Abstract
Heart failure (HF) is a pathophysiologically complex disease that is exceptionally heterogeneous in terms of its etiology. It is associated with unsatisfactorily high mortality, both in-hospital and post-discharge, as well as with very frequent rehospitalizations. High phenotypic variability, coexistence of various hemodynamic disorders (such as changes in systemic and pulmonary vascular resistance, increased central venous pressure, impaired heart cardiac output, and fluid overload) and coexisting metabolic and neurohormonal disorders may eventually lead to impaired systemic perfusion. Congestion that impairs renal perfusion has a significant impact on both glomerular filtration and the renal tubular function. This review article discusses the importance of changes caused by HF in various nephron segments, phenotyping of cardiorenal syndromes, the role of effective natriuresis in decongestion, and the importance of known and new diagnostic biomarkers in predicting renal dysfunction. A better understanding of cardiac and renal interactions may help in selecting an effective, efficient and nephroprotective strategy of treatment for patients with HF.
Highlights
Mutual hemodynamic and neurohormonal interaction of the heart and kidneys determines the exceptional dependence of both organs
Chronic kidney disease (CKD), defined as lowering of estimated glomerular filtration rate
A large meta-analysis involving over 1,000,000 HF patients revealed that the presence of CKD doubles the risk of general mortality.[2]
Summary
Mutual hemodynamic and neurohormonal interaction of the heart and kidneys determines the exceptional dependence of both organs. Heart failure (HF) and kidney disease (KD) often coexist, which carries significant prognostic implications. Chronic kidney disease (CKD), defined as lowering of estimated glomerular filtration rate (eGFR)
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