Tacrolimus and Renal Tubular Toxicity:Mechanism and Prevention
10.3870/j.issn.1672-0741.24.05.007
- VernacularTitle:他克莫司与肾小管毒性:机制与防治
- Author:
Banghuan HU
1
;
Hua SU
1
Author Information
1. 华中科技大学同济医学院附属协和医院肾内科,武汉 430022
- Publication Type:Journal Article
- Keywords:
tacrolimus;
renal tubular toxicity;
mechanism;
drugs for prevention and treatment
- From:
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
2025;54(1):117-122
- CountryChina
- Language:Chinese
-
Abstract:
Tacrolimus(FK506)is the most widely utilized calcineurin inhibitors(CNIs)and serves as the first-line agent in immunosuppressive treatment regimens.FK506 has a narrow therapeutic index,and its pharmacokinetics exhibit significant vari-ability both between and within individuals.High-dose exposure to FK506,whether administered long-term or short-term,can result in nephrotoxicity.Proximal tubule cells in kidney are the only cells that are capable of metabolizing CNIs,and these cells are believed to play a central role in the development of toxicity associated with this class of drugs.The mechanism underlying renal tubular toxicity induced by FK 506 is complex,involving factors such as cellular oxidative stress,inflammatory responses,metabolic dysfunction of renal tubular cells,apoptosis,and the renin-angiotensin system.Despite extensive research,the patho-genesis of FK506-induced tubular toxicity remains incompletely understood.Therefore,this article aims to review the research progress concerning the pathogenesis of tacrolimus-related renal tubular toxicity,as well as its prevention and treatment,to pro-vide a reference for clinical practice and future research.
