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)

Acute renal failure due to intravascular hemolysis is a common clinical problem in North Indian patients. It constituted 21.5 percent of 325 patients dialyzed for acute renal failure over an 11-year period at Chandigarh. Thirty patients had developed acute intravascular hemolysis in association with erythrocyte glucose-6 phosphate dehydrogenase (G-6PD) deficiency, 17 due to copper sulphate intoxication and 8 due to envenomation by snakes. Less frequent causes were insect stings, incompatible blood transfusion, intake of anti-leprosy drug--dapsone in non-G-6PD-deficient patients, and mercuric chloride toxicity in two patients each; naphthalene poisoning in one; and uncertain causes in six patients. Renal histology was available in 55 patients. Acute tubular necrosis was seen in 54 and bilateral diffuse cortical necrosis in one patient. Fifty patients (71.43 percent) survived and 20(28.6 percent) diet. G-6PD erythrocyte deficiency, which is present in 4.5 percent of the North Indian population, was the most frequent cause of acute renal failure in this group.
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PMID:Acute renal failure due to intravascular hemolysis in the North Indian patients. 60 54

Eleven out of a series of twenty-nine patients (37-9%) with acute copper sulphate poisoning developed acute renal failure. Intravascular haemolysis appeared to be the chief factor responsible for renal lesions in these patients. Histological lesions observed in the kidney varied from those of mild shock to well established acute tubular necrosis. In one case, granulomatous lesions were seen in response to tubulorrhexis. Renal failure was the chief indication for dialysis in ten patients, whereas one patient was dialysed primarily for removal of copper. Notwithstanding the adequate control of uraemia by dialysis, only six of the eleven patients recovered. Septicaemia was responsible for death in three, hepatic failure in one and methaemoglobinaemia in another. It is postulated that release of copper from haemolysed red cells during acute haemolytic episodes may initiate, or contribute to, the development of renal damage.
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PMID:Acute renal failure following copper sulphate intoxication. 87 9

In chemical skin injuries, reduction of the time of exposure to the causative agent and recognition of systemic toxicity are necessary to lessen the severity of the insult, reduce morbidity, and maximize survival. During a 17-year period (1969 through 1985), 87 (2.1%) of the 4,212 burned patients admitted to the U.S. Army Institute of Surgical Research sustained chemical burns. Twelve of 87 patients died (13.8%). White phosphorous, the most common causative agent, produced cutaneous injury in 49 patients. Acids (13 patients), alkalies (ten patients), and organic solvents (five patients) were the other common causes of injury. Initial treatment consisted of water lavage. Later wound management was carried out with topical antibiotic therapy and excision and grafting as necessary. Systemic toxicity due to phenol, nitrate, and formate absorption occurred, as did acute tubular necrosis following copper sulfate treatment of white phosphorus burns. Inhalation injury occurred in five patients. A decrease in hospital stay for chemically injured patients was observed. To minimize chemical injury, clothing should be removed promptly and water lavage begun. Systemic toxicity and inhalation injury are rare but often severe and increase mortality.
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PMID:Chemical burns. 336 7

Nephrotoxic lesions induced by cisplatin in rats are characterized by acute tubular necrosis in the outer stripe of the medulla. The purpose of this study was to examine the potential role of changes in metal binding proteins, and iron and copper content in urine and renal tissue in cisplatin-induced nephrotoxicity. Cisplatin was administered intravenously to groups of 20 rats at single doses of 0, 1, 2.5, and 5 mg/kg and rats were sacrificed at 1, 2, 3 and 6 days after treatment. Increased serum BUN and creatinine were observed at a dose of 5 mg/kg cisplatin on day 2 through day 6. Increased urinary copper excretion coincided with necrosis and increased BUN and creatinine on day 3 in the high-dose group. Evidence of renal injury was apparent histologically as karyomegaly at all dose levels as early as 48 hours after injection of cisplatin, prior to increases in urinary copper levels. No change in the distribution of metal binding proteins (transferrin, ferritin, ceruloplasmin, and metallothionein) evaluated by immunohistochemical staining, was seen. Based upon these results, it is unlikely that changes in metal excretion play a primary role in cisplatin-induced nephrotoxicity however, changes in nuclear function indicated by karyomegaly may be involved in early renal injury.
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PMID:Assessment of the possible role of iron and copper in cisplatin-induced nephrotoxicity in the rat. 816 68

