Pathological and functional significance of aging mouse kidneys: clinical implications to reduce the risk of hyper- or hypokalemia in the elderly.

IF 2.9 3区 医学 Q1 UROLOGY & NEPHROLOGY
Itsuro Kazama
{"title":"Pathological and functional significance of aging mouse kidneys: clinical implications to reduce the risk of hyper- or hypokalemia in the elderly.","authors":"Itsuro Kazama","doi":"10.23876/j.krcp.24.012","DOIUrl":null,"url":null,"abstract":"<p><p>Elderly patients are prone to develop hyper- or hypokalemia, since they are susceptible to drugs or diets that affect the urinary or fecal potassium (K+) excretion. In aging mouse kidneys, in addition to glomerulosclerosis, proximal tubular atrophy, and atherosclerosis in renal arterioles, there was diffuse tubulointerstitial fibrosis with a number of inflammatory leukocytes infiltrating into the cortical interstitium. Since these pathological features greatly influence renal K+ handling, slowing the progression of kidney aging would fundamentally reduce the risk of developing hyper- or hypokalemia. Immunohistochemistry demonstrated the overexpression of K+ channels (Kv1.3) in leukocytes within the cortical interstitium, which was strongly associated with \"chronic inflammation\" in aging kidneys and the subsequent progression of renal fibrosis. In our basic studies, antihypertensive drugs (benidipine, nifedipine, verapamil, diltiazem) and anticholesterol drugs (lovastatin, simvastatin, pravastatin) strongly suppressed the leukocyte Kv1.3 channels and thus exerted anti-inflammatory effects. Given such pharmacological properties of these drugs, they may also be useful in slowing the progression of tubulointerstitial fibrosis in aging kidneys and reducing the risk of hyper- or hypokalemia in elderly patients.</p>","PeriodicalId":17716,"journal":{"name":"Kidney Research and Clinical Practice","volume":null,"pages":null},"PeriodicalIF":2.9000,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kidney Research and Clinical Practice","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.23876/j.krcp.24.012","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"UROLOGY & NEPHROLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Elderly patients are prone to develop hyper- or hypokalemia, since they are susceptible to drugs or diets that affect the urinary or fecal potassium (K+) excretion. In aging mouse kidneys, in addition to glomerulosclerosis, proximal tubular atrophy, and atherosclerosis in renal arterioles, there was diffuse tubulointerstitial fibrosis with a number of inflammatory leukocytes infiltrating into the cortical interstitium. Since these pathological features greatly influence renal K+ handling, slowing the progression of kidney aging would fundamentally reduce the risk of developing hyper- or hypokalemia. Immunohistochemistry demonstrated the overexpression of K+ channels (Kv1.3) in leukocytes within the cortical interstitium, which was strongly associated with "chronic inflammation" in aging kidneys and the subsequent progression of renal fibrosis. In our basic studies, antihypertensive drugs (benidipine, nifedipine, verapamil, diltiazem) and anticholesterol drugs (lovastatin, simvastatin, pravastatin) strongly suppressed the leukocyte Kv1.3 channels and thus exerted anti-inflammatory effects. Given such pharmacological properties of these drugs, they may also be useful in slowing the progression of tubulointerstitial fibrosis in aging kidneys and reducing the risk of hyper- or hypokalemia in elderly patients.

老化小鼠肾脏的病理和功能意义:降低老年人高钾血症或低钾血症风险的临床意义。
老年患者容易出现高钾血症或低钾血症,因为他们容易受到药物或饮食的影响,从而影响尿液或粪便中钾(K+)的排泄。在衰老的小鼠肾脏中,除了肾小球硬化、近端肾小管萎缩和肾动脉粥样硬化外,还有弥漫性肾小管间质纤维化,皮质间质内有大量炎性白细胞浸润。由于这些病理特征在很大程度上影响着肾脏对 K+ 的处理,因此减缓肾脏衰老的进程将从根本上降低患高钾血症或低钾血症的风险。免疫组化显示,肾皮质间质内的白细胞中 K+ 通道(Kv1.3)过度表达,这与衰老肾脏中的 "慢性炎症 "以及随后的肾脏纤维化进展密切相关。在我们的基础研究中,降压药(贝尼地平、硝苯地平、维拉帕米、地尔硫卓)和抗胆固醇药(洛伐他汀、辛伐他汀、普伐他汀)能强烈抑制白细胞 Kv1.3 通道,从而发挥抗炎作用。鉴于这些药物的药理特性,它们还可能有助于减缓衰老肾脏中肾小管间质纤维化的进展,降低老年患者出现高钾血症或低钾血症的风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
4.60
自引率
10.00%
发文量
77
审稿时长
10 weeks
期刊介绍: Kidney Research and Clinical Practice (formerly The Korean Journal of Nephrology; ISSN 1975-9460, launched in 1982), the official journal of the Korean Society of Nephrology, is an international, peer-reviewed journal published in English. Its ISO abbreviation is Kidney Res Clin Pract. To provide an efficient venue for dissemination of knowledge and discussion of topics related to basic renal science and clinical practice, the journal offers open access (free submission and free access) and considers articles on all aspects of clinical nephrology and hypertension as well as related molecular genetics, anatomy, pathology, physiology, pharmacology, and immunology. In particular, the journal focuses on translational renal research that helps bridging laboratory discovery with the diagnosis and treatment of human kidney disease. Topics covered include basic science with possible clinical applicability and papers on the pathophysiological basis of disease processes of the kidney. Original researches from areas of intervention nephrology or dialysis access are also welcomed. Major article types considered for publication include original research and reviews on current topics of interest. Accepted manuscripts are granted free online open-access immediately after publication, which permits its users to read, download, copy, distribute, print, search, or link to the full texts of its articles to facilitate access to a broad readership. Circulation number of print copies is 1,600.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信