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)

67Ga scintigraphy was performed in 44 patients with various biopsy proven forms of renal disease and in a further 64 patients, some with clinically diagnosed renal disease and some with non-renal disorders. Renal uptake of gallium at 48 hours was graded by two blinded observers and by tissue ratios determined by computer. All 11 patients with biopsy proven acute drug-induced interstitial nephritis demonstrated intense, diffuse, bilateral renal 67Ga uptake, a phenomenon observed in only five of the other 30 patients with biopsy proven renal disease and in four of the 64 patients with clinical diagnoses only. No patient with acute tubular necrosis demonstrated significant renal gallium uptake. It is suggested that 67Ga scintigraphy is an excellent screening test for the presence of acute interstitial nephritis and helps to identify which patients with unexplained acute renal failure require renal biopsy.
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PMID:Gallium67 scintigraphy in the diagnosis of acute renal disease. 386 87

The nephrotoxic potential of N-(3,5-dichlorophenyl)succinimide (NDPS) was examined, in male Fischer-344 rats. Rats were administered NDPS (0.1, 0.2, 0.4 or 1.0 mmol/kg intraperitoneally (i.p.) or sesame oil (2.5 ml/kg, i.p.), and renal function was monitored at 24 and 48 h. NDPS (0.1 mmol/kg) stimulated organic ion uptake at 48 h. NDPS (0.2 mmol/kg) produced diuresis but did not alter blood urea nitrogen (BUN), kidney weight or organic ion uptake by renal cortical slices at 48 h. High-dose NDPS (0.4 and 1.0 mmol/kg) administration produced diuresis, decreased accumulation of p-aminohippurate (PAH) and tetraethylammonium (TEA), increased BUN and kidney weight and caused acute tubular necrosis. At 24 h, NDPS (0.2 mmol/kg) decreased uptake of PAH and TEA and tended to increase BUN. These results are similar to previous reports of NDPS-induced nephrotoxicity in Sprague-Dawley rats and suggest that either rat model would be suitable for future studies on the mechanism(s) of NDPS-induced nephropathy.
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PMID:N-(3,5-Dichlorophenyl)succinimide nephrotoxicity in the Fischer-344 rat. 397 35

The biochemistry laboratory records of a 400-bed general hospital serving a population of about 120,000 showed that during the three-year period 1966-8 inclusive 487 patients had at some stage during their admission a blood urea of 100 mg/100 ml or more. Ninety per cent. were aged 50 or over, 79% were 60 or over, and 52% were 70 or over.The case notes of all patients with renal failure admitted during 1966 and 1967 were examined together with those of patients under 60 admitted during 1968. Three observers agreed about the most likely cause of the renal failure in 90% of patients whose case notes were available, or 74% of the total. The raised blood urea was thought to be due to "prerenal" factors in 60% of the patients, to acute tubular necrosis in 80%, to obstructive uropathy in 12%, and to "intrinsic" renal disease in 20%. Renal failure precipitated by such factors as cardiac failure, chest infections, cerebrovascular accidents, and shock was particularly common in old people.The hospital survey and replies to a questionnaire sent to all general practitioners in the area suggest that in the three-year period 14 patients may have been suitable for treatment by maintenance haemodialysis or renal transplantation. This represents a rate of about 39 per million per year under the age of 60 and 28 per million per year under 50.
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PMID:Incidence of uraemia and requirements for maintenance haemodialysis. 521 79

A hippuran renogram pattern of the type usually interpreted as indicating urinary tract obstruction was seen in acute tubular necrosis and was present both in the oliguric and in the diuretic phase. It seems that in acute renal failure the renogram does not distinguish urinary tract obstruction from intrinsic renal disease.
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PMID:131-I hippuran renogram in acute renal failure. 556 19

Living cells from the urinary tract can be examined by phase-contrast microscopy in a pellet obtained by centrifugation of 10 ml of freshly voided urine. Once these cells have been identified and classified according to their sources, their respective proportions can be evaluated, thus providing some information on the renal structures affected. Urine sediment examination was performed in 60 cases of acute renal failure in order to determine the relationship between the abnormalities encountered and the clinical or histological diagnosis. An abnormal sediment was always associated with parenchymal acute renal failure. Cellular debris and casts were abundant in acute tubular necrosis and less numerous in toxic acute renal failure than in failure resulting from shock. The finding of deformed erythrocytes was strongly suggestive of glomerular nephropathy, a diagnosis which was confirmed by renal biopsy in almost every case.
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PMID:[Urinary sediment in acute renal insufficiency. Diagnostic and prognostic value of phase-contrast microscopic examination]. 623 86

