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Analgesic nephropathy in rodents

R G Schnellmann¹

¹Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock 72205-7199, USA. rschnell@biomed.uams.edu

Journal of Toxicology and Environmental Health. Part B, Critical Reviews

|March 6, 1998

Summary

The exact causes and mechanisms of analgesic nephropathy remain unknown in humans. Current animal models, like rodents, do not accurately mimic human responses to pain relievers such as acetaminophen and aspirin.

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Area of Science:

Nephrology
Toxicology
Pharmacology

Background:

Analgesic nephropathy is a recognized human condition.
The specific causative agents and underlying mechanisms remain unidentified.

Purpose of the Study:

To review the literature on analgesic nephropathy.
To evaluate the role of acetaminophen and aspirin in renal toxicity.
To assess the suitability of animal models for studying analgesic nephropathy.

Main Methods:

Literature review of studies on analgesic nephropathy.
Analysis of rodent and human data regarding acetaminophen and aspirin exposure.
Evaluation of animal models for disease mimicry.

Main Results:

Chronic acetaminophen does not induce renal papillary necrosis in rodents or humans.
Chronic aspirin causes renal papillary necrosis in rodents, but epidemiological studies do not link aspirin alone to human analgesic nephropathy.
Species differences may explain aspirin's varied effects.
Limited controlled studies exist for combination analgesics.
Rodent models do not accurately replicate human analgesic nephropathy.

Conclusions:

The chemical agents causing human analgesic nephropathy are undetermined.
Mechanisms of analgesic nephropathy require further elucidation.
Current animal models, particularly rodents, are inadequate for studying human analgesic nephropathy.

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