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肾病综合征及其并发症。

The nephrotic syndrome and its complications.

作者信息

Cameron J S

出版信息

Am J Kidney Dis. 1987 Sep;10(3):157-71. doi: 10.1016/s0272-6386(87)80170-1.

DOI:10.1016/s0272-6386(87)80170-1
PMID:3307394
Abstract

Modern views of the pathogenesis and natural history of nephrotic syndrome have changed substantially since the early studies by Cotugno and Bright. Contrary to beliefs held 20 years ago, we do not possess a unique satisfying explanation for the induction, maintenance, and resolution of nephrotic edema, and many concepts firmly established as "classic" are now being revised or reconsidered. These include the relationship between urinary protein losses and hypoalbuminemia, which is complicated by several factors such as daily protein intake, albumin catabolism, and the possible role of albumin loss at extrarenal sites. The influence of lowered plasma albumin on the decrease in plasma volume is also quite complex, due to technical difficulties in measuring plasma volume and turnover of radio-labeled albumin. The most contentious areas are how sodium and water retention are initiated and maintained and the relationship between hypoalbuminemia, plasma oncotic pressure, and edema. While aldosterone excretion and plasma concentrations are elevated in nephrotic patients, data on the renin-angiotensin system are controversial and the renal handling of sodium is related to a host of factors including glomerular filtration rate, altered proximal tubular reabsorption, and the role of vasodilators or vasoconstrictors. The complications of nephrotic syndrome are protean and relatively common. Among those are acute renal failure, thrombosis, infections, and hyperlipidemia. Since the introduction of percutaneous biopsy, the spectrum of lesions underlying nephrotic syndrome has widened considerably, the most common being minimal change, especially in children. There are very few prognostic indicators by which response to treatment may be predicted and these include persistent microscopic hematuria.

摘要

自科图尼奥和布莱特早期的研究以来,对肾病综合征发病机制和自然病程的现代观点已发生了重大变化。与20年前的观点相反,我们对肾病性水肿的诱发、维持和消退并没有一个独特且令人满意的解释,许多被牢固确立为“经典”的概念现在正在被修订或重新考虑。这些包括尿蛋白丢失与低白蛋白血症之间的关系,这因每日蛋白质摄入量、白蛋白分解代谢以及肾外部位白蛋白丢失的可能作用等多种因素而变得复杂。由于测量血浆容量和放射性标记白蛋白周转率存在技术困难,血浆白蛋白降低对血浆容量减少的影响也相当复杂。最具争议的领域是钠和水潴留是如何启动和维持的,以及低白蛋白血症、血浆胶体渗透压和水肿之间的关系。虽然肾病患者醛固酮排泄和血浆浓度升高,但关于肾素 - 血管紧张素系统的数据存在争议,肾脏对钠的处理与许多因素有关,包括肾小球滤过率、近端肾小管重吸收改变以及血管扩张剂或血管收缩剂的作用。肾病综合征的并发症多种多样且相对常见。其中包括急性肾衰竭、血栓形成、感染和高脂血症。自经皮肾活检引入以来,肾病综合征潜在病变的范围已大幅扩大,最常见的是微小病变,尤其是在儿童中。几乎没有可以预测治疗反应的预后指标,其中包括持续性镜下血尿。

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