[Clinicopathological studies of renal cortical necrosis--with special reference to its pathogenesis].
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Experiments were donducted on rats to determine the lowest dose of either phenylbutazone or indomethacin capable of producing papillary necrosis and in each case it was found to be 50 mg/kg body weight. A single dose of oxyphenbutazone (444 mg/kg), a major metabolite of phenylbutazone in man, produced patchy cortical necrosis, which became more extensive during daily administration for 4 days, despite evidence of regeneration. Although papillary necrosis as such was never seen with this substance, there was evidence of damage to the lower nephron in the form of tubular necrosis and calcification.
Three cases of acute bilateral renal cortical necrosis, each with a different clinical course, are discussed. One patient spontaneously recovered renal function after prolonged oliguria. This case should be added to the small number of similar case reports in the literature. The second patient recovered adequate renal function temporarily, but eventually required chronic hemodialysis and renal transplantation. There was pathological evidence of progression from focal to massive cortical necrosis. The third patient never regained renal function, but is well after dialysis and transplantation. The influence of modern theories of pathogenesis of the disease, and increased availability of dialysis, are discussed in relation to the initial prognostic assessment of the patient with cortical necrosis.
Explore the source record for details and available documents.
Explore the source record for details and available documents.