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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Hypertonic saline solution for prevention of renal dysfunction in patients with decompensated heart failure

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Author(s):
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Issa, Victor S. [1] ; Andrade, Lucia [2] ; Ayub-Ferreira, Silvia M. [1] ; Bacal, Fernando [1] ; de Braganca, Ana C. [2] ; Guimaraes, Guilherme V. [1] ; Marcondes-Braga, Fabiana G. [1] ; Cruz, Fatima D. [1] ; Chizzola, Paulo R. [1] ; Conceicao-Souza, Germano E. [1] ; Velasco, Irineu T. [3] ; Bocchi, Edimar A. [1]
Total Authors: 12
Affiliation:
[1] Univ Sao Paulo, Fac Med, Hosp Clin, Heart Inst InCor, BR-05508 Sao Paulo - Brazil
[2] Univ Sao Paulo, Fac Med, Dept Nephrol, Lab Basic Res, BR-05508 Sao Paulo - Brazil
[3] Univ Sao Paulo, Fac Med, Emergency Dept, BR-05508 Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: INTERNATIONAL JOURNAL OF CARDIOLOGY; v. 167, n. 1, p. 34-40, JUL 15 2013.
Web of Science Citations: 17
Abstract

Background: Renal dysfunction is associated with increased mortality in patients with decompensated heart failure. However, interventions targeted to prevention in this setting have been disappointing. We investigated the effects of hypertonic saline solution (HSS) for prevention of renal dysfunction in decompensated heart failure. Methods: In a double-blind randomized trial, patients with decompensated heart failure were assigned to receive three-day course of 100 mL HSS (NaCl 7.5%) twice daily or placebo. Primary end point was an increase in serumcreatinine of 0.3 mg/dL or more. Main secondary end point was change in biomarkers of renal function, including serum levels of creatinine, cystatin C, neutrophil gelatinase-associated lipocalin-NGAL and the urinary excretion of aquaporin 2 (AQP(2)), urea transporter (UT-A(1)), and sodium/hydrogen exchanger 3 (NHE3). Results: Twenty-two patients were assigned to HSS and 12 to placebo. Primary end point occurred in two (10%) patients in HSS group and six (50%) in placebo group (relative risk 0.3; 95% CI 0.09-0.98; P=0.01). Relative to baseline, serum creatinine and cystatin C levels were lower in HSS as compared to placebo (P=0.004 and 0.03, respectively). NGAL level was not statistically different between groups, however the urinary expression of AQP2, UT-A1 and NHE3 was significantly higher in HSS than in placebo. Conclusions: HSS administration attenuated heart failure-induced kidney dysfunction as indicated by improvement in both glomerular and tubular defects, a finding with important clinical implications. HSS modulated the expression of tubular proteins involved in regulation of water and electrolyte homeostasis. (C) 2011 Elsevier Ireland Ltd. All rights reserved. (AU)