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糖尿病中的肾脏

The kidney in diabetes.

作者信息

Mauer S M, Steffes M W, Brown D M

出版信息

Am J Med. 1981 Mar;70(3):603-12. doi: 10.1016/0002-9343(81)90582-9.

Abstract

The kidneys as a target organ for secondary microvascular complications of diabetes mellitus represents a health problem of enormous social cost. Recent studies in man and animals strongly support the concept that the primary responsibility for diabetic nephropathy rests with the metabolic derangements of the diabetic state. However, these metabolic derangements have complex biological effects; it is unlikely that hyperglycemia, per se, produces all of the nephropathic influences of diabetes. Alterations in microvascular hemodynamics in diabetes probably contribute to glomerular pathology. These alterations may be based upon disturbed vasoactive control mechanisms regulating angiotensin and prostaglandin secretion and metabolism. Although much remains to be learned about the pathogenesis of glomerular basement membrane and mesangial thickening in diabetes, these central structural abnormalities appear separable. Mesangial thickening is reversible by cure of the diabetic state in rats whereas glomerular basement membrane thickening is not. Treatment for the diabetic patient with end-stage renal failure has recently improved markedly. Although presently, kidney transplants from living related donors appear best, cadaver transplants and long-term hemodialysis are reasonable options.

摘要

肾脏作为糖尿病继发性微血管并发症的靶器官,是一个社会成本巨大的健康问题。最近在人类和动物身上进行的研究有力地支持了这样一种观点,即糖尿病肾病的主要责任在于糖尿病状态下的代谢紊乱。然而,这些代谢紊乱具有复杂的生物学效应;高血糖本身不太可能产生糖尿病所有的肾病影响。糖尿病微血管血流动力学的改变可能导致肾小球病变。这些改变可能基于调节血管紧张素和前列腺素分泌及代谢的血管活性控制机制紊乱。尽管关于糖尿病中肾小球基底膜和系膜增厚的发病机制仍有许多有待了解之处,但这些核心结构异常似乎是可区分的。在大鼠中,糖尿病状态的治愈可使系膜增厚逆转,而肾小球基底膜增厚则不然。终末期肾衰竭糖尿病患者的治疗最近有了显著改善。尽管目前,来自活体亲属供体的肾移植似乎是最佳选择,但尸体肾移植和长期血液透析也是合理的选择。

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