Proteinuria--a direct cause of renal morbidity?

Proteinuria--a direct cause of renal morbidity?
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蛋白尿——肾脏疾病的直接原因?

DOI:
--
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发表时间:
1994
影响因子:
19.6
通讯作者:
G. Coles
G. Coles
中科院分区:
医学1区
文献类型:
--
作者:
JohnD. Williams;G. Coles

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除此之外,还可能有蛋白尿。大分子通过肾小球基底膜的异常通过本身可能导致一系列事件,从而导致终末期肾病。不仅可以认为蛋白尿可能导致固有的肾小球损害,而且肾小管内大量蛋白质的存在可能会对间质产生破坏性影响。这一点特别重要,因为最近人们的注意力集中在一个众所周知但被忽视的事实上,即肾脏疾病的进展与间质损害关系最好,而不是与肾小球硬化本身相关[3,4]。这篇综述将检验在人类和动物中声称支持“蛋白尿假说”的证据。它还将阐述肾小球通透性增加可能间接导致肾功能下降的机制。
Added to these could be proteinuria. The abnormal passage of macromolecules through the glomerular basement membrane may itself set in train a series of events which leads to end-stage renal disease. Not only can one argue that proteinuria may contribute to intrinsic glomerular damage, but also that the presence of large quantities of protein within the tubules may have a damaging effect on the interstitium. This is particularly relevant since attention has recently focused on a long known but ignored fact that the progression of renal disease correlates best with interstitial damage and not with glomerulosclerosis per se [3, 4]. This review will examine the evidence in both humans and animals which purports to support the "proteinuria hypothesis." It will also address mechanisms whereby increased gbmerular permselectivity might contribute indirectly to a decline in renal function.
同源蛋白负荷诱导的慢性蛋白尿中的肾小球上皮细胞结构和功能。
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