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嘌呤霉素氨基核苷肾病中蛋白尿与尿浓缩功能缺陷的关系

Association of Proteinuria with Urinary Concentration Defect in Puromycin Aminonucleoside Nephrosis.

作者信息

Jo Chor Ho, Kim Sua, Kim Gheun-Ho

机构信息

Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea.

Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea.

出版信息

Electrolyte Blood Press. 2020 Dec;18(2):31-39. doi: 10.5049/EBP.2020.18.2.31. Epub 2020 Dec 28.

DOI:10.5049/EBP.2020.18.2.31
PMID:33408745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7781767/
Abstract

BACKGROUND

Puromycin aminonucleoside (PA) can induce nephrotic syndrome in rats, and proteinuria is an important mediator of tubulointerstitial injury in glomerulopathy. We assumed that glomerular proteinuria may affect tubular function, such as urinary concentration, and investigated whether a urinary concentration defect is associated with proteinuria in puromycin aminonucleoside nephrosis (PAN). We also investigated the defect response to enalapril.

METHODS

Glomerular proteinuria was induced by a single intraperitoneal injection of PA (150mg/kg BW) in male Sprague-Dawley rats. In a half of these rats, enalapril (35mg/kg BW) was administered daily in a food mixture for two weeks. After the animal experiment, kidneys were harvested for immunoblot analysis and histopathologic examination.

RESULTS

Compared with the control group, PA-treated rats had severe proteinuria, polyuria, and a lower urine osmolality. PA treatment induced remarkable tubulointerstitial injury and significant reductions in protein abundances of aquaporin-1 and Na-K-2Cl co-transporter type 2 (NKCC2). Proteinuria significantly correlated with osteopontin expression in the kidney and inversely correlated with renal expression of aquaporin-1, aquaporin-2, and NKCC2. The degree of tubulointerstitial injury significantly correlated with proteinuria, urine output, and osteopontin expression and inversely correlated with urine osmolality and renal expression of aquaporin-1, aquaporin-2, and NKCC2. No significant differences in parameters were found between PA-treated rats with and without enalapril.

CONCLUSION

In PAN, glomerular proteinuria was associated with tubulointerstitial injury and water diuresis. Downregulation of aquaporin-1 and NKCC2 can impair countercurrent multiplication and cause a urinary concentration defect in PAN.

摘要

背景

嘌呤霉素氨基核苷（PA）可诱导大鼠肾病综合征，蛋白尿是肾小球病中肾小管间质损伤的重要介质。我们推测肾小球蛋白尿可能影响肾小管功能，如尿液浓缩功能，并研究了嘌呤霉素氨基核苷肾病（PAN）中尿液浓缩功能缺陷是否与蛋白尿相关。我们还研究了依那普利对该缺陷的反应。

方法

通过单次腹腔注射PA（150mg/kg体重）诱导雄性Sprague-Dawley大鼠出现肾小球蛋白尿。在这些大鼠的一半中，将依那普利（35mg/kg体重）每日添加到食物混合物中给药两周。动物实验结束后，摘取肾脏进行免疫印迹分析和组织病理学检查。

结果

与对照组相比，PA处理的大鼠出现严重蛋白尿、多尿和较低的尿渗透压。PA处理导致显著的肾小管间质损伤，并使水通道蛋白-1和钠-钾-2氯共转运体2（NKCC2）的蛋白丰度显著降低。蛋白尿与肾脏中骨桥蛋白的表达显著相关，与水通道蛋白-1、水通道蛋白-2和NKCC2的肾脏表达呈负相关。肾小管间质损伤的程度与蛋白尿、尿量和骨桥蛋白表达显著相关，与尿渗透压以及水通道蛋白-1、水通道蛋白-2和NKCC2的肾脏表达呈负相关。在接受依那普利治疗和未接受依那普利治疗的PA处理大鼠之间，各项参数未发现显著差异。

结论

在PAN中，肾小球蛋白尿与肾小管间质损伤和水利尿有关。水通道蛋白-1和NKCC2的下调会损害逆流倍增，导致PAN出现尿液浓缩功能缺陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4899/7781767/466bc41042c7/ebp-18-31-g008.jpg
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