serum creatinine concentration, as in the primary glomerulopathies. 3) In primary malignant nephrosclerosis, which is always accompanied by haemolytic-uraemic syndrome, the relative width of the cortical interstitium is not related to the serum creatinine concentration. Chronic renal insufficiency develops in this disease as a result of a fall in glomerular filtration rate to inadequate levels due to impairment of renal perfusion by stenotic changes in the preglomerular vessels. 4) In secondary malignant nephrosclerosis, which is never accompanied by haemolytic-uraemic syndrome, there is, as in the primary glomerulopathies, a significant positive correlation between the relative width of the renal cortical interstitium and the serum creatinine concentration and a significant negative correlation between the relative capillary volume and the serum creatinine concentration. 5) In decompensated benign nephrosclerosis the severity of the renal insufficiency depends largely on the degree of obliteration of the postglomerular capillaries.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

对各类肾血管病变所致慢性肾功能不全的发病机制进行的临床与形态学对比研究结果如下

1)代偿性良性肾硬化症,伴有入球小动脉壁玻璃样变,不会导致肾功能不全,因为在此疾病中相对较少的肾小球(大多位于肾包膜下)会闭塞。2)失代偿性良性肾硬化症中,不仅入球小动脉,而且肾小球和皮质间质均受累,肾皮质间质的相对宽度与血清肌酐浓度之间存在显著正相关,而球后毛细血管的相对体积与血清肌酐浓度之间存在显著负相关,这与原发性肾小球病的情况相同。3)原发性恶性肾硬化症总是伴有溶血尿毒症综合征,其皮质间质的相对宽度与血清肌酐浓度无关。在这种疾病中,慢性肾功能不全是由于肾小球前血管的狭窄性改变导致肾灌注受损,使肾小球滤过率降至不足水平所致。4)继发性恶性肾硬化症从不伴有溶血尿毒症综合征,与原发性肾小球病一样,肾皮质间质的相对宽度与血清肌酐浓度之间存在显著正相关,毛细血管相对体积与血清肌酐浓度之间存在显著负相关。5)在失代偿性良性肾硬化症中,肾功能不全的严重程度在很大程度上取决于球后毛细血管的闭塞程度。(摘要截选至250字)

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