Abstract: Chronic kidney disease (CKD) is a complex pathology, which affects renal structure and function. Nowadays, this disease affects around of 15% of worldwide population. Cardiovascular diseases are the main cause of death in CKD patients. Cardio renal Syndrome, a physiopathological disorder that is not completely understood, e consists in an interdependent relationship between heart and kidneys, where the acute or chronic dysfunction in one organ can induce the same in the other organ. Thus, this makes necessary the investigation and improvement of technologies and markers of cardiovascular damage on the onset of chronic kidney disease. This study aimed to improve the comprehension of the mechanisms involved in the cardio renal syndrome pathogenesis by the analysis of cardiac and inflammatory biomarkers in an experimental model o CKD. As a CKD animal model, were used Wistar rats, in two different groups: SHAM (normal control) and CKD (CKD model) that underwent 5/6 nefrectomy surgeries. Blood samples were collected at the times basal (B),4 and 8 weeks after de surgeries. The serum levels of cardiac troponin I (TnI) were used as myocardial injury marker, and the amino terminal of the brain natriuretic peptide (NT-proBNP was used for express the cardiac wall stretching. Interleukin -6 (IL-6) was used as a marker for inflammatory processes. It was showed increased levels of TnI at the times of 4 and 8 weeks in the CKD group, suggesting the development of myocardial injury secondary to CKD. The NT-proBNP levels remained unchanged between the two groups. IL-6 levels were not increased. The development of an inflammatory process linked to myocardial injury characterizes one of the cardio renal connectors present in cardio renal syndrome, suggesting that this condition was present in the CKD group. The IL-6 and TnI biomarkers showed a promising potential for its applicability for the screening of the cardiovascular consequences of CKD, however, additional studies focusing in its clinical use are still in need.