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)

During a one-year period analgesic and non-steroidal anti-inflammatory drug-(NSAID) associated acute renal failure (ARF) was recorded in 147 of 398 patients registered in 58 nephrology units. This figure represented 36.9% of drug-associated ARF, and 6.8% of total patients with ARF hospitalized during the same period. Drugs involved were primarily glafenin (79), NSAID (62), paracetamol (5) and phenacetin (1 case). Hypersensitivity reactions were documented in 32 patients. Acute tubular necrosis was found in 20, and interstitial nephritis (AIN) in 9 of 34 biopsied patients. All patients in the glafenin group and 71.4% in the NSAID group recovered fully or regained previous renal function (p less than 0.01). Permanent renal damage (9.5% of total cases) was more frequent in patients with AIN than in those with other types of ARF (p less than 0.001). Preventive measures should be especially directed to older patients receiving NSAID, by avoiding the combined use of drugs potentiating their action and by correcting any predisposing factor to ARF.
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PMID:Analgesic and non-steroidal anti-inflammatory drug-associated acute renal failure: a prospective collaborative study. 287 10

During a one-year period, drug-associated acute renal failure (ARF) was prospectively recorded in 398 patients, registered in 58 french nephrology Units. Drugs involved were primarily antibiotics, mainly aminoglycosides, glafenine, non-steroidal antiinflammatory drugs and contrast media. Hypersensitivity reactions were reported in 69 patients. Renal biopsy, performed in 81 instances, showed acute tubular necrosis in 42 and acute interstitial nephritis in 20 patients. Hypotension, sodium depletion and/or cardiac failure were predisposing factors in 198 cases. Fifty patients died, 251 recovered fully or regained previous renal function, and in 93 permanent renal damage remained. Advanced age, oliguria, severe ARF, and preexisting cardiac, hepatic or renal insufficiency were poor prognostic factors. Prevention of drug-associated ARF should be directed to high-risk patients, particularly those receiving aminoglycosides and contrast media.
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PMID:[Acute renal failure associated with drugs or iodinated contrast media. Results of a cooperative multicentric study by the Nephrology Society]. 287 11

A sandwich ELISA assay has been formatted from two commercially available murine monoclonal antibodies, URO-4 and URO-4a, directed against a 120,000 dalton glycoprotein, the adenosine deaminase binding protein (ABP), found on the brush border of the renal proximal tubular epithelial cell. Untimed urine samples from 37 normal individuals and urinary ABP less than 0.1 AU; 37 patients with pure glomerular disease had ABP less than 0.4 AU (with 29, or 76% less than 0.2 AU); 10 patients with pre-renal azotaemia had ABP less than 0.6 (with 8, or 80% less than 0.3 AU). In contrast, 79 patients with post-ischaemic acute tubular necrosis had ABP greater than 0.6 AU. Acute renal failure due to myoglobinuria, contrast dye, and aminoglycoside toxicity were all associated with urinary ABP greater than 1.0 AU. In addition, all six patients with acute bacteraemic pyelonephritis had ABP greater than 0.7 AU, as opposed to ABP less than 0.2 AU in the urines of 12 women with acute cystitis. We conclude that this monoclonal antibody based urinary assay is a sensitive measure of renal proximal tubular injury, reliably distinguishes acute tubular from glomerular disease, and may be helpful in differentiating forms of urinary tract infection.
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PMID:Diagnosis of renal proximal tubular injury by urinary immunoassay for a proximal tubular antigen, the adenosine deaminase binding protein. 288 57

Traditional methods of noninvasively evaluating patients for renal injury do not accomplish the following tasks: reliably distinguish potentially treatable forms of acute renal failure from acute tubular necrosis; provide a sensitive indicator of early allograft rejection in renal transplant recipients, particularly those in the pediatric age group; provide an early warning of incipient drug-induced nephrotoxicity; or serve as an adequate screening test for renal injury due to exposure to occupational or environmental toxins, especially heavy metals. Because of this, considerable effort has been devoted to the development of assays to satisfy these needs. Three approaches include measurement in the urine of low-molecular-weight plasma proteins such as beta 2-microglobulin; a variety of kidney-derived enzymes, such as L-alanine aminopeptidase and N-acetyl-beta-D-glucosaminidase; and specific renal antigens using immunologic detection. The first two of these have not proved to be adequately sensitive or specific, complicated by the frequent loss of activity associated with the physicochemical characteristics of the urine or the presence of pyuria. Despite this, useful information has been obtained. In particular, assays of beta 2-microglobulin urinary excretion and retinol binding protein appear to have clinical utility that should be pursued. Recent experience with a monoclonal antibody-based assay for a unique proximal tubular antigen, the adenosine deaminase binding protein, suggests that a battery of such assays, each directed against an antigen localized to a particular segment of the nephron, may be particularly useful.
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PMID:Noninvasive renal diagnostic studies. 290 37

