{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T01:43:35Z","timestamp":1793065415903,"version":"4.5.0"},"reference-count":144,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,8]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>The transition of AKI to CKD has major clinical significance. As reviewed here, recent studies show that a subpopulation of dedifferentiated, proliferating tubules recovering from AKI undergo pathologic growth arrest, fail to redifferentiate, and become atrophic. These abnormal tubules exhibit persistent, unregulated, and progressively increasing profibrotic signaling along multiple pathways. Paracrine products derived therefrom perturb normal interactions between peritubular capillary endothelium and pericyte-like fibroblasts, leading to myofibroblast transformation, proliferation, and fibrosis as well as capillary disintegration and rarefaction. Although signals from injured endothelium and inflammatory\/immune cells also contribute, tubule injury alone is sufficient to produce the interstitial pathology required for fibrosis. Localized hypoxia produced by microvascular pathology may also prevent tubule recovery. However, fibrosis is not intrinsically progressive, and microvascular pathology develops strictly around damaged tubules; thus, additional deterioration of kidney structure after the transition of AKI to CKD requires new acute injury or other mechanisms of progression. Indeed, experiments using an acute-on-chronic injury model suggest that additional loss of parenchyma caused by failed repair of AKI in kidneys with prior renal mass reduction triggers hemodynamically mediated processes that damage glomeruli to cause progression. Continued investigation of these pathologic mechanisms should reveal options for preventing renal disease progression after AKI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2015010006","type":"journal-article","created":{"date-parts":[[2015,3,26]],"date-time":"2015-03-26T05:15:21Z","timestamp":1427346921000},"page":"1765-1776","source":"Crossref","is-referenced-by-count":685,"title":["Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression"],"prefix":"10.1681","volume":"26","author":[{"given":"Manjeri A.","family":"Venkatachalam","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joel M.","family":"Weinberg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wilhelm","family":"Kriz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anil K.","family":"Bidani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"R1-6-20240223","doi-asserted-by":"crossref","first-page":"967","DOI":"10.1681\/ASN.2012030222","article-title":"Yes, AKI truly leads to CKD.","volume":"23","author":"Hsu","year":"2012","journal-title":"J Am Soc Nephrol"},{"key":"R2-6-20240223","doi-asserted-by":"crossref","first-page":"520","DOI":"10.2215\/CJN.06711208","article-title":"The nexus of acute kidney injury, chronic kidney disease, and World Kidney Day 2009.","volume":"4","author":"Okusa","year":"2009","journal-title":"Clin J Am Soc Nephrol"},{"key":"R3-6-20240223","doi-asserted-by":"crossref","first-page":"58","DOI":"10.1056\/NEJMra1214243","article-title":"Acute kidney injury and chronic kidney disease as interconnected syndromes.","volume":"371","author":"Chawla","year":"2014","journal-title":"N Engl J Med"},{"key":"R4-6-20240223","doi-asserted-by":"crossref","first-page":"F1078","DOI":"10.1152\/ajprenal.00017.2010","article-title":"Acute kidney injury: A springboard for progression in chronic kidney disease.","volume":"298","author":"Venkatachalam","year":"2010","journal-title":"Am J Physiol Renal Physiol"},{"key":"R5-6-20240223","doi-asserted-by":"crossref","first-page":"2555","DOI":"10.2215\/CJN.09560911","article-title":"Acute kidney injury and chronic kidney disease: A work in progress.","volume":"6","author":"Bydash","year":"2011","journal-title":"Clin J Am Soc Nephrol"},{"key":"R6-6-20240223","doi-asserted-by":"crossref","first-page":"1227","DOI":"10.1001\/jama.2009.1364","article-title":"Chronic on acute renal failure: Long-term implications of severe acute kidney injury.","volume":"302","author":"Waikar","year":"2009","journal-title":"JAMA"},{"key":"R8-6-20240223","doi-asserted-by":"crossref","first-page":"90","DOI":"10.1001\/archinte.1960.00270130106013","article-title":"A functional and morphological follow-up study of acute renal failure.","volume":"105","author":"Price","year":"1960","journal-title":"Arch Intern Med"},{"key":"R9-6-20240223","doi-asserted-by":"crossref","first-page":"853","DOI":"10.7326\/0003-4819-68-4-853","article-title":"Arsine-induced anuria. 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