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Both diseases require significant management efforts, and more importantly, HF is often associated with CKD, aggravating the clinical scenario and leading to \u201ccardiorenal syndrome\u201d (CRS). Although clinical studies suggest a bidirectional interaction between HF and CKD, the pathophysiological understanding of CRS remains incomplete. Several mechanisms are involved in CRS, including changes in systemic and renal hemodynamics, endothelial dysfunction, inflammation, and activation of the renin-angiotensin-aldosterone and sympathetic nervous systems. However, the precise mechanisms are still unclear, partly because of the incomplete characterization of experimental models recapitulating CRS. In this review, we analyze recent studies using different animal models of CRS, such as primary HF, primary CKD, and the \u201cdouble-hit\u201d models that have been proposed to investigate the pathophysiology of this condition. In HF models, data on renal pathology showed renal fibrosis, inflammation, and decreased glomerular filtration rate (GFR), whereas kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) were used as markers of early kidney damage. In CKD models, data on heart pathology indicated changes in hemodynamics, increased systolic blood pressure, and the presence of fibrosis. These models provide new insights into the pathophysiological development of CRS, particularly the \u201cdouble-hit\u201d models, which may offer more information about the cross talk between the heart and kidneys. 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