We have described four male patients, aged 21 to 39 years, who had rhabdomyolysis and acute renal failure during parenteral cocaine use. This complication has only recently been attributed to cocaine. Their illnesses behaved clinically like nonoliguric acute tubular necrosis, though renal biopsies were not done. No permanent nerve, muscle, or kidney damage resulted.
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PMID:Cocaine-associated rhabdomyolysis and acute renal failure. 277 92

Multiple factors still influence the high rate of mortality in acute tubular necrosis. Trying to analyze the influence of each risk factor present in an individual patient and the possible interdependence between these factors, as well as to obtain an early prognosis, we have applied a forward analysis to demographic data, acute renal failure origin, need of dialysis, diuresis and clinical conditions in 228 patients, using a multiple linear regression model contained in a computer package. Based on this approach we have found that three variables: deep neurological coma, persistent blood hypotension and assisted respiration have significant influence on mortality. Also, a regression equation was obtained which could be applied as a discriminant score to patient prognosis. This score, calculated with the three aforementioned variables and oliguria when the nephrologist sees the patient for the first time, allows an easy and early prognosis in each patient with acute tubular necrosis.
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PMID:Easy and early prognosis in acute tubular necrosis: a forward analysis of 228 cases. 291 41

Any patient who demonstrates a decrease in urinary output, compromise in hemodynamic parameters, or exposure to nephrotoxic agents will be thoroughly assessed by the critical care nurse for signs or symptoms of acute tubular necrosis (ATN). Prompt recognition of the patient who is at risk, and early nursing interventions, can prevent or improve the course of ATN, the most common form of acute renal failure (ARF).
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PMID:Acute tubular necrosis: preventing complications. 292 Jun 55

Three categories of acute renal failure have been identified: prerenal, postrenal, and renal. Prerenal failure results from decreased perfusion of the kidney and postrenal failure from obstruction distal to the nephron; renal failure, in the surgical setting, usually represents acute tubular necrosis. A rational approach to the diagnosis of acute renal failure is outlined, and the treatment of acute tubular necrosis is discussed. High-risk factors are identified, and the importance of maintaining intravascular volume to prevent acute renal failure is stressed, since the mortality rate may approach 50% in patients in whom this perioperative complication develops.
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PMID:Acute renal failure in the surgical patient: initial diagnosis and treatment. 294 85

We compared early (less than 70 days) cumulative survival, cause of death, and morbidity (defined as the number of organ system failures and reoperations) of 236 patients who needed dialysis for acute tubular necrosis (ATN) after transplantation with that of a control group of 215 transplant patients who had immediate renal function after transplantation. The patients were matched for age, number of transplants, time of transplantation, diabetic status, living-related vs cadaveric donor, and number of HLA matches. There were no differences in cumulative survival after transplantation, causes of death, organ system failure, or surgical complications as evident from the number of reoperations. The ATN patients' overall clinical course was similar to that described for other postsurgical patients with ATN in their native kidneys. We conclude that the poor survival and the surgical complications in patients with postoperative ATN are due to the basic disease and not to acute renal failure or to dialysis. To improve survival, research should be focused on the basic disease and the surgical procedures rather than on dialysis technique.
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PMID:Why do patients with postsurgical acute tubular necrosis die? 299 Mar 83

A 35-yr-old patient developed severe acute tubular necrosis requiring hemodialysis. A [99mTc]dimercaptosuccinic acid scan of the kidneys showed no renal uptake at 4 or 24 hr, but the patient subsequently recovered normal renal function as judged by a normal serum creatinine. Based on this case report and a review of the literature, one cannot assume irreversible loss of function in patients with acute renal failure, based on the absence of radiopharmaceutical uptake by the kidneys.
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PMID:Failure to visualize acutely injured kidneys with technetium-99m DMSA does not preclude recoverable function. 301 25


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