Essential fatty acid deficiency during acute puromycin nephrosis ameliorates late renal injury.

Essential fatty acid deficiency during acute puromycin nephrosis ameliorates late renal injury.
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急性嘌呤霉素肾病期间必需脂肪酸缺乏可改善晚期肾损伤。

DOI:
10.1152/ajprenal.1989.257.5.f798
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发表时间:
1989
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Karnovsky,MJ
Karnovsky,MJ
中科院分区:
--
文献类型:
--
作者:
Diamond,JR;Pesek,I;Ruggieri,S;Karnovsky,MJ

文献摘要

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嘌呤霉素氨基糖苷(PA)肾病与蛋白尿高峰期肾小球巨噬细胞数量显著增加有关。这一观察结果的重要性仍然不确定。必需脂肪酸缺乏(EFAD)饮食消耗正常大鼠肾小球的常驻巨噬细胞和改变肾小球类花生酸代谢。在这项研究中,我们发现,EFAD饮食,仅在急性肾病阶段的持续时间,显着改善复发性蛋白尿,肾功能不全,和形态学损伤特征的晚期,复发阶段的慢性氨基糖苷类肾病。肾小球巨噬细胞数量,孤立的肾小球血栓素B2的生产,和循环白细胞和单核细胞计数显着减少肾病大鼠EFAD饮食2周后PA注射,这在时间上对应于峰值蛋白尿。EFAD饮食在慢性氨基糖苷肾病晚期提供保护和在急性肾病期降低肾小球巨噬细胞数量的确切机制仍有待阐明。
Puromycin aminonucleoside (PA) nephrosis is associated with a significant increase in the glomerular macrophage number during peak proteinuria. The significance of this observation remains uncertain. An essential fatty acid-deficient (EFAD) diet depletes normal rat glomeruli of resident macrophages and alters glomerular eicosanoid metabolism. In this study, we found that an EFAD diet, administered only for the duration of the acute nephrotic phase, significantly ameliorated the recurrent albuminuria, renal dysfunction, and morphological injury characteristic of the late, recurrent phase of chronic aminonucleoside nephrosis. Glomerular macrophage number, isolated glomerular thromboxane B2 production, and circulating leukocyte and monocyte counts were significantly reduced in nephrotic rats on the EFAD diet 2 wk after PA injection, which temporally corresponds to peak albuminuria. The exact mechanism(s) by which the EFAD diet conferred protection in the late phase of chronic aminonucleoside nephrosis and lowered glomerular macrophage number during the acute nephrotic phase remain to be elucidated.