Affiliation:
1. Department of Clinical Biochemistry, Frimley Park Hospital NHS Foundation Trust, Frimley, Surrey GUI6 JUJ
2. Department of Clinical Biochemistry, Royal Surrey County Hospital NHS Foundation Trust, Guildford, Surrey, GU2 7XX, UK
Abstract
Background 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. Methods 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. Results 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. Conclusions 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.
Subject
Clinical Biochemistry,General Medicine
Cited by
20 articles.
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