Renal dysfunction in chronic heart failure is driven by shared risk factors and complex pathophysiological interactions, where reduced GFR strongly relates to increased mortality and morbidity.
Renal dysfunction is extremely common in patients with chronic heart failure (CHF). Although the pathogenesis of reduced glomerular filtration rate (GFR) may differ between patients and even over time within an individual, the result is the same: reduced GFR is strongly related to increased mortality and morbidity. Potential explanations for the renal impairment include shared aetiological risk factors, such as atherosclerosis, hypertension, endothelial dysfunction and inflammation. Furthermore, a complex series of pathophysiological interactions exists between these two organ systems; an abnormality in one system will in general adversely impact on the other, resulting in a vicious cycle of disease progression. Improved understanding of the aetiology of reduced GFR in patients with CHF is fundamental to identifying appropriate therapies. Whilst reduced cardiac output and thereby renal perfusion is undoubtedly important, other factors, such as increased central venous pressure and anaemia may be amenable to therapeutic intervention.
Damman et al. (Sat,) conducted a review in Chronic heart failure and renal dysfunction. Renal dysfunction in chronic heart failure is driven by shared risk factors and complex pathophysiological interactions, where reduced GFR strongly relates to increased mortality and morbidity.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: