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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

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

Macrophages are highly plastic leukocytes that differentiate from monocytes following their entry into extravascular tissues. Macrophages can enter various tissues under inflammatory or non-inflammatory conditions and assume different functions and phenotypes according to the cues they receive from the environment. The notion that inflammation in general and macrophage responses in particular affect physiological phenomena that were previously considered to be not immune-related has enhanced and broadened our understanding of macrophage function during inflammation and its resolution....