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Role of inflammation in the pathogenesis of cardiorenal syndrome in a rat myocardial infarction model

Authors
Cho, EunjungKim, MinaKo, Yoon SookLee, Hee YoungSong, MyeongjinKim, Myung GyuKim, Hyoung-KyuCho, Won-YongJo, Sang-Kyung
Issue Date
11월-2013
Publisher
OXFORD UNIV PRESS
Keywords
inflammation; kidney; myocardial infarction
Citation
NEPHROLOGY DIALYSIS TRANSPLANTATION, v.28, no.11, pp.2766 - 2778
Indexed
SCIE
SCOPUS
Journal Title
NEPHROLOGY DIALYSIS TRANSPLANTATION
Volume
28
Number
11
Start Page
2766
End Page
2778
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/101723
DOI
10.1093/ndt/gft376
ISSN
0931-0509
Abstract
Cardiorenal syndrome is now frequently recognized, and the combined dysfunction of heart and kidney increases morbidity and mortality. This study aimed to investigate possible mechanisms that underlie renal damage following heart dysfunction using a rat myocardial infarction model, focusing on the inflammatory pathway. Rats were randomized into four groups: normal, volume depletion, sham operation and myocardial infarction (MI). MI was induced by the ligation of the left coronary artery and a volume depletion model was produced by low-salt diet and furosemide injection. Biochemical, histological and flow cytometric analyses were performed at 3 days and 4 and 8 weeks after MI. On Day 3 following MI, the development of subclinical acute kidney injury was identified through significantly increased serum and urine neutrophil gelatinase-associated lipocalin level. We detected the increase of activated monocytes (CC chemokine receptor 2 ED-1) in peripheral blood, along with the infiltration of ED-1 macrophages and the increment of nuclear p65 in the kidney of MI rats, suggesting the contribution of nuclear factor-kappa B-mediated inflammation in the development of Type 1 cardiorenal syndrome (CRS). The inflammatory cytokines, interleukin-6 and tumour necrosis factor- (TNF-) mRNA expression, as well as microvascular endothelial permeability and tubular cell apoptosis, significantly increased in the kidneys of MI rats. At 4 and 8 weeks after MI, tubular cell apoptosis, ED-1 macrophage infiltration and interstitial fibrosis increased in MI rats, and these chronic changes were significantly mitigated by systemic monocyte/macrophage depletion using liposome clodronate. This study identifies the possible important role of inflammatory response as a mediator of heartkidney crosstalk in CRS.
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