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微量白蛋白尿:心血管疾病的标志物还是制造者?

Microalbuminuria: marker or maker of cardiovascular disease.

机构信息

Department of Elderly Medicine, Rotherham General Hospital, Rotherham, UK. ahmedhafiz @ hotmail.com

出版信息

Nephron Exp Nephrol. 2011;119 Suppl 1:e6-10. doi: 10.1159/000328015. Epub 2011 Aug 10.

DOI:10.1159/000328015
PMID:21832857
Abstract

Advancing age is associated with albuminuria and vascular changes. This review will explore the putative links between the two. Vascular ageing involves endothelial dysfunction as well as increased arterial diameter, wall thickness and stiffness, ultimately leading to arterial sclerosis. This process is accelerated by a defective vascular repair process. Endothelial dysfunction is likely to be involved in the initiation and development of microalbuminuria. It is often followed by the development and progression of atherosclerosis. Initially, microalbuminuria is reversible but becomes fixed with the progression of vascular structural changes including glomerulosclerosis. The prevalence of microalbuminuria increases with age and has been shown to be a marker of widespread microvasculopathy at various levels including cerebral, cardiac and renal microcirculations. This has been linked to endpoint clinical events, with microalbuminuria increasing the risk of cognitive impairment and strokes, cardiovascular disease outcomes, and progression to end-stage renal failure. Evidence of microvascular damage such as microalbuminuria associated with increased cardiovascular risk may suggest that microvascular damage and dysfunction predate overt macrovascular disease. Microalbuminuria and reduced glomerular filtration rate (GFR) may be markers of different pathologic processes. It is likely that microalbuminuria and reduced GFR simply represent, respectively, the spectrum of renal vascular manifestations from systemic endothelial dysfunction (microvascular disease) to systemic atherosclerosis (macrovascular disease).

摘要

随着年龄的增长,白蛋白尿和血管变化有关。这篇综述将探讨这两者之间的潜在联系。血管老化涉及内皮功能障碍以及动脉直径、壁厚度和僵硬度的增加,最终导致动脉硬化。这个过程被一个有缺陷的血管修复过程加速。内皮功能障碍可能参与了微量白蛋白尿的发生和发展。它通常伴随着动脉粥样硬化的发展和进展。最初,微量白蛋白尿是可逆的,但随着包括肾小球硬化在内的血管结构变化的进展而变得固定。微量白蛋白尿的患病率随着年龄的增长而增加,并且已经表明它是包括大脑、心脏和肾脏微循环在内的各级广泛微血管病的标志物。这与终点临床事件有关,微量白蛋白尿增加了认知障碍和中风、心血管疾病结局以及进展为终末期肾衰竭的风险。与增加的心血管风险相关的微血管损伤的证据,如微量白蛋白尿,可能表明微血管损伤和功能障碍早于明显的大血管疾病。微量白蛋白尿和肾小球滤过率(GFR)降低可能是不同病理过程的标志物。微量白蛋白尿和 GFR 降低可能只是分别代表了从全身内皮功能障碍(微血管疾病)到全身动脉粥样硬化(大血管疾病)的肾脏血管表现谱。

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