Worsening Renal Function in Patients With Acute Decompensated Heart Failure Treated With Ultrafiltration: Predictors and Outcomes

BackgroundUltrafiltration (UF) is used to treat patients with diuretic-resistant acute decompensated heart failure. The aim of this study was to identify predictors and the effect of worsening renal failure (WRF) on mortality in patients treated with UF.Methods and ResultsBased on changes in serum creatinine, 99 patients treated with UF were divided into WRF and control groups. Overall creatinine increased from 1.9 ± 9.7 to 2.2 ± 2.0 mg/dL (P < .001), and WRF developed in 41% of the subjects. The peak UF rate was higher in the WRF group in univariate analysis (174 ± 45 vs 144 ± 42 mL/h; P = .03). Based on multivariate analysis, aldosterone antagonist treatment (odds ratio [OR] 3.38, 95% confidence interval [CI] 1.17–13.46, P = .04), heart rate ≤65 beats/min (OR 6.03, 95% CI 1.48–48.42; P = .03), and E/E′ ≥15 (OR 3.78, 95% CI 1.26–17.55; P = .04) at hospital admission were associated with WRF. Patients with baseline glomerular filtration rate (GFR) ≤60 mg/dL who developed WRF during UF had a 75% 1-year mortality rate.ConclusionsWRF occurred frequently during UF. Increased LV filling pressures, lower heart rate, and treatment with aldosterone antagonist at hospital admission can identify patients at increased risk for WRF. Patients with baseline GFR ≤60 mg/dL and WRF during UF have an extremely high 1-year mortality rate.     

Biochemical Evidence of Mild Hepatic Dysfunction Identifies Decompensated Heart Failure Patients With Reversible Renal Dysfunction

BackgroundDifferentiation of HF-induced renal dysfunction (RD) from irreversible intrinsic kidney disease is challenging, likely related to the multifactorial pathophysiology underlying HF-induced RD. In contrast, HF-induced liver dysfunction results in characteristic laboratory abnormalities. Given that similar pathophysiologic factors are thought to underlie both conditions, and that the liver and kidneys share a common circulatory environment, patients with laboratory evidence of HF-induced liver dysfunction may also have a high incidence of potentially reversible HF-induced RD.Methods and ResultsHospitalized patients with a discharge diagnosis of HF were reviewed (n = 823). Improvement in renal function (IRF) was defined as a 20% improvement in estimated glomerular filtration rate (eGFR). An elevated international normalized ratio (INR; odds ratio [OR] 2.8; P < .001), bilirubin (BIL; OR 2.2; P < .001), aspartate aminotransferase (AST; OR 1.8; P = .004), and alanine aminotransferase (ALT; OR 2.1; P = .001) were all significantly associated with IRF. Among patients with baseline RD (eGFR ≤45 mL min^?1 1.73 m^?2), associations between liver dysfunction and IRF were particularly strong (INR: OR 5.7 [P < .001]; BIL: OR 5.1 [P < .001]; AST: OR 2.9 [P = .005]; ALT: OR 4.8 [P < .001]).ConclusionsBiochemical evidence of mild liver dysfunction is associated with reversible RD in decompensated HF patients. In the absence of methodology to directly identify HF-induced RD, signs of HF-induced dysfunction of other organs may serve as an accessible method by which HF-induced RD is recognized.     

The Kidney in Heart Failure: The Role of Venous Congestion

Heart failure can lead to renal impairment, an interaction now termed “cardiorenal syndrome.” The prevalent physiological explanation for the renal impairment that accompanies heart failure centers around the forward failure hypothesis, which emphasizes the role of left ventricular dysfunction in causing edema, and the backward failure hypothesis, which singles out venous congestion as the dominant mechanism of edema and reduced glomerular filtration rate. In this review, we provide an appraisal on venous congestion, an extremely important contributor that has received little attention. We also summarize the pharmacology of loop diuretics, explain current understanding of diuretic resistance, and address controversies regarding decongestive treatments.     

