Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dose-response and sequential studies of 2-bromoethylamine hydrobromide (BEA) nephrotoxicosis were carried out using Swiss ICR mice. For the dose-response study, 150 male mice, 30 per group, were injected intraperitoneally (ip) with 100, 200, 300, 400 or 500 mg BEA/kg and ten from each group were killed 1, 3 or 5 days after treatment. For the sequential study, 80 male mice were injected ip with 300 mg BEA/kg and ten were killed at 0.5, 1, 2, 3, 6, 12 or 18 hr, or 10 days after treatment. Control mice (10-15) in both studies were given 0.15 ml of 0.9% NaCl solution injected ip and were killed after 1, 3 or 5 days in the former study and after 18 hr of 10 days in the latter study. Mortality and the extent of the renal lesions were dose dependent. The percentage of mice with tubular necrosis varied from 0 in mice given 100 mg BEA/kg to 100 in mice given 400 mg BEA/kg. The percentage of mice with renal papillary necrosis was also dose dependent and varied from 0 in the 100 mg/kg group to 72 in the 400 mg/kg group. Degeneration of proximal tubules was detected 2 hr after treatment. Three hours after treatment, grossly, the renal cortex was diffusely pale and, microscopically, there was marked acute tubular necrosis. Epithelial cells lining the cortical tubules were regenerating 3 days after treatment. By 10 days after treatment cortical interstitial fibrosis was marked with many tubules lined by regenerating epithelium and many tubules were dilated. BEA-induced nephrotoxicosis in the mouse was primarily an acute cortical tubular necrosis.
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PMID:Acute cortical tubular necrosis in the Swiss ICR mouse induced by 2-bromoethylamine hydrobromide. 237 94

Non-narcotic analgesics have acute and chronic effects on the kidney. Until quite recently chronic effects have received much more attention than acute effects. Renal papillary necrosis attributed to prolonged intake of analgesic compounds was first described from Switzerland in the 1950s, and subsequently in many countries including Scandinavia, Australia, Belgium and Canada. Renal papillary necrosis is now accepted as an effect of over-the-counter analgesic compounds and has also been recorded with many individual non-steroidal anti-inflammatory drugs (NSAIDs). Evidence suggests that uroepithelial tumours also occur as a complication of prolonged abuse of analgesic compounds. Clinical evidence associating renal papillary necrosis with compound analgesics and NSAIDs has been backed up by experimental evidence showing that these drugs cause renal papillary necrosis in animals. Acute effects of non-narcotic analgesics have been described mainly in association with aspirin and NSAIDs. In high renin states, including salt-depleted normal subjects, NSAID administration may be associated with an acute decrease in renal function, which is more obvious in patients who have underlying renal disease. Clinical syndromes which occur in association with NSAIDs include oedema, hyperkalaemia and acute renal failure and the acute nephrotic syndrome. Acute renal failure may be associated with acute interstitial nephritis and the nephrotic syndrome or may be due to acute tubular necrosis. Patients who have the nephrotic syndrome show fusion of foot processes of glomerular epithelial cells on electron microscopy as well as acute interstitial nephritis. Patients who suffer these episodes of acute renal function deterioration associated with NSAIDs recover slowly after withdrawal of the drugs, and the recovery may not be complete.
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PMID:Effects of non-narcotic analgesics on the kidney. 355 79

Most antipyretic analgesics can cause acute nephrotoxic effects, including acute tubular necrosis, acute interstitial nephritis, glomerular toxicity, and functional changes, such as "salicyl edema," following large doses of sodium salicylate. Most functional changes are related to acute suppression of prostaglandin synthesis, "the acute prostaglandin-effect," and have been primarily noted with the use of indomethacin. The association between prolonged and excessive consumption of compound analgesics and the development of renal disease and renal failure, characterized by renal papillary necrosis, is now well established. Studies in several countries have shown that the incidence of analgesic nephropathy as an indication for dialysis and transplantation corresponds to the per capita consumption of phenacetin in compound analgesics. Analgesic nephropathy, which is part of a wider clinical syndrome, the analgesic syndrome, is uncommon following the use of single analgesics. Analgesic nephropathy and the analgesic syndrome are discussed in detail, including the development of uroepithelial tumors.
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PMID:Renal effects of antipyretic analgesics. 635 70