The diagnostic value of renal scintiscans in patients with acute or chronic renal failure has not been emphasized other than for the estimation of renal size. 131I OIH, 67gallium, 99mTcDTPA, glucoheptonate and DMSA all may be valuable in a variety of specific settings. Acute renal failure due to acute tubular necrosis, hepatorenal syndrome, acute interstitial nephritis, cortical necrosis, renal artery embolism, or acute pyelonephritis may be recognized. Data useful in the diagnosis and management of the patient with obstructive or reflux nephropathy may be obtained. Radionuclide studies in patients with chronic renal failure may help make apparent such causes as renal artery stenosis, chronic pyelonephritis or lymphomatous kidney infiltration. Future correlation of scanning results with renal pathology promises to further expand nuclear medicine's utility in the noninvasive diagnosis of renal disease.
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PMID:Nuclear medicine in acute and chronic renal failure. 628 57

The retrospective review of 115 case-histories of patients with acute renal failure (ARF) seen over the last two years showed that etiologies were distributed as follows: acute tubular necrosis in 65% of cases, urinary tract obstruction in 16%, acute glomerulonephritis in 3,5%, acute interstitial nephritis (AIN) in 8% and acute microvascular nephropathy in 3,5%. The diagnostic value of renal biopsy in ARF is discussed. In spite of recent advances in the treatment of ARF, the mortality rate remains as high as 48%. This is mainly due to current etiologic circumstances, to the age of the patients and to the complications of ARF, with infectious complications being the most serious. Urea nitrogen accumulation is not a poor prognosis factor. Furosemide in high doses does not alter the prognosis but reduces the total number of dialysis indications (81% in 1970, 60% in 1980), the number of dialysis sessions per patient (1 only in 62% of patients), and the duration of the ARF episode (mean duration: 10,7 days).
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PMID:[Current aspects of acute renal failure]. 629 41

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

Patients with renal disease are at risk of further deterioration of renal function and acute tubular necrosis when subjected to anaesthesia and surgery. Optimal fluid loading and careful selection of anaesthetic techniques and agents, appropriate monitoring and the use of mannitol and dopamine assist in the maintenance of renal blood flow and help preserve renal function in these patients. In association with renal failure, physiological changes in other systems result in reduced oxygen supply to the tissues, metabolic disturbances, impairment of the coagulation and immune defence mechanisms and an increased risk of cardiac and cerebrovascular catastrophe. Although many anaesthetic techniques including regional analgesia may be used successfully in these patients caution with most drugs, especially pethidine, phenoperidine, suxamethonium and all non-depolarising neuromuscular relaxants is recommended. Of the volatile anaesthetics currently available, halothane is the agent of choice. Oxygen therapy and close monitoring of cardiorespiratory function are necessary postoperatively.
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PMID:Anaesthesia for the patient with impaired renal function. 635 49

Renal insufficiency occurs in some, but not all, patients with multiple myeloma and Bence Jones proteinuria. Many of these patients are found to have a distinctive renal lesion characterized by distal nephron cast formation. It has been proposed that the specific Bence Jones protein (BJP) which is produced by a myeloma tumor may play an important role in the genesis of this cast nephropathy and that patients excreting BJPs with the highest isoelectric points (pI) are those most likely to develop this cast nephropathy. We have utilized a rat model of multiple myeloma to further evaluate the relationship between Bence Jones proteinuria and the development of myeloma cast nephropathy. This model employed immunoglobulin-secreting tumors obtained from a unique strain of rats in which they spontaneously develop. These tumors were transplanted to a homologous strain of rats and the effect on renal function and morphology in these rats were evaluated. Four different kappa light chain synthesizing tumors were studied. Following transplantation of the tumors, all rats were maintained on a diet designed to produce an acid urine (pH 5.5 to 6.0) and maximal urinary concentration (2000 to 3000 mOsm/kg). Among the rats excreting BJP of pI 6.7, 17 of 18 had virtually normal renal histology. Of the 15 rats with BJP of pI 7.6, 11 also had normal renal histology. However, 12 of 12 rats excreting BJP of pI 5.2 developed a distal nephron, light chain containing cast nephropathy. In the pI 4.3 group, 6 of 12 rats developed acute tubular necrosis, and the remaining six animals sustained a less severe lesion which was characterized by the presence of bland hyaline casts. The mean serum creatinine level obtained at the time of sacrifice was elevated (compared to that found in sham-operated controls) in the pI 5.2 group (P less than 0.001) and the pI 4.3 group (P less than 0.01) but not in the pI 6.7 or 7.6 groups. These results do not support the concept that cationic BJP's are more nephrotoxic than those that carry a more negative charge and indicate that other factors must determine the nephrotoxicity of a given BJP.
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PMID:Myeloma kidney cast nephropathy in a rat model of multiple myeloma. 641 38


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