Clonal Hematopoiesis of Indeterminate Potential (CHIP) is associated with an increased risk of acute kidney injury (AKI). The study, published in *Nature Medicine*, investigates the link between CHIP and AKI using large epidemiological databases and mouse models. Key findings include: - **Epidemiological Study**: In the UK Biobank cohort, CHIP was associated with a 34% higher risk of developing AKI (HR 1.34, 95% CI 1.29–1.40). This association was more pronounced in cases requiring dialysis (HR 1.65, 95% CI 1.24–2.20). The risk increased with the frequency of variant alleles, with an HR of 1.19 for every 10% increase in allele frequency. - **Meta-analysis**: Across three prospective cohorts (UK Biobank, Atherosclerosis Risk in Communities, and Cardiovascular Health Study), the overall risk of AKI associated with CHIP was 26% (HR 1.26, 95% CI 1.19–1.34). - **Experimental Models**: In mouse models, Tet2-deficient mice showed more severe AKI and poorer recovery compared to wild-type mice. These mice also exhibited increased inflammation, macrophage infiltration, and fibrosis. Similar results were observed in Jak2 heterozygous mice. - **Long-term Outcomes**: In the unilateral ureteral obstruction (UUO) model, Tet2-deficient mice showed more severe inflammation, macrophage infiltration, and fibrosis at 28 days post-obstruction. The study suggests that CHIP is a significant risk factor for AKI, with a causal link demonstrated in animal models. This research opens new avenues for diagnostic and therapeutic approaches to manage AKI. However, the study lacks a therapeutic proposal and the UUO model is not a standard model for AKI.Clonal Hematopoiesis of Indeterminate Potential (CHIP) is associated with an increased risk of acute kidney injury (AKI). The study, published in *Nature Medicine*, investigates the link between CHIP and AKI using large epidemiological databases and mouse models. Key findings include: - **Epidemiological Study**: In the UK Biobank cohort, CHIP was associated with a 34% higher risk of developing AKI (HR 1.34, 95% CI 1.29–1.40). This association was more pronounced in cases requiring dialysis (HR 1.65, 95% CI 1.24–2.20). The risk increased with the frequency of variant alleles, with an HR of 1.19 for every 10% increase in allele frequency. - **Meta-analysis**: Across three prospective cohorts (UK Biobank, Atherosclerosis Risk in Communities, and Cardiovascular Health Study), the overall risk of AKI associated with CHIP was 26% (HR 1.26, 95% CI 1.19–1.34). - **Experimental Models**: In mouse models, Tet2-deficient mice showed more severe AKI and poorer recovery compared to wild-type mice. These mice also exhibited increased inflammation, macrophage infiltration, and fibrosis. Similar results were observed in Jak2 heterozygous mice. - **Long-term Outcomes**: In the unilateral ureteral obstruction (UUO) model, Tet2-deficient mice showed more severe inflammation, macrophage infiltration, and fibrosis at 28 days post-obstruction. The study suggests that CHIP is a significant risk factor for AKI, with a causal link demonstrated in animal models. This research opens new avenues for diagnostic and therapeutic approaches to manage AKI. However, the study lacks a therapeutic proposal and the UUO model is not a standard model for AKI.