Abstract -- The incidence of chronic renal failure in combination with cardiovascular events is increasing and the co-existence of the diseases leads to an extremely bad prognosis and often lethal outcome. The combination of cardiac and renal dysfunction, i.e. the cardio-renal interaction, leads to amplified progression of failure of the individual organs. This was also studied in an experimental rat model where a myocardial infarction (MI) was induced in unilateral nephrectomized rats and several cardiac, renal and neurohumoral parameters were measured. This study confirmed that MI enhances progressive renal damage in this experimental rat model, evidenced by increased levels of proteinuria and focal glomerulosclerosis. In this review, I tried to find the underlying mechanisms of the cardio-renal interaction. Therefore, the main consequences of MI were described, which include inflammation, hemodynamic changes and activation of the renin-angiotensin system (RAS). In addition to this, the consequences of unilateral nephrectomy on the residual kidney were described, including reduced glomerular filtration rate (GFR), hypertrophy of the contralateral kidney and slightly higher protein excretion levels. Since the RAS exerts multiple effects on both the heart and kidneys, and inhibition of the RAS via angiotensin converting enzyme-inhibitors (ACEi) have contributed greatly to the treatment of cardiac and renal failure, the RAS seems to be the most evident link in the cardio-renal interaction. This provides great perspectives for the future to conduct further research on the cardio-renal interaction.
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