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)

An animal model is described in which mild transitory renal impairment is induced with glycerol and the nephrotoxic effects of cephalosporin antibiotics and furosemide studied. Cephaloridine and cephalothin were found to produce extensive acute tubular necrosis in rats when given in subnephrotoxic doses in combination with furosemide; this damage occurred at serum antibiotic levels not much higher than those obtained in clinical practice. No significant renal damage was found with cephalexin or Cephapirin given in equivalent dosage. It is suggested that the cephalosporin antibiotics should be used with caution in the presence of even minor transient renal impairment and particularly if furosemide is being given concurrently.
Can Med Assoc J 1972 Sep 09
PMID:Relative nephrotoxicity of cephalosporin antibiotics in an animal model. 507 52

Of 41 cases of acute paracetamol poisoning one died of gastrointestinal haemorrhage and acute massive necrosis of the liver, three became jaundiced, and 13 others had biochemical evidence of hepatocellular damage. Liver damage is a toxic effect which is present in most patients who ingest more than 15 g. of paracetamol. One patient with liver damage survived renal failure due to acute tubular necrosis. It is suggested that the renal lesion was also the result of paracetamol overdosage.Profound hypoglycaemia and metabolic acidosis may also complicate severe poisoning. Plasma levels of para-aminophenol fall rapidly, and procedures currently used to enhance the elimination of the drug cannot be expected to prevent development of hepatic damage.
Br Med J 1970 Sep 05
PMID:Acute paracetamol poisoning. 531 16

a 17-year-old gravida 1, para 0, single white girl who had undergone criminal abortion, presented at the hospital with high fever and red urine. Her vital signs were monitored and laboratory tests were performed. A total abdominal hysterectomy and salpingo-oophorectomy were performed because of gangrenous uterus and ovaries. The patient developed postoperative complications and blood transfusion was performed. The criminal abortion was induced using some type of liquid (eg., Lysol) that was injected into the uterus transvaginally. The use of Lysol, soap and detergents in criminal abortion produces an area of tissue necrosis. The compounds are also absorbed into the bloodstream. The necrotic tissue is susceptible to infection, while the part which is absorbed into the bloodstream is nephrotoxic, hepatotoxic and produces hemolysis. Common complications of septic abortion are pelvic abscesses; metastatic abscesses; tetanus; renal insufficiency; cortical necrosis; and acute tubular necrosis. Coagulation abnormalities, as well as the psychological, economic and legal aspects of septic abortion are also discussed. It is hoped that all physicians would actively support legislation which would liberalize abortion laws.
Conn Med 1970 Sep
PMID:Medical grand rounds at Yale-New Haven Hospital. Septic abortion. 550 61

The mushroom metabolite gamma-L-glutaminyl-3,4-dihydroxybenzene (GDHB) was found to have an LD50 of 100 to 200 mg/kg in neonatal C57Bl/6J mice. Adult mice given 200 mg/kg GDHB showed histopathologic evidence of proximal convoluted tubular injury as early as 2 hours after injection, which progressed by 24 hours to profound acute tubular necrosis. Focal acinar epithelial cell necrosis in the pancreas was also observed. The time course and location of the injury suggested that appearance of the ultimate toxic metabolite could be due to cleavage of GDHB by gamma-glutamyl transpeptidase (GGTP). The reaction in vitro of GDHB with crude porcine GGTP resulted in the release of 4-amino-catechol which air oxidized to 2-hydroxy--4-iminoquinone (HIQ), a known sulfhydryl reagent and cytotoxic compound. Synthesis of N2-methyl-gamma-glutaminyl-3,4-dihydroxybenzene (MeGDHB) provided a compound whose oxidized derivatives, when compared with those of GDHB, had similar half-wave potentials and visible absorption maxima. MeGDHB was resistant to cleavage by GGTP and was without apparent toxicitiy at 2-3 times the LD50 of GDHB. Therefore, cleavage by GGTP, an enzymatic transformation accessible to GDHB but unavailable to MeGDHB, is proposed as the mechanism of activation of the mushroom metabolite. The following pathogenic sequence is indicated: 1) release of 4-aminocatechol from GDHB by the action of GGTP and 2) irreversible injury resulting both from the generation of free radicals by the autoxidation of 4-aminocatechol and from the reaction of HIQ with cellular nucleophils, particularly sulfhydryl groups.
Am J Pathol 1980 Sep
PMID:The role of gamma-glutamyl transpeptidase in the nephrotoxicity of an Agaricus bisporus metabolite. 610 87

Intrarenal pressure was measured in kidney-transplant recipients in an attempt to differentiate between graft rejection and cyclosporin nephrotoxicity. Intrarenal pressure was measured directly through a fine needle inserted into the kidney and connected to a manometer. Blood cyclosporin levels were monitored regularly, and renal biopsy specimens were obtained whenever renal function deteriorated. 32 recipients of renal allografts were studied 1 to 270 days after transplantation. 129 pressure readings were obtained during normal renal function, rejection, nephrotoxicity, and acute tubular necrosis (ATN). Rejection but not toxicity or ATN caused a highly significant rise in intrarenal pressure. No complications were encountered apart from transient haematuria in 1 patient. This simple test may therefore be of value in monitoring renal-transplant patients who are receiving cyclosporin.
Lancet 1983 Sep 24
PMID:Fine-needle intrarenal manometry: a new test for rejection in cyclosporin-treated recipients of kidney transplants. 613 42

