Increased Single-Nephron GFR in Normal Adults: Too Much of a Good Thing . . . or Maybe Not?

Increased Single-Nephron GFR in Normal Adults: Too Much of a Good Thing . . . or Maybe Not?
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正常成人单肾单位 GFR 增加:好事太多了。

DOI:
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发表时间:
2018
影响因子:
13.2
通讯作者:
R. Steiner
R. Steiner
中科院分区:
医学1区
文献类型:
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作者:
R. Steiner

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已经确定了。活检标本根据肾单位(即肾小球加肾小管)的数量和大小以及肾小球硬化(>10% 的肾小球)、动脉硬化(>50% 的内膜增厚)和间质纤维化进行分级。根据测量的 GFR 除以总肾单位数计算每个个体的平均 sngfr,总肾单位数定义为活检中功能肾单位的密度与计算机断层扫描上总肾皮质体积的乘积,即 sngfr = GFR/[(肾单位密度)×(总皮质体积)]。正常肾脏捐赠者的皮质体积随着 GFR 的增加而增加。因此,对于任何给定的 GFR,功能肾单位密度的降低是平均 sngfr 较高的主要决定因素。在任何年龄段内,个体平均 sngfr 差异很大,但在各个年龄组中,组平均值相似,为 80 ± 40 nl/min。在整个队列中,平均 sngfr 的增加与肾小球硬化和动脉硬化有关,但与间质纤维化无关。较高的平均 sngfr 还与体重指数增加和出生时肾单位禀赋较低有关。对于许多肾脏病学家来说,这项研究表明肾小球过度滤过会导致活检标本异常。表面上健康的个体似乎发生了微妙的超滤损伤。然而,作者警告说,较高的平均 sngfrs 很可能是对肾单位损失的次要有益适应。由于肾脏显微解剖结构的变化,对他们研究结果的解释也变得复杂。在不同的人类研究人群中,平均肾单位数量变化高达 13 倍,平均肾小球体积变化高达 7 倍。在单个肾脏内,肾小球体积可变化多达 8 倍。这可能会给大多数人一个
had been determined. Biopsy specimens were graded for nephron (ie, glomerulus plus tubule) number and size and glomerular sclerosis (>10% of glomeruli), arteriosclerosis (>50% intimal thickening), and interstitial fibrosis. An average sngfr was calculated for each individual from measured GFR divided by total nephron number, which was defined as the product of the density of functioning nephrons on biopsy and total renal cortical volume on computed tomography, that is, sngfr = GFR/[(nephron density) × (total cortical volume)]. Cortical volume increases as GFR increases in normal kidney donors. Therefore, for any given GFR, reduced density of functioning nephrons was the major determinant of a higher average sngfr. Within any age bracket, individual average sngfrs varied widely, but across age groups, group averages were similar, at 80 ± 40 nl/min. In the cohort as a whole, increasing average sngfr was associated with glomerulosclerosis and arteriosclerosis, but not interstitial fibrosis. Higher average sngfrs were also associated with increasing body mass index and measures of low nephron endowment at birth. To many nephrologists, this study would suggest that glomerular hyperfiltration contributed to biopsy specimen abnormalities. Subtle hyperfiltration damage seemed to occur in ostensibly healthy individuals. However, the authors cautioned that higher average sngfrs could well have been a secondary beneficial adaptation to nephron loss. Interpretation of their findings is also complicated by variations in kidney microanatomy. In various human study populations, average nephron number varies up to 13-fold, and mean glomerular volume varies up to 7-fold. Within an individual kidney, glomerular volumes can vary as much as 8-fold. This may give most individuals a
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发表时间: 2017-01-01
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