Renal impairment in heart failure (HF) patients has been increasingly recognized as an independent risk factor for morbidity and mortality. In the most recent European and American guidelines for HF management, renal dysfunction was considered an index of poor prognosis independent of the presence of other traditionally investigated risk factors. Different mechanisms appear to be implicated in worsening renal function in patients with acute decompensated HF (ADHF) in contrast to chronic HE In patients with acute ADHF, renal impairment has been attributed to renal hypoperfusion due to reduced cardiac output and decreased systemic blood pressure. In these patients, neurohormonal activation of the renin-angiotensin and sympathetic nervous systems plays a key role. In chronic and clinically stable HF, other mechanisms, including microvascular damage, oxidative stress, inflammation, and fibrosis, lead to a reduced number of functioning nephrons. Differentiating transient functional changes in renal filtration and acute renal tubular injury with loss of functioning nephrons is a critical step in understanding cardiorenal syndromes and selection of patients for novel therapeutic approaches. [Rev Cardiovasc Med. 2011;12(4):186-199 doi: 10.3909/ricm0581 (C) 2011 MedReviews (R), LLC

Clinical Impact of Renal Dysfunction in Heart Failure

Ronco C
2011

Abstract

Renal impairment in heart failure (HF) patients has been increasingly recognized as an independent risk factor for morbidity and mortality. In the most recent European and American guidelines for HF management, renal dysfunction was considered an index of poor prognosis independent of the presence of other traditionally investigated risk factors. Different mechanisms appear to be implicated in worsening renal function in patients with acute decompensated HF (ADHF) in contrast to chronic HE In patients with acute ADHF, renal impairment has been attributed to renal hypoperfusion due to reduced cardiac output and decreased systemic blood pressure. In these patients, neurohormonal activation of the renin-angiotensin and sympathetic nervous systems plays a key role. In chronic and clinically stable HF, other mechanisms, including microvascular damage, oxidative stress, inflammation, and fibrosis, lead to a reduced number of functioning nephrons. Differentiating transient functional changes in renal filtration and acute renal tubular injury with loss of functioning nephrons is a critical step in understanding cardiorenal syndromes and selection of patients for novel therapeutic approaches. [Rev Cardiovasc Med. 2011;12(4):186-199 doi: 10.3909/ricm0581 (C) 2011 MedReviews (R), LLC
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/3293527
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