The effect of cyclosporine and steroids on early renal allograft function and eventual graft outcome was analyzed in 100 recipients; 33 recipients of living related donor (LRD) and 67 recipients of cadaveric donor (CAD) allografts were studied. A concurrent population of 47 CAD recipients treated with azathioprine and steroids was used for comparison. Recipients received oral cyclosporine (14 mg/kg) 48 hours (LRD) or 6-12 hours (CAD) pretransplant. No cases of acute tubular necrosis (ATN) were observed in the LRD recipients. The incidence of posttransplant ATN was similar in the cyclosporine-treated (41%) and in the azathioprine-treated (45%) CAD recipients (P = ns). Cyclosporine-treated CAD kidneys preserved less than 24 hr experienced a lower rate of ATN (P less than .01) using simple cold storage (31%), as compared with hypothermic pulsatile perfusion (57%). One-month creatinine nadirs were higher in cyclosporine-treated than in azathioprine-treated recipients, using median values for each group. One-year actuarial patient survival for cyclosporine-treated LRD recipients was 97%; CAD recipients, 94%, and azathioprine-treated CAD recipients, 91%. Graft survival rates in the same groups were 91%, 76%, and 55%, respectively. The major causes of graft loss in cyclosporine-treated patients were nonimmunologic. It is concluded that cyclosporine and prednisone are a safe, efficacious combination for LRD and CAD renal transplantation. The possibility of nephrotoxicity leading to impaired graft function in the early posttransplant period should not preclude the administration of cyclosporine prior to alloantigen presentation.
Transplantation 1983 Sep
PMID:The effect of cyclosporine on early graft function in human renal transplantation. 635 68

Plasma oxalate was measured with use of the enzyme oxalate oxidase (EC 1.2.3.4; normal values 3.3 +/- 1.5 mumol/L, n = 24) in 50 patients with different degrees of renal failure. The following mean concentrations +/- SD (in mumol/L) were found: for glomerular diseases, 12.7 +/- 7.8 (n = 21); tubular diseases, 20.4 +/- 14.0 (n = 16); chronic renal failure before dialysis, 32.5 +/- 13.5, and after dialysis, 17.8 +/- 3.8 (n = 10); and primary hyperoxalemia, 72.2 +/- 14.5 14.5 (n = 2). The course of plasma oxalate was followed in one of these two patients after renal transplantation and in a patient recovering from acute tubular necrosis. No significant differences were found between patients with glomerular and tubular disorders. Overall, plasma oxalate was correlated with plasma creatinine in patients with glomerular and tubular diseases and dialysis patients (r = .84, P less than .001). Patients with primary hyperoxalemia had values outside the 95% confidence area of the regression line. It is concluded that the values obtained with this method, although probably still tending to overestimate the true oxalate concentration to some extent, provide reliable information about relative differences in plasma oxalate levels. In patients with terminal renal failure, plasma oxalate sometimes rises to levels at which deposition of calcium oxalate in tissues can occur.
Am J Kidney Dis 1984 Sep
PMID:Plasma oxalate concentration in chronic renal disease. 638 28

Status epilepticus is a medical emergency. Recent experimental studies have shown that permanent brain damage can occur after only 60 minutes of uncontrolled seizure activity. Cardiac arrhythmias are a common cause of death. Other complications include rhabdomyolysis, acute tubular necrosis and neurogenic pulmonary edema. Management is divided into three phases: stabilization of the patient, termination of the seizures and diagnostic evaluation.
Am Fam Physician 1983 Sep
PMID:Status epilepticus. 661 91

Myoglobinuria, which occurs more frequently than previously believed, may lead to acute tubular necrosis and renal failure. It may be recurrent and can result in permanent renal damage. Three cases of myoglobinuria with acute renal failure and abnormal sonograms are reported.
J Ultrasound Med 1983 Sep
PMID:Sonographic findings in myoglobinuric renal failure and their clinical implications. 663 65

2'-Deoxycoformycin (2'-dCF), a tight-binding inhibitor of adenosine deaminase, was administered to 26 pediatric patients with acute lymphoblastic leukemia in a Phase I study. Doses ranged from 0.25 to 1.0 mg/kg given i.v. for 3 consecutive days. Common toxicity included nausea, vomiting, diarrhea, hepatocellular enzyme elevations, and conjunctivitis. Lymphopenia occurred in all patients. The most serious adverse effects were acute tubular necrosis and central nervous system toxicity, which appeared to be dose related. In addition, two patients given the 0.75-mg/kg dose developed severe hepatic toxicity, although this could not be ascribed definitively to 2'-dCF. Antitumor activity was observed in eight patients, two of whom experienced a complete remission. Inhibition of lymphoblast adenosine deaminase activity was noted in the majority of cases and was observed at all doses. Antileukemic activity occurred at doses of 2'-dCF which were not associated with limiting toxicities. These results suggest that 2'-dCF is active against acute lymphoblastic leukemia and that a starting dose of 0.5 mg/kg/day be utilized in Phase II studies.
Cancer Res 1981 Sep
PMID:Phase I study of 2'-deoxycoformycin in acute lymphoblastic leukemia. 697 90


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