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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Accepted causes (acute insults) and risk factors for the development of acute renal failure were defined, quantitatively assessed, and tested for statistical significance in 143 patients with acute tubular necrosis. Sixty-two percent of patients had more than one acute insult, and 48 percent had more than one suspected risk factor. Hypotension, excessive aminoglycoside exposure, pigmenturia, and dehydration were identified as highly significant acute insults, while it was concluded that sepsis and administration of radiocontrast material could not be incriminated as causes of acute tubular necrosis. An additive interaction between acute insults was demonstrated, and the severity of acute renal failure was related to the number and severity of acute insults. Patients with oliguric renal failure had more severe acute insults than patients with nonoliguric renal failure. Preexisting renal disease and chronic hypertension were significant risk factors, the latter only when hypotension had been one of the acute insults. An age of more than 59 years, gout and/or chronic hyperuricemia, diabetes, and long-term diuretic administration were not found to be significant risk factors.
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PMID:Acute renal failure. Multivariate analysis of causes and risk factors. 711 78

During the past decade the formation of neutrophil extracellular traps (NETs) has been recognized as a unique modality of pathogen fixation (sticky extracellular chromatin) and pathogen killing (cytotoxic histones and proteases) during host defense, as well as collateral tissue damage. Numerous other triggers induce NET formation in multiple forms of sterile inflammation, including thrombosis, gout, obstruction of draining ducts, and trauma. Whether neutrophils always die along with NET release, and if they do die, how, remains under study and is most likely context dependent. In certain settings, neutrophils release NETs while undergoing regulated necrosis-for example, necroptosis. NETs and extracellular traps (ETs) released by macrophages also have been well documented in kidney diseases-for example, in various forms of acute kidney injury. Histones released from ETs and other sources are cytotoxic and elicit inflammation, contributing to necroinflammation of the early-injury phase of acute tubular necrosis in antineutrophil cytoplasmic antibody-related renal vasculitis, anti-glomerular basement membrane disease, lupus nephritis, and thrombotic microangiopathies. Finally, acute kidney injury-related releases of dying renal cells or ETs promote remote organ injuries-for example, acute respiratory distress syndrome. In this review, we summarize what is known about the release of ETs from neutrophils and macrophages in the kidney, the available experimental evidence, and ongoing discussions in the field.
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PMID:Extracellular traps in kidney disease. 3046 65