Clinical Impact of Changes in Hemodynamic Indices of Contractile Function During Treatment of Acute Decompensated Heart Failure

Background

The objective of this work was to determine the impact of improving right ventricular versus left ventricular stroke work indexes (RVSWI vs LVSWI) during therapy for acute decompensated heart failure (ADHF).

Effect of Losartan on the Cardiac and Renal Function in Patients With Chronic Heart Failure

Objectives To explore the effect of losartan on cardiac and renal function in patients with chronic heart failure (CHF). Methods Sixty-five patients with CHF were divided into two groups using a randomized, control and single blind method: losartan group (n=30) and convention group (n=35), with a treatment course of 8 weeks for both groups. The concentrations of cystatin C (cys C) in serum, microamount albumin (MA) in urine were measured by immunoturbidimetry. The concentration of aquaporin-2(AQP-2)was determined by enzyme-linked-immunosorbent assay (ELISA) and the heart contractile function was measured by echocardiography before and after treatment respectively. Results Comparing with routine treatment group, left ventricular end-diastolic dimension (LVEDd) decreased significantly, while left ventricular ejection fraction(LVEF)and left ventricular fractional shortening (LVFS) increased significantly in losartan group. The levels of cys C in serum and MA, AQP-2 in urine were significantly lower in losartan group than in routine treatment group. Conclusion Losartan can improve cardiac and renal function in patients with CHF.     

Levosimendan Improves Renal Function in Patients with Acute Decompensated Heart Failure: Comparison with Dobutamine

Background Levosimendan is a relatively new cardiac inotropic agent with calcium sensitizing activity. This study was conducted to investigate the effects of levosimendan (L) and dobutamine (D) on renal function in patients hospitalized with decompensated heart failure (HF). Method The present study included 88 consecutive patients hospitalized with acutely decompensated HF (New York Heart Association (NYHA) Class 3–4) requiring inotropic therapy. Patients were randomized 2:1 to either L or D for intravenous inotropic support. Diuretic therapy was kept constant during infusions. Renal function values, including serum creatinine (CR), blood urea nitrogen, 24-h urinary output levels and calculated glomerular filtration rate (GFR) were measured just prior to and 24 h after the infusions in all patients, and 48 and 72 h after the infusions in every second patient in both groups. The pre and post-infusion values of renal function and left ventricular ejection fraction (LVEF) were evaluated. Results LVEF increased significantly in both groups. Those in L showed a significant improvement in calculated GFR after 24 h, whereas those in D showed no significant change (median in change in L:+15.3%, median change in D: −1.33%). Furthermore, in the L group a significant improvement was observed in calculated GFR after 72 h compared to baseline levels, whereas in D no significant change (median change in L:+45.45%, median change in D: +0.09%) was seen. Both agents improved 24-h urinary output. Conclusion Levosimendan seems to provide beneficial effects in terms of improvement in renal function compared to dobutamine in patients with heart failure who require inotropic therapy.     

A Patient with Heart Failure and Worsening Kidney Function

There is high prevalence of CKD, defined by reduced GFR, in patients with heart failure. Reduced kidney function is associated with increased morbidity and mortality in this patient population. The cardiorenal syndrome (CRS) involves a bidirectional relationship between the heart and kidneys whereby dysfunction in either may exacerbate the function of the other, but this syndrome has been difficult to precisely define because it has many complex physiologic, biochemical, and hormonal abnormalities. The pathophysiology of CRS is not completely understood, but potential mechanisms include reduced kidney perfusion due to decreased forward flow, increased right ventricular and venous pressure, and neurohormonal adaptations. Treatment options include inotropic medications; diuretics; ultrafiltration; and medications, such as β-blockers, inhibitors of the renin-angiotensin-aldosterone system, and more novel treatments that focus on unique aspects of the pathophysiology. Recent observational studies suggest that treatments that result in a decrease in venous pressure and lead to hemoconcentration may be associated with improved outcomes. Patients with CRS that is not responsive to medical interventions should be considered for ventricular assist devices, heart transplantation, or combined heart and kidney transplantation.     

