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Here, we combine SARS-CoV-2 variants with genome-edited kidney organoids and clinical data to investigate tropism, mechanism, and therapeutics. SARS-CoV-2 specifically infects organoid proximal tubules among diverse cell types. Infections produce replicating virus, apoptosis, and disrupted cell morphology, features of which are revealed in the context of polycystic kidney disease. Cross-validation of gene expression patterns in organoids reflects proteomic signatures of COVID-19 in the urine of critically ill patients indicating interferon pathway upregulation. SARS-CoV-2 viral variants alpha, beta, gamma, kappa, and delta exhibit comparable levels of infection in organoids. Infection is ameliorated in\n                    <jats:italic>ACE2\u2013\/\u2013<\/jats:italic>\n                    organoids and blocked via treatment with de novo\u2013designed spike binder peptides. Collectively, these studies clarify the impact of kidney infection in COVID-19 as reflected in organoids and clinical populations, enabling assessment of viral fitness and emerging therapies.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.154882","type":"journal-article","created":{"date-parts":[[2021,11,12]],"date-time":"2021-11-12T13:00:18Z","timestamp":1636722018000},"source":"Crossref","is-referenced-by-count":45,"title":["Cross-validation of SARS-CoV-2 responses in kidney organoids and clinical populations"],"prefix":"10.1172","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9212-0576","authenticated-orcid":true,"given":"Louisa","family":"Helms","sequence":"first","affiliation":[{"name":"Department of Medicine;"},{"name":"Division of Nephrology;"},{"name":"Kidney Research Institute;"},{"name":"Institute for Stem Cell and Regenerative Medicine;"},{"name":"Department of Laboratory Medicine and 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