Renal toxicity of non-narcotic analgesics. At-risk patients and prescribing applications.

Abstract

Acute and chronic renal damage may occur with many analgesics. Acute effects on the kidney occur mainly with aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs). One of the most obvious effects in healthy individuals is fluid retention which is thought to be mediated through inhibition of the renal effects of prostaglandins. Aspirin and NSAIDs also cause a decrease in glomerular filtration rate and renal blood flow and although these changes may occur in healthy individuals they are more pronounced in high renin states and in patients with pre-existing renal disease. Clinical syndromes associated with the renal effects of NSAIDs include oedema, acute renal failure and the nephrotic syndrome. Advanced age, dehydration, concurrent diuretic use and pre-existing renal disease are risk factors for these syndromes. Chronic effects of non-narcotic analgesics on the kidney were suspected before their acute effects became apparent. The key chronic renal lesion in the kidney attributed to prolonged ingestion of non-narcotic analgesics is renal papillary necrosis. The incidence of analgesic-associated renal papillary necrosis in different countries has generally paralleled the national regular use of analgesics. Although phenacetin was widely implicated as the cause of renal papillary necrosis, there is now increasing evidence that aspirin and other NSAIDs may cause renal papillary necrosis in patients who have not taken phenacetin. There is some evidence that this problem is reduced by legislative control of over-the-counter sales. Uroepithelial tumours have also been attributed to chronic abuse of analgesic mixtures. Such tumours are characterised by a reversal of the usual sex ratio, being more common in females.