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柠檬酸铁对慢性肾脏病小鼠模型的肾保护作用。

Renoprotective effects of ferric citrate in a mouse model of chronic kidney disease.

作者信息

Hanudel Mark R, Czaya Brian, Wong Shirley, Jung Grace, Chua Kristine, Qiao Bo, Gabayan Victoria, Ganz Tomas

机构信息

Division of Pediatric Nephrology, Department of Pediatrics, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, MDCC A2-383, Los Angeles, CA, 90095-1752, USA.

Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.

出版信息

Sci Rep. 2022 Apr 23;12(1):6695. doi: 10.1038/s41598-022-10842-4.

DOI:10.1038/s41598-022-10842-4
PMID:35461329
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9035171/
Abstract

In chronic kidney disease, ferric citrate has been shown to be an effective phosphate binder and source of enteral iron; however, the effects of ferric citrate on the kidney have been less well-studied. Here, in Col4α3 knockout mice-a murine model of progressive chronic kidney disease, we evaluated the effects of five weeks of 1% ferric citrate dietary supplementation. As expected, ferric citrate lowered serum phosphate concentrations and increased serum iron levels in the Col4α3 knockout mice. Consistent with decreased enteral phosphate absorption and possibly improved iron status, ferric citrate greatly reduced circulating fibroblast growth factor 23 levels. Interestingly, ferric citrate also lessened systemic inflammation, improved kidney function, reduced albuminuria, and decreased kidney inflammation and fibrosis, suggesting renoprotective effects of ferric citrate in the setting of chronic kidney disease. The factors mediating possible ferric citrate renoprotection, the mechanisms by which they may act, and whether ferric citrate affects chronic kidney disease progression in humans deserves further study.

摘要

在慢性肾脏病中,柠檬酸铁已被证明是一种有效的磷结合剂和肠内铁源;然而,柠檬酸铁对肾脏的影响尚未得到充分研究。在此,在Col4α3基因敲除小鼠(一种进行性慢性肾脏病的小鼠模型)中,我们评估了为期五周的1%柠檬酸铁饮食补充的效果。正如预期的那样,柠檬酸铁降低了Col4α3基因敲除小鼠的血清磷浓度,并提高了血清铁水平。与肠内磷吸收减少以及铁状态可能改善一致,柠檬酸铁大大降低了循环成纤维细胞生长因子23水平。有趣的是,柠檬酸铁还减轻了全身炎症,改善了肾功能,减少了蛋白尿,并减轻了肾脏炎症和纤维化,提示柠檬酸铁在慢性肾脏病背景下具有肾脏保护作用。介导柠檬酸铁可能的肾脏保护作用的因素、它们可能起作用的机制以及柠檬酸铁是否影响人类慢性肾脏病进展值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/14e32aae14fd/41598_2022_10842_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/86ae3632953b/41598_2022_10842_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/514ed8ed8d9f/41598_2022_10842_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/ec5e59cf3ff4/41598_2022_10842_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/53a801481f39/41598_2022_10842_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/14e32aae14fd/41598_2022_10842_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/86ae3632953b/41598_2022_10842_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/514ed8ed8d9f/41598_2022_10842_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/ec5e59cf3ff4/41598_2022_10842_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/53a801481f39/41598_2022_10842_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/073d/9035171/14e32aae14fd/41598_2022_10842_Fig5_HTML.jpg

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Nephrol Dial Transplant. 2021 Sep 17. doi: 10.1093/ndt/gfab271.
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Erythropoiesis-independent effects of iron in chronic kidney disease.铁在慢性肾脏病中的非促红细胞生成作用
Pediatr Nephrol. 2022 Apr;37(4):777-788. doi: 10.1007/s00467-021-05191-9. Epub 2021 Jul 9.
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Calcium phosphate microcrystals in the renal tubular fluid accelerate chronic kidney disease progression.肾管状液中的磷酸钙微晶加速慢性肾病进展。
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Orphan nuclear receptor ERR-γ regulates hepatic FGF23 production in acute kidney injury.孤儿核受体ERR-γ在急性肾损伤中调节肝脏成纤维细胞生长因子23的产生。
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Excessive fibroblast growth factor 23 promotes renal fibrosis in mice with type 2 cardiorenal syndrome.过量的成纤维细胞生长因子 23 可促进 2 型心肾综合征小鼠的肾纤维化。
Aging (Albany NY). 2021 Jan 15;13(2):2982-3009. doi: 10.18632/aging.202448.
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