Potential effects of aggressive decongestion during the treatment of decompensated heart failure on renal function and survival.
BACKGROUND
Overly aggressive diuresis leading to intravascular volume depletion has been proposed as a cause for worsening renal function during the treatment of decompensated heart failure. If diuresis occurs at a rate greater than extravascular fluid can refill the intravascular space, the concentration of such intravascular substances as hemoglobin and plasma proteins increases. We hypothesized that hemoconcentration would be associated with worsening renal function and possibly would provide insight into the relationship between aggressive decongestion and outcomes.


RESULTS
Subjects in the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness trial limited data set with a baseline/discharge pair of hematocrit, albumin, or total protein values were included (336 patients). Baseline-to-discharge increases in these parameters were evaluated, and patients with >or=2 in the top tertile were considered to have evidence of hemoconcentration. The group experiencing hemoconcentration received higher doses of loop diuretics, lost more weight/fluid, and had greater reductions in filling pressures (P<0.05 for all). Hemoconcentration was strongly associated with worsening renal function (odds ratio, 5.3; P<0.001), whereas changes in right atrial pressure (P=0.36) and pulmonary capillary wedge pressure (P=0.53) were not. Patients with hemoconcentration had significantly lower 180-day mortality (hazard ratio, 0.31; P=0.013). This relationship persisted after adjustment for baseline characteristics (hazard ratio, 0.16; P=0.001).


CONCLUSIONS
Hemoconcentration is significantly associated with measures of aggressive fluid removal and deterioration in renal function. Despite this relationship, hemoconcentration is associated with substantially improved survival. These observations raise the question of whether aggressive decongestion, even in the setting of worsening renal function, can positively affect survival.
Testani
Jeffrey M
JM
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA. jeffrey.testani@uphs.upenn.edu
Chen
Jennifer
J
McCauley
Brian D
BD
Kimmel
Stephen E
SE
Shannon
Richard P
RP
D000328:Adult; D000368:Aged; D001798:Blood Proteins / Q000378:metabolism; D001810:Blood Volume; D045604:Extracellular Fluid / Q000378:metabolism; D005260:Female; D005919:Glomerular Filtration Rate; D006333:Heart Failure / Q000188:drug therapy* / Q000401:mortality*; D006400:Hematocrit; D006801:Humans; D007668:Kidney / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D011669:Pulmonary Wedge Pressure; D012709:Serum Albumin / Q000378:metabolism; D049993:Sodium Chloride Symporter Inhibitors / Q000627:therapeutic use*; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000627:therapeutic use*; D016896:Treatment Outcome; D017725:Ventricular Pressure
D001798:Blood Proteins; D012709:Serum Albumin; D049993:Sodium Chloride Symporter Inhibitors; D049994:Sodium Potassium Chloride Symporter Inhibitors