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首页> 外文期刊>American Journal of Physiology >Glomerular hypertrophy precedes albuminuria and segmental loss of podoplanin in podocytes in Munich-Wistar-Fromter rats
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Glomerular hypertrophy precedes albuminuria and segmental loss of podoplanin in podocytes in Munich-Wistar-Fromter rats

机译：肾小球肥大先于蛋白尿和慕尼黑-Wistar-Fromter大鼠足细胞中podoplanin的部分丢失

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摘要

Focal segmental glomerulosclerosis (FSGS) is a common cause of end-stage renal disease. Albuminuria is a risk factor for FSGS and is influenced by environmental, genetic, and sex-specific factors. Podocytes play a central role in the development of albuminuria, but the precise relationship between early glomerular and podocyte-associateddamage and albuminuria is unclear. Furthermore, experimental findings demonstrate a sex difference in development of albuminuria and FSGS. We investigated the early glomerular changes in male Munich-Wistar-Fromter (MWF) rats, which spontaneously develop albuminuria, and male albuminuria-resistant spontaneously hypertensive rats (SHR). In addition, since female MWF rats are protected from overt proteinuria and progressive renal disease, we compared the phenotypic changes in podocytes during early development of albuminuria in male and female MWF rats. In male MWF rats, glomerular hypertrophy preceded the onset of albuminuria and was greater than in male SHR. Albuminuria developed starting at 6 wk of age and coincided with focal and segmental loss of podoplanin, increased expression of desmin, entrapment of albumin in affected podocytes, and focal and segmental foot process effacement at the ultrastructural level. Other podocyte-associated molecules, such as nephrin and zonula occludens 1, were unaffected. Early glomerular hypertrophy and podocyte damage did not differ between male and female MWF rats. Our data show for the first time that albuminuria in male and female MWF rats is preceded by glomerular hypertrophy and accompanied by focal and segmental loss of podoplanin when FSGS was not yet present.
机译：局灶性节段性肾小球硬化症（FSGS）是终末期肾脏疾病的常见原因。蛋白尿是FSGS的危险因素，并受环境，遗传和性别特异性因素的影响。足细胞在白蛋白尿的发展中起着核心作用，但是尚不清楚早期肾小球和足细胞相关损伤与白蛋白尿之间的确切关系。此外，实验结果表明，蛋白尿和FSGS的发展存在性别差异。我们调查了雄性慕尼黑-Wistar-Fromter（MWF）大鼠的早期肾小球变化，该大鼠自发发展白蛋白尿和雄性白蛋白尿抵抗性自发性高血压大鼠（SHR）。此外，由于雌性MWF大鼠受到保护，免受明显的蛋白尿和进行性肾脏疾病的影响，我们比较了雌性和MWF大鼠白蛋白尿早期发育过程中足细胞的表型变化。在雄性MWF大鼠中，肾小球肥大先于蛋白尿，且大于雄性SHR。白蛋白尿从6周龄开始发展，并伴有podoplanin的局灶性和节段性丢失，结节蛋白表达增加，受影响的足细胞中白蛋白的包裹以及超微结构水平的局灶性和节段性足突消失。其他足细胞相关分子，如肾素和小带闭塞1，均未受影响。雄性和雌性MWF大鼠之间的早期肾小球肥大和足细胞损伤没有差异。我们的数据首次显示，在不存在FSGS的情况下，雄性和雌性MWF大鼠的白蛋白尿先于肾小球肥大，并伴有podoplanin的局灶性和节段性丢失。

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