scholarly journals Serum and Urine Albumin and Response to Loop Diuretics in Heart Failure

2019 ◽  
Vol 14 (5) ◽  
pp. 712-718 ◽  
Author(s):  
Antonios Charokopos ◽  
Matthew Griffin ◽  
Veena S. Rao ◽  
Lesley Inker ◽  
Krishna Sury ◽  
...  
Keyword(s):  
Heart Failure ◽  
Serum Albumin ◽  
Transitional Care ◽  
Care Center ◽  
Loop Diuretics ◽  
Human Heart Failure ◽  
Diuretic Resistance ◽  
Urine Albumin ◽  
Patients With Heart Failure ◽  
Diuretic Efficiency

Background and objectivesDiuretic resistance can limit successful decongestion of patients with heart failure. Because loop diuretics tightly bind albumin, low serum albumin and high urine albumin can theoretically limit diuretic delivery to the site of action. However, it is unknown if this represents a clinically relevant mechanism of diuretic resistance in human heart failure.Design, setting, participants, & measurementsIn total, 208 outpatients with heart failure at the Yale Transitional Care Center undergoing diuretic treatment were studied. Blood and urine chemistries were collected at baseline and 1.5 hours postdiuretic administration. Urine diuretic levels were normalized to urine creatinine and adjusted for diuretic dose administered, and diuretic efficiency was calculated as sodium output per doubling of the loop diuretic dose. Findings were validated in an inpatient heart failure cohort (n=60).ResultsSerum albumin levels in the outpatient cohort ranged from 2.4 to 4.9 g/dl, with a median of 3.7 g/dl (interquartile range, 3.5–4.1). Serum albumin had no association with urinary diuretic delivery (r=−0.05; P=0.52), but higher levels weakly correlated with better diuretic efficiency (r=0.17; P=0.02). However, serum albumin inversely correlated with systemic inflammation as assessed by plasma IL-6 (r=−0.35; P<0.001), and controlling for IL-6 eliminated the diuretic efficiency-serum albumin association (r=0.12; P=0.12). In the inpatient cohort, there was no association between serum albumin and urinary diuretic excretion (r=0.15; P=0.32) or diuretic efficiency (r=−0.16; P=0.25). In the outpatient cohort, 39% of patients had microalbuminuria, and 18% had macroalbuminuria. There was no correlation between albuminuria and diuretic efficiency after adjusting for kidney function (r=−0.02; P=0.89). Results were similar in the inpatient cohort.ConclusionsSerum albumin levels were not associated with urinary diuretic excretion, and urinary albumin levels were not associated with diuretic efficiency.

scholarly journals Oral Metolazone Versus Intravenous Chlorothiazide as an Adjunct to Loop Diuretics for Diuresis in Acute Decompensated Heart Failure With Reduced Ejection Fraction

2018 ◽  
Vol 54 (6) ◽  
pp. 351-357 ◽  
Author(s):  
Brian C. Bohn ◽  
Rim M. Hadgu ◽  
Hannah E. Pope ◽  
Jerrica E. Shuster
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Oral Formulation ◽  
Loop Diuretics ◽  
Reduced Ejection Fraction ◽  
Significant Difference ◽  
Patients With Heart Failure ◽  
Total Urine

Background: Thiazide diuretics are often utilized to overcome loop diuretic resistance when treating acute decompensated heart failure (ADHF). In addition to a large cost advantage, several pharmacokinetic advantages exist when administering oral metolazone (MTZ) compared with intravenous (IV) chlorothiazide (CTZ), yet many providers are reluctant to utilize an oral formulation to treat ADHF. The purpose of this study was to compare the increase in 24-hour total urine output (UOP) after adding MTZ or CTZ to IV loop diuretics (LD) in patients with heart failure with reduced ejection fraction (HFrEF). Methods and Results: From September 2013 to August 2016, 1002 patients admitted for ADHF received either MTZ or CTZ in addition to LD. Patients were excluded for heart failure with preserved ejection fraction (HFpEF) (n = 469), <24-hour LD or UOP data prior to drug initiation (n = 129), or low dose MTZ/CTZ (n = 91). A total of 168 patients were included with 64% receiving CTZ. No significant difference was observed between the increase in 24-hour total UOP after MTZ or CTZ initiation (1458 [514, 2401] mL vs 1820 [890, 2750] mL, P = .251). Conclusions: Both MTZ and CTZ similarly increased UOP when utilized as an adjunct to IV LD. These results suggest that while thiazide agents can substantially increase UOP in ADHF patients with HFrEF, MTZ and CTZ have comparable effects.

