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Abstract
One of the particularities that develops the cardiorenal syndrome (CRS) is a circle in which as a consequence of the low cardiac output there is an alteration in the balance of nitric oxide and in the release of antidiuretic hormone, among others; induction of renal vasoconstriction and increased reabsorption in the proximal tubule of water and sodium reduces the supply of water and sodium at the level of the distal tubule, which causes a decrease in the diuresis of the natriuretic peptide and increases sensitivity to the action of aldosterone (secreted by the adrenal glands) which acts in the conservation of sodium and secreting potassium and increasing blood pressure). This explains that in patients with cardiac insufficiency (CI), one of the most evident characteristics is hypervolemia and sodium retention. Recent data support that, in CRS, fluid and sodium retention and subsequent resistance to diuretics cause progressive volume overload and worsening of HF, with reduced cardiac output and increased renal dysfunction. Consequently, a situation with a poor prognosis and few alternative options is generated.
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