title: Importance of venous congestion for worsening of renal function in advanced decompensated heart failure.
abstract: OBJECTIVE
  To determine whether venous congestion, rather than impairment of cardiac output, is primarily associated with the development of worsening renal function (WRF) in patients with advanced decompensated heart failure (ADHF).
  
  
  BACKGROUND
  Reduced cardiac output is traditionally believed to be the main determinant of WRF in patients with ADHF.
  
  
  METHODS
  A total of 145 consecutive patients admitted with ADHF treated with intensive medical therapy guided by pulmonary artery catheter were studied. We defined WRF as an increase of serum creatinine >/=0.3 mg/dl during hospitalization.
  
  
  RESULTS
  In the study cohort (age 57 +/- 14 years, cardiac index 1.9 +/- 0.6 l/min/m(2), left ventricular ejection fraction 20 +/- 8%, serum creatinine 1.7 +/- 0.9 mg/dl), 58 patients (40%) developed WRF. Patients who developed WRF had a greater central venous pressure (CVP) on admission (18 +/- 7 mm Hg vs. 12 +/- 6 mm Hg, p < 0.001) and after intensive medical therapy (11 +/- 8 mm Hg vs. 8 +/- 5 mm Hg, p = 0.04). The development of WRF occurred less frequently in patients who achieved a CVP <8 mm Hg (p = 0.01). Furthermore, the ability of CVP to stratify risk for development of WRF was apparent across the spectrum of systemic blood pressure, pulmonary capillary wedge pressure, cardiac index, and estimated glomerular filtration rates.
  
  
  CONCLUSIONS
  Venous congestion is the most important hemodynamic factor driving WRF in decompensated patients with advanced heart failure.
authors.affiliation: Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Wilfried
authors.initials: W
authors.lastname: Mullens
authors.affiliation: Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Zuheir
authors.initials: Z
authors.lastname: Abrahams
authors.affiliation: Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Gary S
authors.initials: GS
authors.lastname: Francis
authors.affiliation: Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: George
authors.initials: G
authors.lastname: Sokos
authors.affiliation: Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: David O
authors.initials: DO
authors.lastname: Taylor
authors.affiliation: Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: Randall C
authors.initials: RC
authors.lastname: Starling
authors.affiliation: Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio.
authors.forename: James B
authors.initials: JB
authors.lastname: Young
authors.affiliation: Department of Cardiovascular Medicine, Kaufman Center for Heart Failure, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio. Electronic address: tangw@ccf.org.
authors.forename: W H Wilson
authors.initials: WHW
authors.lastname: Tang
mesh_terms: D000368:Aged; D002302:Cardiac Output; D002496:Central Venous Pressure; D003404:Creatinine / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000503:physiopathology*; D006801:Humans; D006940:Hyperemia / Q000097:blood / Q000150:complications* / Q000503:physiopathology*; D007674:Kidney Diseases / Q000097:blood / Q000209:etiology* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index
chemical_list: D003404:Creatinine