{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T09:21:47Z","timestamp":1788168107673,"version":"build-2803163510"},"reference-count":137,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,8,8]],"date-time":"2026-08-08T00:00:00Z","timestamp":1786147200000},"content-version":"am","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"name":"Birla Institute of Technology"},{"name":"Science-Pilani, Pilani"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Acute kidney injury (AKI) affects 10%\u201315% of hospitalized patients, and nearly one-quarter progress to chronic kidney disease (CKD), reflecting a failure to recognize the temporally dynamic continuum linking these conditions. This review synthesizes emerging evidence demonstrating that AKI-to-CKD continuum unfolds through four mechanistically distinct phases: (1) hyperacute injury (0\u201324 h), defined by bioenergetic collapse, mitochondrial permeability transition, oxidative stress, and early inflammatory priming; (2) acute response\u2014persistent AKI (1\u20137 days), dominated by coordinated pyroptotic\u2013apoptotic\u2013necroptotic cell death (PANoptosis) and lipid peroxidation-driven ferroptosis, impaired mitophagy, aberrant G2\/M arrest, and amplified cytokine release; (3) acute kidney disease (AKD) (2\u20138 weeks) characterized by maladaptive repair mechanisms, encompassing persistent TGF-\u03b2\/SMAD signaling, metabolic reprogramming toward glycolysis, mechanotransductive YAP\/TAZ activation, endothelial rarefaction, and stabilization of pro-fibrotic non-coding RNA networks; and (4) CKD (&amp;gt;12 weeks), where irreversible extracellular matrix deposition, chronic hypoxia, immune dysregulation, and established myofibroblast phenotypes perpetuate fibrosis. Three universal processes integrate these stages: (1) epigenetic injury memory through chromatin remodeling at pro-fibrotic loci, (2) metabolic reprogramming and epigenetic crosstalk, involving substrates such as S-adenosylmethionine and \u03b1-ketoglutarate, reinforcing self-perpetuating renal fibrosis, and (3) renal functional reserve. However, substrate availability and cellular contexts are temporally variable, rendering phase-agnostic, single-target approaches ineffective because they fail to align with the evolving molecular environments. A temporally informed, multi-phase strategy that targets these universal mechanisms at optimal time-windows is crucial for preventing or attenuating this irreversible AKI-to-CKD continuum.<\/jats:p>","DOI":"10.1093\/ndt\/gfag180","type":"journal-article","created":{"date-parts":[[2026,8,8]],"date-time":"2026-08-08T11:50:11Z","timestamp":1786189811000},"source":"Crossref","is-referenced-by-count":1,"title":["The acute kidney injury\u2013chronic kidney disease continuum: mechanisms and therapeutic interventions"],"prefix":"10.1093","author":[{"ORCID":"https:\/\/orcid.org\/0009-0008-8325-6912","authenticated-orcid":false,"given":"Hrushikesh Vikas","family":"Kulkarni","sequence":"first","affiliation":[{"name":"Department of Pharmacy, Birla Institute of Technology and Science, Pilani , Pilani Campus, Vidya Vihar, Pilani, Rajasthan ,","place":["India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4261-445X","authenticated-orcid":false,"given":"Shrikant Ramesh","family":"Mulay","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Birla Institute of Technology and Science, Pilani , Hyderabad Campus, Jawahar Nagar, Kapra Mandal, Medchal District, Telangana ,","place":["India"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4627-5504","authenticated-orcid":false,"given":"Anil Bhanudas","family":"Gaikwad","sequence":"additional","affiliation":[{"name":"Department of Pharmacy, Birla Institute of Technology and Science, Pilani , Pilani Campus, Vidya Vihar, Pilani, Rajasthan ,","place":["India"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2026,8,8]]},"reference":[{"key":"2026083104563332700_bib1","doi-asserted-by":"publisher","first-page":"241","DOI":"10.1016\/S0140-6736(24)02385-7","article-title":"Acute kidney injury","volume":"405","author":"Ostermann","year":"2025","journal-title":"Lancet"},{"key":"2026083104563332700_bib2","doi-asserted-by":"publisher","first-page":"14261","DOI":"10.1038\/s41598-025-96236-8","article-title":"Acute kidney injury in hospitalized patients with real-life analysis of incidence and clinical impact in Italian hospitals (the SIN-AKI study)","volume":"15","author":"Esposito","year":"2025","journal-title":"Sci Rep"},{"key":"2026083104563332700_bib3","doi-asserted-by":"publisher","first-page":"2572","DOI":"10.3390\/jcm14082572","article-title":"Unpacking KDIGO Guidelines: prioritizing and applying exposures and susceptibilities for AKI in clinical practice","volume":"14","author":"Wetterstrand","year":"2025","journal-title":"J Clin Med"},{"key":"2026083104563332700_bib4","doi-asserted-by":"publisher","first-page":"1482","DOI":"10.2215\/CJN.00710113","article-title":"World incidence of AKI: a meta-analysis","volume":"8","author":"Susantitaphong","year":"2013","journal-title":"Clin J Am Soc Nephrol"},{"key":"2026083104563332700_bib5","doi-asserted-by":"publisher","first-page":"1411","DOI":"10.1007\/s00134-015-3934-7","article-title":"Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study","volume":"41","author":"Hoste","year":"2015","journal-title":"Intensive Care Med"},{"key":"2026083104563332700_bib6","doi-asserted-by":"publisher","first-page":"479","DOI":"10.1093\/joneph\/aajaf075","article-title":"When to start and discontinue kidney replacement therapy in acute kidney injury patients? 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