Corticosteroids Significantly Increase Serum Cystatin C Concentration without Affecting Renal Function in Symptomatic Heart Failure.

Abstract

Human cystatin C is a single non-glycosylated polypeptide chain consisting of 120 amino acid residues. Its concentration in the circulation is mainly determined by glomerular filtration rate. However, non-renal factors, i.e., drugs, may dramatically affect its levels in the circulation. The aim of this study was to evaluate the effect of corticosteroid treatment on serum cystatin C concentration in patients with symptomatic heart failure. Fifty-six symptomatic heart failure patients were treated with prednisone. Concentrations of serum cystatin C and serum creatinine were recorded at baseline, and after about 2 weeks of treatment. Twenty-four hour urinary creatinine was also measured to directly calculate glomerular filtration rate. Prednisone treatment significantly increased serum cystatin C concentration from 1.24 +/- 0.40 mg/L at baseline to 1.61 +/- 0.80 mg/L at the end of study (p < 0.05). However, the elevation in serum cystatin C concentration was not associated with renal function impairment. Prednisone not only significantly decreased serum creatinine concentrations from 89.66 +/- 28.63 pmol/L at baseline to 76.55 +/- 20.80 micromol/L after prednisone treatment (p < 0.05), but also significantly increased fractional excretion of sodium and urine flow rate. The data also showed there was a slight and but nonstatistically significant increase in glomerular filtration rate in such patients after prednisone treatment. Important non-renal factors, such as corticosteroids, can influence cystatin C concentration. Thus, it needs to be considered when interpreting cystatin C values in patients with heart failure receiving corticosteroid therapy.