{"doi":"10.1016/j.kint.2022.02.023","title":"Kidney repair and regeneration: perspectives of the NIDDK (Re)Building a Kidney consortium","abstract":"Acute kidney injury impacts ∼13.3 million individuals and causes ∼1.7 million deaths per year globally. Numerous injury pathways contribute to acute kidney injury, including cell cycle arrest, senescence, inflammation, mitochondrial dysfunction, and endothelial injury and dysfunction, and can lead to chronic inflammation and fibrosis. However, factors enabling productive repair versus nonproductive, persistent injury states remain less understood. The (Re)Building a Kidney (RBK) consortium is a National Institute of Diabetes and Digestive and Kidney Diseases consortium focused on both endogenous kidney repair mechanisms and the generation of new kidney tissue. This short review provides an update on RBK studies of endogenous nephron repair, addressing the following questions: (i) What is productive nephron repair? (ii) What are the cellular sources and drivers of repair? and (iii) How do RBK studies promote development of therapeutics? Also, we provide a guide to RBK’s open access data hub for accessing, downloading, and further analyzing data sets. Acute kidney injury impacts ∼13.3 million individuals and causes ∼1.7 million deaths per year globally. Numerous injury pathways contribute to acute kidney injury, including cell cycle arrest, senescence, inflammation, mitochondrial dysfunction, and endothelial injury and dysfunction, and can lead to chronic inflammation and fibrosis. However, factors enabling productive repair versus nonproductive, persistent injury states remain less understood. The (Re)Building a Kidney (RBK) consortium is a National Institute of Diabetes and Digestive and Kidney Diseases consortium focused on both endogenous kidney repair mechanisms and the generation of new kidney tissue. This short review provides an update on RBK studies of endogenous nephron repair, addressing the following questions: (i) What is productive nephron repair? (ii) What are the cellular sources and drivers of repair? and (iii) How do RBK studies promote development of therapeutics? Also, we provide a guide to RBK’s open access data hub for accessing, downloading, and further analyzing data sets. Despite advances in kidney care and efforts to delay development of chronic kidney disease (CKD), acute kidney injury (AKI) and progression to CKD remains a major health care burden.1Mehta R.L. Cerdá J. Burdmann E.A. et al.International Society of Nephrology's 0by25 initiative for acute kidney injury (zero preventable deaths by 2025): a human rights case for nephrology.Lancet. 2015; 385: 2616-2643Google Scholar The (Re)Building a Kidney consortium (RBK) is a National Institute of Diabetes and Digestive and Kidney Diseases consortium tasked with finding ways to improve kidney repair and forestalling progression to CKD, as well as devising innovative approaches to generation and engraftment of kidney replacement tissue.2The RBK consortiumThe NIDDK rebuilding a kidney consortium.https://www.rebuildingakidney.orgDate accessed: December 1, 2021Google Scholar Forestalling progression of CKD requires an understanding of endogenous kidney repair mechanisms and discriminating between productive repair and nonproductive, profibrotic conditions. Mouse models show that nephron tubules have an intrinsic regenerative potential3Kusaba T. Lalli M. Kramann R. et al.Differentiated kidney epithelial cells repair injured proximal tubule.Proc Natl Acad Sci U S A. 2014; 111: 1527-1532Google Scholar; however, on repeated injury, cells can be diverted to a nonproductive senescent state. RBK research groups focus on ischemia-reperfusion injury (IRI) to induce AKI because it is the most common cause of AKI and, as an experimental model in mice, can be performed with variable ischemic durations to produce mild or severe tubule injury and model the AKI-to-CKD progression. Whole kidney RNA-sequencing characterization after murine ischemia-reperfusion following recovery from IRI for 12 months provided clues about repair processes and the AKI-CKD transition4Liu J. Ku","journal":"Kidney International","year":2022,"id":239015,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":51,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9588,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2022-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":34474,"name":"Joseph V. Bonventre","orcid":"0000-0001-7144-386X","position":1,"is_corresponding":false},{"id":650193,"name":"Jeffrey A. Hubbell","orcid":"0000-0003-0276-5456","position":2,"is_corresponding":false},{"id":372140,"name":"Neil A. Hukriede","orcid":"0000-0002-9655-9030","position":3,"is_corresponding":false},{"id":263339,"name":"Benjamin D. Humphreys","orcid":"0000-0002-6420-8703","position":4,"is_corresponding":false},{"id":70342,"name":"Carl Kesselman","orcid":"0000-0003-0917-1562","position":5,"is_corresponding":false},{"id":279574,"name":"M. Todd Valerius","orcid":"0000-0001-8143-9231","position":6,"is_corresponding":false},{"id":323733,"name":"Andrew P. McMahon","orcid":"0000-0002-3779-1729","position":7,"is_corresponding":false},{"id":279205,"name":"Stuart J. Shankland","orcid":"0000-0002-4616-8330","position":8,"is_corresponding":false},{"id":342879,"name":"Jason A. Wertheim","orcid":"0000-0001-5680-1067","position":9,"is_corresponding":false},{"id":650190,"name":"Michael White","orcid":"0000-0002-9615-2249","position":10,"is_corresponding":false},{"id":865146,"name":"Mark P. de Caestecker","orcid":null,"position":11,"is_corresponding":false},{"id":535491,"name":"Iain A. Drummond","orcid":"0000-0003-3734-1231","position":12,"is_corresponding":false},{"id":753625,"name":"Bilal A. Naved","orcid":"0000-0001-5870-624X","position":0,"is_corresponding":true}],"reference_count":40,"raw_metadata":null,"created_at":"2026-07-19T00:22:36.865157Z","pmid":"35276204","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}