Association between renal iron accumulation and renal interstitial fibrosis in a rat model of chronic kidney disease
Autor: | Akiyo Eguchi, Tohru Masuyama, Aya Fujii, Yoshiro Naito, Toshihiro Iwasaku, Makiko Oboshi, Yoshitaka Okuhara, Hisashi Sawada, Daisuke Morisawa, Shinichi Hirotani |
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Rok vydání: | 2015 |
Předmět: |
Male
medicine.medical_specialty Normal diet Physiology Iron Gene Expression Blood Pressure Iron Chelating Agents Kidney urologic and male genital diseases Benzoates Nephrectomy Rats Sprague-Dawley Fibrosis Internal medicine Internal Medicine medicine Renal fibrosis Animals Renal Insufficiency Chronic business.industry Deferasirox Kidney metabolism Glomerulosclerosis Triazoles medicine.disease female genital diseases and pregnancy complications Rats Proteinuria Endocrinology medicine.anatomical_structure Nephritis Interstitial Cardiology and Cardiovascular Medicine business medicine.drug Kidney disease |
Zdroj: | Hypertension Research. 38:463-470 |
ISSN: | 1348-4214 0916-9636 |
DOI: | 10.1038/hr.2015.14 |
Popis: | Iron accumulation is associated with the pathophysiology of chronic kidney disease (CKD). Renal fibrosis is a final common feature that contributes to the progression of CKD; however, little is known about the association between renal iron accumulation and renal interstitial fibrosis in CKD. Here we investigate the effects of iron chelation on renal interstitial fibrosis in a rat model of CKD. CKD was induced by 5/6 nephrectomy in Sprague-Dawley rats. At 8 weeks after operation, 5/6 nephrectomized rats were administered an oral iron chelator, deferasirox (DFX), in chow for 8 weeks. Other CKD rats were given a normal diet. Sham-operative rats given a normal diet served as a control. CKD rats exhibited hypertension, glomerulosclerosis and renal interstitial fibrosis. Iron chelation with DFX did not change hypertension and glomerulosclerosis; however, renal interstitial fibrosis was attenuated in CKD rats. Consistent with these findings, renal gene expression of collagen type III and transforming growth factor-β was increased in CKD rats compared with the controls, while iron chelation suppressed these increments. In addition, a decrease in vimentin along an increase in E-cadherin in renal gene expression was observed in CKD rats with iron chelation. CKD rats also showed increased CD68-positive cells in the kidney, whereas its increase was attenuated by iron deprivation. Similarly, increased renal gene expression of CD68, tumor necrosis factor-α and monocyte chemoattractant protein-1 was suppressed in CKD rats with iron chelation. Renal iron accumulation seems to be associated with renal interstitial fibrosis in a rat model of CKD. |
Databáze: | OpenAIRE |
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