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Clinical Medicine Insights: Urology

Analgesic Nephropathy—A Painful Progression

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Clinical Medicine Insights: Urology 2016:9 7-10

Review

Published on 05 Oct 2016

DOI: 10.4137/CMU.S13179


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Abstract

One of the dreaded complications of long term analgesic intake is nephrotoxicity characterized by chronic interstitial nephritis and papillary necrosis. Much of the literature of its epidemiology dates back to 1960s and its impact on present day society is not well documented. Non steroidal anti inflammatory agents reduce pain by blocking prostaglandin generation. Prostaglandins have renal vaso dilatory effects in states of volume depletion to counteract the vasoconstrictive pressor hormones. Earlier analgesic tablets contained a mixture of aspirin, phenacetin and caffeine. Phenacetin and its metabolites have nephrotoxic potential and incidence of analgesic nephropathy was brought down in countries where it was banned. The concentration of phenacetin and its metabolite acetaminophen is increased at the tip of renal papilla due to counter current concentrating mechanism of the loop of henle. These are potent oxidants leading to cell injury due to lipid peroxidation, though their effects are normally counterbalanced by anti oxidant glutathione. Glutathione deficiency at the medulla can be precipitated by co ingestion of aspirin. The exact dose of analgesics which needs to be ingested is unclear but a daily ingestion of 5–8 tablets over 5 years results in clinical nephrotoxicity. The histopathology is one of chronic interstitial nephritis with renal fibrosis. Clinically the patient presents with polyuria, asthenia and anemia. The diagnosis is suspected in a patient with progressive chronic kidney disease without proteinuria. CT imaging of the kidneys show irregular scarred kidneys with papillary calcification and necrosis. Recently, COX-2 inhibitors are promoted as renal safe drugs, but may not be so given the multiple case reports of renal toxicity in post marketing surveys. The treatment of analgesic nephropathy includes discontinuation of offending drug, protein restricted diet, control of blood pressure and statins. In conclusion analgesic nephropathy is a preventable cause of chronic kidney disease and both the patients and treating physicians should be mindful of the potential nephrotoxcity of nonsteroidal anti inflammatory agents when administered for prolonged periods without monitoring renal function.



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