We first show that CHIP is associated with incident AKI in three large population-based cohorts and is more pronounced for CHIP with driver mutations in genes other than DNMT3A, such as TET2 and JAK2. We then show that non-DNMT3A-CHIP is associated with a nonresolving AKI pattern in the Assessment, Serial Evaluation, and Subsequent Sequelae in Acute Kidney Injury (ASSESS)-AKI and Vanderbilt’s Biobank (BioVU) cohorts. This evidence concerns the gene JAK2 and acute kidney injury.