Interactive and potentially independent roles of renin-angiotensin-aldosterone system blockade and the development of cardiorenal syndrome, type 1 on in-hospital mortality among elderly patients admitted with acute decompensated congestive heart failure

Jose Iglesias,1–4 Savan Ghetiya,5 Kandria J Ledesma,6 Chirag S Patel,7 Jerrold S Levine8,9 1Department of Medicine, Subsection of Nephrology, Rowan University School of Osteopathic Medicine, Stratford, NJ, USA; 2Department of Medicine, Subsection of Nephrology, Jersey Shore University Medical Center, Neptune, NJ, USA; 3Department of Medicine Section of Nephrology, Robert Wood Johnson School of Medicine, New Brunswick, NJ, USA; 4Department of Medicine, Subsection of Nephrology, RWJ Barnabas Health Community Medical Center, Toms River, NJ, USA; 5Department of Medicine, Coney Island University Medical Center, New York, NY, USA; 6American University of Antigua College of Medicine, Coolidge, Antigua and Barbuda; 7Department of Medicine, Jersey Shore University Medical Center, Neptune, NJ, USA; 8Department of Medicine, Section of Nephrology, University of Illinois at Chicago, Chicago, IL, USA; 9Department of Medicine Section of Nephrology, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA Purpose: Cardiorenal syndrome type 1 (CRS1), defined as worsening renal function from acute decompensated congestive heart failure (ADCHF), is complicated by the fact that CRS1 limits the use of common therapeutic strategies, such as angiotensin converting-enzyme inhibitors (ACEIs) or angiotensin II-receptor blockers (A2RB). The present study examines retrospectively the role of ACEI/A2RB usage on in-hospital mortality among elderly ADCHF patients, in particular those who developed CRS1.Methods: We retrospectively examined the effects of ACEI/A2RB usage and CRS1 development (in-hospital change in serum creatinine ≥0.3 mg/dL or ≥0.5 mg/dL), as well as their potential interaction, on in-hospital mortality among elderly ADCHF patients (aged ≥65 years). Employing univariate and multivariate analyses, we performed risk-factor analysis on a cohort of 419 patients (51 nonsurvivors [12.2%]) for whom we had complete clinical and laboratory data (median f