EVIDENCE FOR A PATHOGENIC LINKAGE BETWEEN GLOMERULAR HYPERTROPHY AND SCLEROSIS
EVIDENCE FOR A PATHOGENIC LINKAGE BETWEEN GLOMERULAR HYPERTROPHY AND SCLEROSIS
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DOI：
10.1016/s0272-6386(12)80347-7
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发表时间：
1991-06-01
影响因子：
13.2
通讯作者：
ICHIKAWA, I
中科院分区：
文献类型：
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作者：
FOGO, A;ICHIKAWA, I
免疫或非免疫机制的原发性肾脏疾病导致大量肾单位群的丧失。据推测，功能性肾单位的最初丧失引起残余肾单位的功能和代谢的改变，其本身是自我造成的，导致肾单位的进一步丧失。这种恶性循环的最终结果是终末期肾脏。各种病理生理机制的潜在作用进行了探讨。这些研究表明肾小球肥大和硬化之间存在密切联系。单个肾小球的分析显示这两个参数的双相模式。肾小球硬化的早期发展沿着肾小球肥大，随着肾小球大小的缩小，硬化的进一步发展。因此，我们建议，在最初的肾单位损失后，残余的肾小球暴露于增加的生长促进因子，这是自我施加的性质，由于其能力，以产生过量的细胞外基质在系膜区。当过量的基质使肾小球毛细血管腔闭塞时，出现典型的硬化性病变。这是一个恶性和加速的过程，因为硬化会导致肾单位数量进一步减少，从而使生长促进因子的影响更大，甚至对最初有抵抗力的肾小球也是如此。
Primary renal disease of immunologic or nonimmunologic mechanisms induces loss of substantial nephron population. It is presumed that the initial loss of functioning nephrons causes alterations of function and metabolism in remnant nephrons, which per se are self-inflictive, leading to further loss of nephrons. The ultimate outcome of this vicious cycle is the end-stage kidney. The potential role of various pathophysiologic mechanisms has been explored. These studies have shown a tight link between glomerular hypertrophy and sclerosis. Analysis of individual glomeruli show a biphasic pattern of these two parameters. Early development of glomerular sclerosis takes place along with the hypertrophy of the glomerulus, and further advancement of sclerosis occurs with shrinkage in glomerular size. Thus, we propose that, after initial nephron loss, the remnant glomeruli are exposed to increased growth-promoting factors, which are self-inflictive in nature due to their capacity to produce excessive amounts of extracellular matrix in the mesangial area. When the excessive matrix obliterates the glomerular capillary lumen, a typical sclerotic lesion appears. This is a vicious and accelerating process, since sclerosis induces further reduction in the nephron population, thereby imposing greater influence of growth-promoting factors even on glomeruli that are initially resistant.