title: The Acute Kidney Injury to Chronic Kidney Disease Transition: A Potential Opportunity to Improve Care in Acute Kidney Injury.
abstract: Recent controlled trials, epidemiological analyses and basic research studies offer a comprehensive view of the short and long-term clinical repercussion of de novo acute kidney injury or AKI. While most post-AKI patients recover their baseline renal function, a significant number, approximately ~20% of those affected, will go on to develop long term illness characterized by an increase in late stage CKD, cardiovascular complications, and increased death rates. When AKI occurs in hospitalized patients, selected demographic and laboratory results can be incorporated into risk calculators that identify those at higher risk for long-term complications. This review touches on some of the salient epidemiological studies of the AKI to CKD transition. It also focuses on certain recent advancements in our understanding of the biological and functional impact of AKI on the renal tubule repair mechanism, as well as the important role that genetic, epigenetic, biochemical and inflammatory events, seemingly beneficial to the re-establishment of normal renal function, can be offset by mediators of progressive fibrosis and irreversible structural changes. Characterization of basic processes that mediate the AKI to CKD transition reveals promising pharmacological and biological agents that hopefully will one day be used in the early stages of AKI to prevent its deadly consequences.
authors.forename: Carlos E
authors.initials: CE
authors.lastname: Palant
authors.forename: Richard L
authors.initials: RL
authors.lastname: Amdur
authors.forename: Lakhmir S
authors.initials: LS
authors.lastname: Chawla
mesh_terms: D058186:Acute Kidney Injury / Q000150:complications* / Q000453:epidemiology / Q000235:genetics / Q000628:therapy; D015415:Biomarkers; D006801:Humans; D006973:Hypertension / Q000209:etiology; D051793:Hypoxia-Inducible Factor 1 / Q000502:physiology; D035683:MicroRNAs / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D051436:Renal Insufficiency, Chronic / Q000453:epidemiology / Q000209:etiology*
chemical_list: D015415:Biomarkers; D051793:Hypoxia-Inducible Factor 1; D035683:MicroRNAs; D017382:Reactive Oxygen Species