Effect of fenofibrate treatment for hyperlipidaemia on serum creatinine and cystatin C

The increase in creatinine in patients on fibrate therapy is well-recognized, but its mechanism is not clearly understood. A study by Hottelart et al. suggested that fibrate-induced creatininaemia was due to the effect of fibrates on creatinine metabolism as opposed to a decline in renal function. To address this hypothesis, we have monitored renal function in a group of hyperlipidaemic patients before commencing fibrate treatment and after three months of therapy.

We studied 12 subjects (10 men, 2 women), median age 43.5 y (range 33-70 y). Serum creatinine, cystatin C, creatine kinase and fasting lipids were measured.

We observed statistically significant increases in concentrations of serum creatinine (P < 0.005) and cystatin C(P < 0.01). Concentrations of both analytes increased in 10 (83.3%) of the patients. In these patients, the median increases were 15.1% (range 5.5-23.2%) for creatinine and 9.9% (range 1.1-26.1%) for cystatin C.

These results suggest that the decrease in estimated glomerular filtration rate, observed in patients undergoing fibrate therapy, is a genuine effect on kidney function rather than a change in creatinine metabolism as previously postulated, since the rises in serum creatinine concentration were reflected by rises in cystatin C, an independent marker of renal function.