scholarly journals Transitional Care Interventions for Patients with Heart Failure: An Integrative Review

2020 ◽  
Vol 17 (8) ◽  
pp. 2925 ◽  
Author(s):  
Hai Mai Ba ◽  
Youn-Jung Son ◽  
Kyounghoon Lee ◽  
Bo-Hwan Kim
Keyword(s):  
Heart Failure ◽  
Hospital Readmission ◽  
Transitional Care ◽  
Hospital Readmissions ◽  
Recovery Period ◽  
Functional Decline ◽  
Integrative Review ◽  
Patients With Heart Failure ◽  
Ed Visits ◽  
The Common

Heart failure (HF) is a life-limiting illness and presents as a gradual functional decline with intermittent episodes of acute deterioration and some recovery. In addition, HF often occurs in conjunction with other chronic diseases, resulting in complex comorbidities. Hospital readmissions for HF, including emergency department (ED) visits, are considered preventable. Majority of the patients with HF are often discharged early in the recovery period with inadequate self-care instructions. To address these issues, transitional care interventions have been implemented with the common objective of reducing the rate of hospital readmission, including ED visits. However, there is a lack of evidence regarding the benefits and adverse effects of transitional care interventions on clinical outcomes and patient-related outcomes of patients with HF. This integrative review aims to identify the components of transitional care interventions and the effectiveness of these interventions in improving health outcomes of patients with HF. Five databases were searched from January 2000 to December 2019, and 25 articles were included.

The Effects of Diuresis on the Pharmacokinetics of the Loop Diuretics Furosemide and Torsemide in Patients with Heart Failure

1998 ◽  
Vol 104 (6) ◽  
pp. 533-538 ◽  
Author(s):  
Stephen S Gottlieb ◽  
Meenakshi Khatta ◽  
Derek Wentworth ◽  
David Roffman ◽  
Michael L Fisher ◽  
...  
Keyword(s):  
Heart Failure ◽  
Loop Diuretics ◽  
Patients With Heart Failure

scholarly journals Urine and Serum Albumin are Not Major Determinants of Diuretic Resistance in Heart Failure

2016 ◽  
Vol 22 (8) ◽  
pp. S17 ◽  
Author(s):  
Antonios Charokopos ◽  
Jennifer S. Hanberg ◽  
Veena S. Rao ◽  
J. Samuel Broughton ◽  
Mahlet Assefa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Serum Albumin ◽  
Diuretic Resistance ◽  
Urine And Serum

Applying the Transitional Care Model to Elderly Patients with Heart Failure

2000 ◽  
Vol 14 (3) ◽  
pp. 53-63 ◽  
Author(s):  
M. Brian Bixby ◽  
Joanne Konick-McMahon ◽  
Catherine G. McKenna
Keyword(s):  
Heart Failure ◽  
Elderly Patients ◽  
Transitional Care ◽  
Care Model ◽  
Patients With Heart Failure

Non-competitive immunochemiluminometric assay for cardiotrophin-1 detects elevated plasma levels in human heart failure

2002 ◽  
Vol 102 (4) ◽  
pp. 411-416 ◽  
Author(s):  
Leong L. NG ◽  
Russell J. O'BRIEN ◽  
Bettina DEMME ◽  
Sonja JENNINGS
Keyword(s):  
Heart Failure ◽  
Amino Acids ◽  
Plasma Levels ◽  
Limit Of Detection ◽  
Linear Increase ◽  
Full Length ◽  
Human Heart Failure ◽  
Competitive Assay ◽  
Coefficients Of Variation ◽  
Patients With Heart Failure

Cardiotrophin-1 (CT-1) leads to a specific form of ventricular hypertrophy characterized by sarcomeres added in series, and has been reported to be elevated in heart failure. Previous competitive assays for CT-1 necessitate the extraction of plasma and involve prolonged incubations. We describe the development of a non-competitive assay for CT-1 that can measure plasma levels without the need for extraction. Two antibodies specific for the mid-section (amino acids 105-120) and C-terminal (amino acids 186-199) portions of CT-1 were developed in rabbits. One antibody was immobilized and used as the capture antibody. The other antibody was affinity purified and biotinylated. Unextracted plasma was incubated with these antibodies, and detection was with methylacridinium ester-labelled streptavidin. Plasma was obtained from 40 patients with heart failure and 40 normal control subjects. The non-competitive assay demonstrated a linear increase in chemiluminescence (measured as relative light units) with increasing amounts of full-length recombinant CT-1, with no evidence of a hook effect at high concentrations. The lower limit of detection was 2.9 fmol/ml. Intra-assay coefficients of variation ranged from 3.1% to 4.2% in the 10-40fmol/well concentration range, and interassay coefficients of variation ranged from 3.5% to 4.5% in the 550-950fmol/ml range. Measurements of CT-1 levels in patients with heart failure (median 166.5fmol/ml; range 49.5-2788fmol/ml) revealed very significantly elevated levels compared with those in normal controls (median 43.5fmol/ml; range 11.2-258.6fmol/ml; P < 0.0001 by Mann-Whitney test). At a CT-1 concentration of 68fmol/ml, sensitivity and specificity were 95% and 82.5% respectively. Thus this new non-competitive immunochemiluminometric assay for CT-1 could successfully detect full-length recombinant CT-1 in unextracted plasma, and demonstrated that plasma levels of CT-1 were significantly elevated in patients with heart failure.

