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NDT Advance Access published online on November 26, 2008

Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfn643
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



Non-phenacetin analgesics and analgesic nephropathy

Clinical assessment of high users from a case-control study [1]*

Paul Michielsen1, Lothar Heinemann2, Michael Mihatsch3, Peter Schnülle4, Helmut Graf 5 and Karl-Martin Koch6

1 Faculty of Medicine, University of Leuven, Belgium 2 Centre for Epidemiology & Health Research, Berlin, Germany 3 Institute of Pathology, University Hospital, Basel, Switzerland 4 Medical Faculty of Mannheim, University of Heidelberg, Germany 5 Krankenanstalt Rudolfstiftung, Vienna, Austria 6 Clinic for Nephrology, Hannover Medical School, Germany

Correspondence and offprint requests to: Paul Michielsen, Acacialaan 54, Herent B3020, Belgium. E-mail: paul.michielsen{at}med.kuleuven.be



  Abstract

Background. A recent large-scale case-control study on analgesic nephropathy (SAN) [1] found no increased risk of end-stage renal disease (ESRD) in users of combined or single formulations of phenacetin-free analgesics. In a subgroup of 22 high users, however, a dose-dependent increased risk was found, which raised the question if these patients presented or not with analgesic nephropathy (AN).

Methods. The individual questionnaires of this subgroup of high users were reviewed, and the total lifetime intake of different types of analgesics was calculated. For evidence of AN, the following data were considered: (1) the amount and type of analgesics consumed, (2) the cause of ESRD, as diagnosed by the nephrologist in charge of the patient and (3) renal imaging and other relevant laboratory data.

Results. This group of ESRD patients consumed on average 7.8 kg of antipyretic analgesics (range 30.8–2.7 kg) over an average of 21.5 years (range 35–6 years). Single analgesics were exclusively used by 12 patients (54.5%) and combined analgesics by 5 patients (22.7%), while 5 patients used both. None of the patients was diagnosed as having AN, and a review of the questionnaires did not disclose evidence suggestive of AN. The possibility that, irrespective of AN, the analgesic (ab)use contributed to the progression of existing renal diseases cannot be answered in the absence of well-defined criteria. The data supporting the existence of such an analgesic-associated nephropathy (AAN) are, however, not consistent and most likely due to confounding by indication.

Conclusion. In a group of ESRD patients with high use of non-phenacetin analgesics, no evidence of AN was found. There is no evidence that (ab)use of analgesics or NSAIDs other than phenacetin leads to a pathologically or clinically defined renal disease that could be named AN or AAN.

Keywords: analgesic-associated nephropathy; analgesic nephropathy; combined analgesics; NSAID; phenacetin


* This publication is dedicated to the memory of Professor Fokke J. van der Woude (1953–2006).

Received for publication: 15. 5.08
Accepted in revised form: 21.10.08


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