Abstract 14706: Atorvastatin Would Prevent Chronic Kidney Injury in Patients With Chronic Heart Failure - A Prospective Randomized-Controlled Study -
Background: Chronic heart failure (CHF) and renal impairment frequently coexist. Statins have been evaluated for renoprotective effects in patients with coronary heart disease and dyslipidemia, and atorvastatin has been shown to improve renal function in those patients. However, there is little information available on the effect of atorvastatin on chronic kidney injury in CHF patients.
Methods: We enrolled 38 mild to moderate CHF outpatients (NYHA class 1.9±0.6, ischemic origin: 54%) with left ventricular ejection fraction (LVEF) < 40% (28±8%) and serum creatinine < 3.0mg/dl. These patients were randomly assigned to receive atorvastatin (10mg/d) or conventional treatment for heart failure, and were prospectively followed up for at least three years. The measurement of serum creatinine level (sCr) was measured at entry, and repeated every at least 6 month after the entry, and chronic kidney injury (CKI) was defined as an increase of more than 0.3mg/dl in baseline sCr value. Furthermore, the circulating levels of Interleukin-6, high-sensitive CRP and oxidized low-density lipoprotein (oxLDL) as a maker of oxidative stress, were also measured before and after 6 months of treatment.
Results: There were no significant differences in age, gender, NYHA class, LVEF, or sCr at the entry between patients with (n=19) and without atorvastatin (n=19). At 6 months after the entry, oxLDL was significantly lower in patients with than without atorvastatin (86±26 to 115±44 U/l, p=0.02), while there were no significant differences in LVEF, Interleukin-6, or high-sensitive CRP between them. After a mean follow-up of 4.9±2.7 years, 14 patients had CKI. Patients with atorvastatin had a significantly lower risk of CKI than those without (27% vs 53%, p=0.016, hazard ratio 0.28(0.09-0.89)).
Conclusion: Long-term atorvastatin therapy would prevent chronic kidney injury in patients with CHF, which might be brought out partially by the reduction of oxidative stress.
- © 2013 by American Heart Association, Inc.