scholarly journals Mechanism and management of diuretic resistance in congestive heart failure

2012 ◽  
Vol 17 (1) ◽  
pp. 44-46
Author(s):  
Dipankar Chandra Nag ◽  
AKM Murshed ◽  
Rajashis Chakrabortty ◽  
Md Raziur Rahman
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Sodium Intake ◽  
Diuretic Therapy ◽  
Compensatory Hypertrophy ◽  
Loop Diuretics ◽  
Thick Ascending Limb ◽  
Diuretic Resistance ◽  
First Line Therapy ◽  
Advanced Stages

Diuretic drugs are used almost universally in patients with congestive heart failure, most frequently the potent loop diuretics. Despite their unproven effect on survival, their indisputable efficacy in relieving congestive symptoms makes them first line therapy for most patients. In the treatment of more advanced stages of heart failure diuretics may fail to control salt and water retention despite the use of appropriate doses. Diuretic resistance may be caused by decreased renal function and reduced and delayed peak concentrations of loop diuretics in the tubular fluid, but it can also be observed in the absence of these pharmacokinetic abnormalities. When the effect of a short acting diuretic has worn off, postdiuretic salt retention will occur during the rest of the day. Chronic treatment with a loop diuretic results in compensatory hypertrophy of epithelial cells downstream from the thick ascending limb and consequently its diuretic effect will be blunted. Strategies to overcome diuretic resistance include restriction of sodium intake, changes in dose, changes in timing, and combination diuretic therapy. DOI: http://dx.doi.org/10.3329/jdnmch.v17i1.12193 J. Dhaka National Med. Coll. Hos. 2011; 17 (01): 44-46

Editor’s Choice-Diuretic resistance in acute heart failure

2018 ◽  
Vol 7 (4) ◽  
pp. 379-389 ◽  
Author(s):  
Frederik H Verbrugge
Keyword(s):  
Heart Failure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Acute Heart Failure ◽  
Filtration Rate ◽  
Loop Diuretic ◽  
Volume Overload ◽  
Renal Perfusion ◽  
Loop Diuretics ◽  
Diuretic Resistance

Diuretic resistance is a powerful predictor of adverse outcome in acute heart failure (AHF), irrespectively of underlying glomerular filtration rate. Metrics of diuretic efficacy such as natriuresis, urine output, weight loss, net fluid balance, or fractional sodium excretion, differ in their risk for measurement error, convenience, and biological plausibility, which should be taken into account when interpreting their results. Loop diuretic resistance in AHF has multiple causes including altered drug pharmacokinetics, impaired renal perfusion and effective circulatory volume, neurohumoral activation, post-diuretic sodium retention, the braking phenomenon and functional as well as structural adaptations in the nephron. Ideally, these mechanisms should guide specific treatment decisions with the goal of achieving complete decongestion. Therefore, volume overload needs to be identified correctly to avoid poor diuretic response due to electrolyte depletion or dehydration. Next, renal perfusion should be optimised if possible and loop diuretics should be prescribed above their threshold dose. Addition of thiazide-type diuretics should be considered when a progressive decrease in loop diuretic efficacy is observed with prolonged use (i.e., the braking phenomenon). Furthermore, thiazide-type diuretics are a useful addition in patients with low glomerular filtration rate. However, they limit free water excretion and are relatively contraindicated in cases of hypotonic hyponatremia, where acetazolamide is the better option. Finally, ultrafiltration should be considered in patients with refractory diuretic resistance as persistent volume overload after decongestive treatment is associated with worse outcomes. Whether more upfront use of any of these individually tailored decongestion strategies is superior to monotherapy with loop diuretics remains to be shown by adequately powered randomised clinical trials.

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