从“虚损痨瘵，燮理气阴"探讨糖尿病肾病铁死亡病机及防治思路

打开文本图片集

[中图分类号]R256

[文献标志码]A [文章编号]doi：10.3969/j.issn.1674-070X.2026.01.017

[Abstract]Based onthetheoryof "treatingconsumptivedeficiencybyharmonizingqiandyin"，thispaperexplores ferroptosis-centeredpathologicalmechanismsandcorespondingpreventionandtreatmentstrategiesfordiabetickidneydisease （DKD）.Dficiencyofthesplenandkidneyservesastherotcause，whiledamp-heat，phlegm-stasis，andturbidity-toxin representthemanifestations.Together，thesefactorsdisruptironhomeostasis，characterizedbydownregulationofsolutecarrer family7member11（SLC7A11，xCT）andglutathioneperoxidase4（GPX4）andupregulationoflong-chainacyl-CoAsynthetase familymember4（ACSL4）.Theseimbalancetriggrslipidperoxidationandferroptosis，damagingrenaltubularepithelialcels and podocytes.Subsequently，through damage-associated molecularpaterns （DAMPs）， transforming growth factor- ⋅{ （TGF- ⋅{ /Smad， andnucleotidebindingoligomezationdomain-likereceptorprotein3（NRP3）signalingpathways，itpromotesfboblastactivation andcollgendeposition，ultimatelyleadingtorenalfibrosis.Gudedbytheconceptof"preventingadiseasebeforeitarises"， athree-tierpreventionandtreatmentstrategyisproposed：inearlysagerengtheningthesplen，eplenishingqouing yin，andtrafoinsodiidtdtoicees，tetofal; duringthemoderatestage，clearingheatandremovingtoxins，circulating bloodandunblockingcolaterals，whilesyneristially modulating thenuclearfactorE2-relatedfactor2（Nrf2）GPX4，ACSL4，aswellastheTGF-β/Smadaxis，tosuppressinflamation andfibrosisamplification；inthelatestage，reiforcinghealthyqi，consolidatingtheroot，warmingyanganddisinhibitingwater， while integrating toxinremoving，collteralunblocking，andrenal protection，toallviatesymptomsand improveprognosis.

[Keywords]diabetickidneydisease;feroptosis;consumptivedeficiency;harmonizingqiandyin;deficiencyofth spleen and kidney；solute carrier family 7 member11; long-chain acyl-CoA synthetase family member 4

糖尿病肾病（diabetickidneydisease，DKD）是糖尿病最主要的微血管并发症，也是终末期肾病（end-stagerenaldisease，ESRD）的首要病因，其发病隐匿、病程迁延，临床以持续性蛋白尿、肾功能进行性下降为主要特征，最终可进展至不可逆的肾衰竭。（剩余17604字）