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Randomized controlled trials have demonstrated the benefits of guideline-directed medical therapy in the outpatient setting for treatment of chronic heart failure. However, the benefits of continuation (or discontinuation) of major chronic heart failure therapies when treating acute heart failure during hospitalization are less clear. Real and anticipated worsening renal function, hyperkalemia and hypotension are the three major reasons for discontinuation of renin-angiotensin-aldosterone system inhibitors during hospitalization, and a failure to resume renin-angiotensin-aldosterone system inhibitors before discharge could worsen cardiovascular outcomes. Available data, mostly observational, shows that continuation or initiation of renin-angiotensin-aldosterone system inhibitors appears efficacious, safe, and well tolerated in majority of acute heart failure patients during hospitalization. Worsening renal function portends poor prognosis only if associated with congestion in acute heart failure, and clinicians should not de-escalate diuretic therapy routinely for worsening renal function.

Worsening renal function in patients with heart failure with preserved ejection fraction is associated with poor outcomes. Pulmonary arterial capacitance is a novel right heart catheterization derived hemodynamic metric representing pulmonary arterial tree distensibility and right ventricle afterload. Given the strong association between heart failure, pulmonary hypertension, and kidney function, the goal of this study is to investigate the correlation between Pulmonary arterial capacitance and long-term renal function in patients with heart failure with preserved ejection fraction. In this retrospective single center study, data from 951 patients with the diagnosis of heart failure, who underwent right heart catheterization were analyzed. Eight hundred and one patients with reduced ejection fraction, end-stage kidney disease on hemodialysis, acute myocardial infarction, and severe structural valvular disorders, were excluded. Pulmonary arterial capacitance was calculated as the stroke volume divided by pulmonary artery pulse pressure (mL/mmHg). Hemodynamic and clinical variables including baseline renal function were obtained at the time of the right heart catheterization, and renal function was also obtained at 3-5 years after right heart catheterization. The final cohort consisted of 150 subjects with a mean age 68 ( ± 14.2) years, 93 (62%) were female. The mean value for Pulmonary arterial capacitance was 2.82 ( ± 2.22) mL/mm Hg and the mean Glomerular Filtration Rate was 60.32 mL/min/l.73 m² ( ± 28.36). After multivariate linear regression analysis (including baseline Estimated Glomerular Filtration Rate as one of the variates), only age and Pulmonary arterial capacitance greater than 2.22 mL/mm Hg were predictors of long term Glomerular Filtration Rate. Pulmonary arterial capacitance as a novel right heart catheterization index could be a predictor of long-term renal function in patients with heart failure with preserved ejection fraction.

Low serum sodium concentration has long been recognized as an established marker of short- and long-term morbidity and mortality in patients with heart failure (HF), and is commonly included in various risk prediction models. Mechanisms leading to hyponatremia (e.g. maladaptive neurohormonal activation) could also lead to concurrent decline in serum chloride levels. Besides, chloride has distinct biological roles (e.g. modulation of renal tubular sodium transporters) that are relevant to the pathophysiology and therapy of HF, making it a potent cardiorenal connector. Several clinical studies have recently reported on a potentially overlooked link between low serum chloride levels and adverse outcomes in patients with a wide variety of HF syndromes, which could indeed be stronger than that of sodium. While evidence on predictive value of chloride is accumulating in various patient populations and settings, the limited available interventional studies have so far yielded conflicting results. It remains to be elucidated whether hypochloremia represents a marker of disease severity and prognosis, or it is an actual pathogenetic mechanism, hence being a potential novel target of therapy. Current ongoing studies are designed to better understand the mechanistic aspects of the role of hypochloremia in HF and shed light on its clinical applicability.

End-stage kidney disease (ESKD) and heart failure (HF) often coexist and must be managed simultaneously. Multidisciplinary collaboration between nephrology and cardiology is critical when treating patients with such complicated physiology. There is no "one-size-fits-all" approach to the evaluation of patients with new left ventricular systolic dysfunction, and diagnostic testing should be adapted to an individual's risk factors. Guideline-directed medical therapy (GDMT) for systolic heart failure should be employed in these patients. While limited randomized data exist, observational data and post hoc analyses suggest that GDMT, including renin angiotensin aldosterone system inhibitors, is associated with improved cardiovascular outcomes and can be safely initiated at low doses with close monitoring of kidney function in this population. Volume status is typically managed through ultrafiltration, so close communication between cardiology and nephrology is necessary to achieve a patient's optimal dry weight and mitigate intradialytic hypotension. Patient education and engagement regarding sodium and fluid restriction is crucial, and symptom burden should be reassessed following changes to the dialysis regimen.

The curve that describes the relationship between glomerular filtration rate (GFR) and cardiovascular risk is U-shaped, indicating that both reduced GFR (kidney failure) and elevated GFR (glomerular hyperfiltration) are equivalent cardiovascular risk factors. The elevated cardiovascular risk associated with abnormal GFR is not explained by standard cardiovascular risk factors. The relationship between GFR and all-cause mortality follows a similar pattern, so that altered GFR (either low or high) increases the risk for overall mortality. Glomerular hyperfiltration is an adaptive process that arises under conditions that demand improved kidney excretory capacity, such as animal protein ingestion and kidney failure. Unlike vegetable protein, animal protein consumption increases dietary acid load and requires an elevation of the GFR to restore acid-base balance. The loss of functioning nephrons in diseased kidneys requires a compensatory increase of the GFR in the nephrons that remain working to enhance whole-kidney GFR. A major factor that raises GFR is the pancreatic hormone glucagon. Glucagon infusion and endogenous glucagon release increase GFR in healthy subjects and patients with kidney failure. In addition to its kidney hemodynamic effect, glucagon causes insulin resistance. Like hyperglucagonemia, insulin resistance develops across the entire spectrum of abnormal GFR, from glomerular hyperfiltration to advanced kidney disease. Insulin resistance is associated with subclinical vascular injury in the general population and patients with diabetes and kidney failure, being a strong cardiovascular risk factor in these population groups. Animal protein consumption activates glucagon secretion and promotes insulin resistance, having a detrimental effect on cardiovascular disease and renal outcomes.