Chagas’ disease, caused by the protozoan Trypanosoma cruzi, where estimated 8 million people are infected in worldwide, mainly in Latin America causing incapacity in infected individuals and more than 10. 000 deaths per year. The pathophysiological mechanisms of the genesis of cardiac involvement, both acute and chronic, are still not completelly understood. However, in experimental models, a relationship was observed between the levels of parasitemia and the high intensity of acute myocarditis with the severity of cardiac symptoms during the chronic phase. Patients with congestive heart failure may present with renal insufficiency and anemia. This triad is denominated the cardio-anemic-renal syndrome. Our results demonstrate that in the early stages of infection there is a transient but marked renal disfunction in mice infected with T. cruzi. In addition, interference in renal/cardiovascular axis, such as the renin angiotensin-aldosterone system block, decreases the mortality of the animals around 30%. Kidney damage during the infection with T. cruzi is underestimated. Experimental results showed the pathophysiological interconnections with the evolution of acute heart failure. We hope from the results compilation to suggest new diagnostic and therapeutic protocols that minimize cardiac symptomatology during the acute phase and the onset of dilated cardiomyopathy during the chronic phase.