There are conflicting reports on the ability of aspirin as a single agent to cause acute or chronic renal failure in experimental animals. Chronic administration of aspirin alone over 18 to 68 weeks in doses of 120 to 500 mg/kg/d has been reported to cause renal papillary necrosis in rats. However, some investigators have been unable to produce renal papillary necrosis in other species or in rats given lower divided doses comparable to therapeutic doses used in humans. In a variety of rat strains, aspirin administered as a single high dose intravenously or by oral gavage produces acute tubular necrosis of proximal tubules, rarely accompanied by renal papillary necrosis in susceptible strains. Several human studies have addressed the chronic nephrotoxicity of aspirin alone or relative risk of end-stage renal disease in association with aspirin use after correction for other analgesics. With the exception of one case control study demonstrating a low, but statistically significant risk of end-stage renal disease in association with aspirin use, all other case control studies and several prospective studies have been unable to identify a significant risk of chronic renal failure in patients using aspirin alone in therapeutic doses. In healthy adults, short-term aspirin administration in therapeutic doses has no effect on creatinine clearance, urine volume, osmolar clearance, or sodium and potassium excretion. However, in predisposed individuals with glomerulonephritis, cirrhosis, and chronic renal insufficiency, and in children with congestive heart failure, short-term aspirin use in therapeutic doses may precipitate reversible acute renal failure. Acute aspirin intoxication (>300 mg/kg) frequently causes acute renal failure and doses of 500 mg/kg may be lethal. Chronic salicylate intoxication has been reported to cause reversible or irreversible acute renal failure in association with a pseudosepsis syndrome.
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PMID:Does aspirin cause acute or chronic renal failure in experimental animals and in humans? 866 25

A 17-year-old healthy girl was admitted to our hospital with diffuse abdominal pain and decreased oral intake of about 11 days duration. About a week prior to admission, she had taken naproxen, 250 mg four times a day for 4 days. Physical examination was normal except for diffuse abdominal tenderness on deep palpation. Investigations revealed high serum BUN (42 mg/dl) and creatinine (4.0 mg/dl). Serum electrolytes and complement (C3, C4) levels and urinalysis were normal. Antinuclear-antibody and anti-dsDNA were negative. Kidney biopsy revealed renal papillary necrosis, acute tubular necrosis, and focal interstitial nephritis. A diagnosis of nonoliguric acute renal failure due to naproxen nephrotoxicity was made. She received intravenous hydration, and oral steroids, which was gradually discontinued in 3 months. A follow-up at 4 months revealed normal renal function with a serum creatinine of 1.1 mg/dl, BUN 7 mg/dl, and normal urinalysis. The report highlights a need for caution while using naproxen or any other nonsteroidal anti-inflammatory drugs, even for a short duration.
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PMID:Renal papillary necrosis induced by naproxen. 1277 22

NSAIDs are commonly used drugs. Even with the advent of selective COX-2 inhibitors, nephrotoxicity still remains a concern. The adverse effects of NSAIDs are mediated via inhibition of prostaglandin synthesis from arachidonic acid by non-specific blocking of the enzyme cyclooxygenase leading to vasoconstriction and reversible mild renal impairment in volume contracted states. When unopposed, this may lead to acute tubular necrosis and acute renal failure. NSAIDs also produce interstitial nephritis with or without nephrotic syndrome secondary to minimal change disease. Although this presents as acute renal failure, it can progress in some cases to chronic renal failure. Papillary necrosis has been incriminated in the development of chronic renal failure secondary to NSAIDs. In patients on long term NSAIDs without acute or chronic renal failure, subclinical renal dysfunction such as reduced creatinine clearance and impaired urine concentrating ability has been shown to be present. Although this sub-clinical dysfunction is reversible on withdrawal of NSAIDs, some reports have suggested a persistent residual dysfunction. Even with a wide range of NSAIDs at our disposal, a renal safe NSAID is yet to be discovered.
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PMID:NSAIDs and kidney. 1584 59

Diseases of the kidney often have their names shortened, creating an arcane set of acronyms which can be confusing to both radiologists and clinicians. This review of renal pathology aims to explain some of the most commonly used acronyms within the field. For each entity, a summary of the clinical features, pathophysiology, and radiological findings is included to aid in the understanding and differentiation of these entities. Discussed topics include acute cortical necrosis, autosomal dominant polycystic kidney disease, angiomyolipoma, autosomal recessive polycystic kidney disease, acute tubular necrosis, localized cystic renal disease, multicystic dysplastic kidney, multilocular cystic nephroma, multilocular cystic renal cell carcinoma, medullary sponge kidney, paroxysmal nocturnal hemoglobinuria, renal papillary necrosis, transitional cell carcinoma, and xanthogranulomatous pyelonephritis.
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PMID:Sorting the Alphabet Soup of Renal Pathology: A Review. 2692 91