Cardiorenal syndrome type 1 (CRS1) is acute kidney injury (AKI) due to rapid worsening of cardiac function, and is a common cause of AKI. Ischemic AKI and subsequent chronic kidney disease (CKD) is mainly investigated by using the model of renal pedicle clamp (ischemia-reperfusion injury: IRI) which models renal transplant warm ischemia. However, results from IRI do not mimic clinical CRS1. We have previously identified a cardiac-derived soluble factor, cardiac LIM protein (CSRP3), which mediates renal function. We hypothesized that the phenotype of AKI-CKD transition differs between animal models of systemic ischemia and renal-limited ischemia.