Relationship of Liver Stiffness With Congestion in Patients Presenting With Acute Decompensated Heart Failure

Objective

The significance of liver stiffness (LS) in the setting of cardiovascular congestion during the course of acute decompensated heart failure (ADHF) is under investigation. The aim of this study was to assess LS with the use of transient elastography (TE) and its associations with volume overload as determined by means of bioimpedance vector analysis (BIVA) in ADHF.

Worsening Renal Function and Outcome in Heart Failure Patients With Preserved Ejection Fraction and the Impact of Angiotensin Receptor Blocker Treatment

Background

Worsening renal function (WRF) associated with renin-angiotensin-aldosterone system (RAAS) inhibition does not confer excess risk in heart failure patients with reduced ejection fraction (HFrEF).

Objectives

The goal of this study was to investigate the relationship between WRF and outcomes in heart failure patients with preserved ejection fraction (HFpEF) and the interaction with RAAS blockade.

Methods

In 3,595 patients included in the I-PRESERVE (Irbesartan in Heart Failure With Preserved Ejection Fraction) trial, change in estimated glomerular filtration rate (eGFR) and development of WRF after initiation of irbesartan or placebo were examined. We examined the association between WRF and the first occurrence of cardiovascular death or heart failure hospitalization (primary outcome in this analysis) and the interaction with randomized treatment.

Results

Estimated GFR decreased early with irbesartan treatment and remained significantly lower than in the placebo group. WRF developed in 229 (6.4%) patients and occurred more frequently with irbesartan treatment (8% vs. 4%). Overall, WRF was associated with an increased risk of the primary outcome (adjusted hazard ratio [HR]: 1.43; 95% confidence interval [CI]: 1.10 to 1.85; p = 0.008). Although the risk related to WRF was greater in the irbesartan group (HR: 1.66; 95% CI: 1.21 to 2.28; p = 0.002) than with placebo (HR: 1.09; 95% CI: 0.66 to 1.79; p = 0.73), the interaction between treatment and WRF on outcome was not significant in an adjusted analysis.

Conclusions

The incidence of WRF in HFpEF was similar to that previously reported in HFrEF but more frequent with irbesartan than with placebo. WRF after initiation of irbesartan treatment in HFpEF was associated with excess risk, in contrast to WRF occurring with RAAS blockade in HFrEF.     

Utilization Pattern of Mineralocorticoid Receptor Antagonists in Contemporary Patients Hospitalized With Acute Decompensated Heart Failure: A Single-Center Experience

BackgroundRecent studies have broadened the potential use of mineralocorticoid receptor antagonist (MRA) in patients with systolic heart failure after cardiovascular hospitalization. Real-world data on safety and tolerability of MRA initiation during hospitalization for acute decompensated heart failure (ADHF) are lacking. We examined the patterns of utilization of MRAs in patients admitted for ADHF in contemporary clinical practice.Methods and ResultsWe reviewed consecutive hospitalized patients admitted with a primary diagnosis of ADHF from March to June 2011. The treatment patterns of MRA use or discontinuation before, during, and after hospitalization were reviewed and analyzed retrospectively. In the study cohort of 500 patients, 106 patients (21%) were on MRAs before admission. During hospitalization, preadmission and newly started MRAs were discontinued in 64 out of 177 (36%), with worsening renal function being the most common identifiable reason. In a multivariate analysis, high admission creatinine was the only significant predictor of MRA discontinuation during hospitalization (P = .01). Of the 394 patients who did not receive MRA before admission, 81 were eligible for MRAs, but only 17 (21%) were initiated. After a median follow up of 57 days, 21 additional patients discontinued MRAs; of 72 eligible patients for MRA, 55 patients (76%) were still appropriately taking it.ConclusionsDespite recent data, MRAs are still underutilized in patients admitted with ADHF who are otherwise eligible for it. Elevated serum creatinine and worsening of renal function are the most common cause of in-hospital discontinuation, which highlights the importance of meticulous follow-up after MRA initiation.