TY - JOUR
T1 - Relationship between heart failure treatment and development of worsening renal function among hospitalized patients
AU - Butler, Javed
AU - Forman, Daniel E.
AU - Abraham, William T.
AU - Gottlieb, Stephen S.
AU - Loh, Evan
AU - Massie, Barry M.
AU - O'Connor, Christopher M.
AU - Rich, Michael W.
AU - Stevenson, Lynne Warner
AU - Wang, Yongfei
AU - Young, James B.
AU - Krumholz, Harlan M.
N1 - Funding Information:
Supported by Biogen, Inc, Cambridge, Mass.
PY - 2004/2
Y1 - 2004/2
N2 - Background: Among patients who are hospitalized with heart failure (HF), worsening renal function (WRF) is associated with worse outcomes. Whether treatment for HF contributes to WRF is unknown. In this study, we sought to assess whether acute treatment for patients who were hospitalized with HF contributes to WRF. Methods: Data were collected in a nested case-control study on 382 subjects who were hospitalized with HF (191 patients with WRF, defined as a rise in serum creatinine level >26.5 μmol/L [0.3 mg/dL], and 191 control subjects). The association of medications, fluid intake/output, and weight with WRF was assessed. Results: Calcium channel blocker (CCB) use and loop diuretic doses were higher in patients on the day before WRF (25% vs 10% for CCB; 199 ± 195 mg vs 143 ± 119 mg for loop diuretics; both P <.05). There were no significant differences in the fluid intake/output or weight changes in the 2 groups. Angiotensin-converting enzyme (ACE) inhibitor use was not associated with WRF. Other predictors of WRF included elevated creatinine level at admission, uncontrolled hypertension, and history of HF or diabetes mellitus. Higher hematocrit levels were associated with a lower risk. Vasodilator use was higher among patients on the day before WRF (46% vs 35%, P <.05), but was not an independent predictor in the multivariable analysis. Conclusions: Several medical strategies, including the use of CCBs and a higher dose of loop diuretics, but not ACE inhibitors, were associated with a higher risk of WRF. Although assessment of inhospital diuresis was limited, WRF could not be explained by greater fluid loss in these patients. Determining whether these interventions are responsible for WRF or are markers of higher risk requires further investigation.
AB - Background: Among patients who are hospitalized with heart failure (HF), worsening renal function (WRF) is associated with worse outcomes. Whether treatment for HF contributes to WRF is unknown. In this study, we sought to assess whether acute treatment for patients who were hospitalized with HF contributes to WRF. Methods: Data were collected in a nested case-control study on 382 subjects who were hospitalized with HF (191 patients with WRF, defined as a rise in serum creatinine level >26.5 μmol/L [0.3 mg/dL], and 191 control subjects). The association of medications, fluid intake/output, and weight with WRF was assessed. Results: Calcium channel blocker (CCB) use and loop diuretic doses were higher in patients on the day before WRF (25% vs 10% for CCB; 199 ± 195 mg vs 143 ± 119 mg for loop diuretics; both P <.05). There were no significant differences in the fluid intake/output or weight changes in the 2 groups. Angiotensin-converting enzyme (ACE) inhibitor use was not associated with WRF. Other predictors of WRF included elevated creatinine level at admission, uncontrolled hypertension, and history of HF or diabetes mellitus. Higher hematocrit levels were associated with a lower risk. Vasodilator use was higher among patients on the day before WRF (46% vs 35%, P <.05), but was not an independent predictor in the multivariable analysis. Conclusions: Several medical strategies, including the use of CCBs and a higher dose of loop diuretics, but not ACE inhibitors, were associated with a higher risk of WRF. Although assessment of inhospital diuresis was limited, WRF could not be explained by greater fluid loss in these patients. Determining whether these interventions are responsible for WRF or are markers of higher risk requires further investigation.
UR - http://www.scopus.com/inward/record.url?scp=10744231948&partnerID=8YFLogxK
U2 - 10.1016/j.ahj.2003.08.012
DO - 10.1016/j.ahj.2003.08.012
M3 - Article
C2 - 14760333
AN - SCOPUS:10744231948
SN - 0002-8703
VL - 147
SP - 331
EP - 338
JO - American heart journal
JF - American heart journal
IS - 2
ER -