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analgesic/necrosis

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The induction of renal papillary necrosis in Gunn rats by analgesics and analgesic mixtures.

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Homozygous members of the mutant Gunn strain of Wistar rats genetically lack the enzyme uridine diphosphate glucuronyl transferase. "High" and "low" dose gavage feeding for 18-34 days of an analgesic mixture containing aspirin, phenacetin and caffeine (APC) confirmed the previously reported

Papillary necrosis in experimental analgesic nephropathy.

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A proprietary aspirin, phenacetin, and caffeine preparation given to rats in a dose equivalent to that taken by patients with analgesic nephropathy produced papillary necrosis in 55%. There was a higher incidence in rats deprived of fluids overnight.Papillary necrosis was not noted in rats receiving

Analgesic renal papillary necrosis.

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Analgesic nephropathy is well recognised. This is a retrospective review of 19 patients with the disease, who presented at Groote Schuur Hospital over a 4-year period. The diagnosis was made on historical and clinical grounds and on the radiological manifestations of papillary necrosis. The mean age

Pathophysiologic mechanisms in analgesic-induced papillary necrosis.

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The nonnarcotic analgesics have been implicated as a significant cause of chronic renal failure worldwide. Epidemiologic studies of habitual abuse and necropsy studies show a strong relationship between the two. Animal studies designed to elucidate underlying mechanisms have been hampered because
The risk of renal papillary necrosis and renal dysfunction due to the chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) is unknown. In a prospective study of 259 heavy analgesic users seen in a general medical hospital over an 11-year-period beginning in January 1982, 69 new cases of

Cause of analgesic-induced renal papillary necrosis.

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It is proposed that analgesic-induced papillary necrosis is due to a progressive narrowing of small blood-vessels of the renal papilla and renal pelvis.

Analgesic-induced renal papillary necrosis in the Gunn rat: the comparative nephrotoxicity of aspirin and phenacetin.

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Homozygous Gunn rats, mutant Wistars genetically lacking glucuronyl transferase, develop renal papillary necrosis after single oral doses of aspirin and of phenacetin. The lesion appears significantly more frequently with aspirin than phenacetin, and at lower doses. The model is a convenient one

Analgesic abuse, renal papillary necrosis and concomitant drug intake.

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In a retrospective survey of 145 patients coming to autopsy at a hospital in Sydney, 31 were found to have some form of renal papillary necrosis (RPN). Sixteen (52%) of those abused analgesic mixtures, there being a marked female preponderance (70%). A further two cases may have been linked with

2,3,6-triaminopyridine, a metabolite of the urinary tract analgesic phenazopyridine, causes muscle necrosis and renal damage in rats.

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Some aromatic polyamines form very stable free radicals and readily undergo autoxidation with concomitant formation of 'active oxygen' species. These substances cause necrosis of striated muscle in rats, and it has been suggested that this is due to free radical formation and disruption of energy
There has been no cogent hypothesis to explain the molecular basis of analgesic and non-steroidal anti-inflammatory drug (NSAID) associated renal papillary necrosis (RPN) and upper urothelial carcinoma (UUC). The microsomal cytochrome P-450 enzyme system may generate reactive intermediates which
BACKGROUND We examined the changes in cerebrospinal fluid (CSF) concentrations of prostaglandin E2 (PGE2) and tumor necrosis factor-alpha (TNF-alpha) after intraplantar administration of complete Freund's adjuvant (CFA) in rats. In addition, we investigated whether different analgesic drugs orally
OBJECTIVE There is a disparity in the animal models used to study pain in rheumatoid arthritis (RA), which tends to be acute in nature, and models used to assess the pathogenesis of RA. The latter models, like human RA, are lymphocyte-driven and polyarthritic. We assessed pain behavior and

[Nephropathy caused by analgesics. papillary necrosis and chronic interstitial nephritis due to abuse of analgesics containing phenacetin].

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Necrosis in situ: a form of renal papillary necrosis seen in analgesic nephropathy.

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