1988 Volume 19 Issue 4 Pages 767-772
Although there are some reports which state that phenacetin is unlikely to be theprimary causative agent in analgesic nephropathy (Prescott, 1982), 80% of the 285phenacetin abusers observed in our clinic between 1962 and 1979 were suffering fromchronic interstitial nephritis (Nitzsche et al., 1980). In order to ascertain whether phenacetin itself or one of its metabolites is responsible for this nephritis we have comparedthe pharmacokinetics and metabolic profile of phenacetin in 2 groups of phenacetinabusers with and without nephritis.
Phenacetin (900 mg), contained in gelatin capsules, was administered orally after anovernight fast. Blood and urine samples were collected. Plasma and urine concentrations of unchanged phenacetin and its major metabolites were determined by HPLCwith spectrophotometric detection (254 nm).
Urinary elimination of phenacetin and metabolites was quantified as the total amount (percentage of dose) in 24 h.
The results suggest that the cause of nephritis in susceptible phenacetin abusers isnot associated with altered elimination of either phenacetin itself or the metabolitesmeasured in this study.