This is the first reported case of human fatality associated with zinc intoxication following a massive ingestion of coins. Four hundred and sixty-one coins were removed form the gastrointestinal tract of a schizophrenic patient during the course of hospitalization. Many of the post-1981 pennies, which consist primarily of zinc, showed severe corrosion due to their prolonged contact with acidic gastric juice. The patient presented with clinical manifestations consistent with the local corrosive as well as systemic effects of zinc intoxication and died 40 days after admission with multi-system organ failure. Tissue samples of the kidneys, pancreas, and liver obtained at autopsy revealed acute tubular necrosis, mild fibrosis, and acute massive necrosis, respectively, and contained high levels of zinc. The overall effects of zinc intoxication on the various organ systems, possible hematological derangement, and the impairment of copper absorption as well as the outcome with treatment are discussed.
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PMID:Zinc toxicity following massive coin ingestion. 918 31

Positron emission tomography (PET) is perfectly suited for quantitative imaging of the kidneys, and the recent improvements in detector technology, computer hardware, and image processing software add to its appeal. Multiple positron emitting radioisotopes can be used for renal imaging. Some, including carbon-11, nitrogen-13, and oxygen-15, can be used at institutions with an on-site cyclotron. Other radioisotopes that may be even more useful in a clinical setting are those that either can be obtained from radionuclide generators (rubidium-82, copper-62) or have a sufficiently long half-life for transportation (fluorine-18). The clinical use of functional renal PET studies (blood flow, glomerular filtration rate) has been slow, in part because of the success of concurrent technologies, including single-photon emission computed tomography (SPECT) and planar gamma camera imaging. Renal blood flow studies can be performed with O-15-labeled water, N-13-labeled ammonia, rubidium-82, and copper-labeled PTSM. With these tracers, renal blood flow can be quantified using a modified microsphere kinetic model. Glomerular filtration can be imaged and quantified with gallium-68 EDTA or cobalt-55 EDTA. Measurements of renal blood flow with PET have potential applications in renovascular disease, in transplant rejection or acute tubular necrosis, in drug-induced nephropathies, ureteral obstruction, before and after revascularization, and before and after the placement of ureteral stents. The most important clinical application for imaging glomerular function with PET would be renovascular hypertension. Molecular imaging of the kidneys with PET is rather limited. At present, research is focused on the investigation of metabolism (acetate), membrane transporters (organic cation and anion transporters, pepT1 and pepT2, GLUT, SGLT), enzymes (ACE), and receptors (AT1R). Because many nephrological and urological disorders are initiated at the molecular and organelle levels and may remain localized at their origin for an extended period of time, new disease-specific molecular probes for PET studies of the kidneys need to be developed. Future applications of molecular renal imaging are likely to involve studies of tissue hypoxia and apoptosis in renovascular renal disease, renal cancer, and obstructive nephropathy, monitoring the molecular signatures of atherosclerotic plaques, measuring endothelial dysfunction and response to balloon revascularization and restenosis, molecular assessment of the nephrotoxic effects of cyclosporine, anticancer drugs, and radiation therapy. New radioligands will enhance the staging and follow-up of renal and prostate cancer. Methods will be developed for investigation of the kinetics of drug-delivery systems and delivery and deposition of prodrugs, reporter gene technology, delivery of gene therapy (nuclear and mitochondrial), assessment of the delivery of cellular, viral, and nonviral vectors (liposomes, polycations, fusion proteins, electroporation, hematopoietic stems cells). Of particular importance will be investigations of stem cell kinetics, including local presence, bloodborne migration, activation, seeding, and its role in renal remodeling (psychological, pathological, and therapy induced). Methods also could be established for investigating the role of receptors and oncoproteins in cellular proliferation, apoptosis, tubular atrophy, and interstitial fibrosis; monitoring ras gene targeting in kidney diseases, assessing cell therapy devices (bioartificial filters, renal tubule assist devices, and bioarticial kidneys), and targeting of signal transduction moleculas with growth factors and cytokines. These potential new approaches are, at best, in an experimental stage, and more research will be needed for their implementation.
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PMID:Future direction of renal positron emission tomography. 1635 95

Chromium copper arsenate (CCA) was used for the protection of wood building materials until the restriction by EPA in 2002. During a short period of time 14-24h, a comparative nephrotoxicity study was performed regarding the effects of CCA and its compounds per se. Histopathological and histochemical features were correlated with the concentration of the total arsenic and chromium in mice kidney. Animals were subcutaneously injected with CCA (7.2mg/kg arsenic and 10.2mg/kg chromium per body weight), CrO3 (10.2mg/kg), As2O5 (7.2 mg/kg) and NaCl (0.9%) per se. The histopathological examination of the renal sections evidenced acute tubular necrosis in the groups of animals exposed to CCA (in both periods of time). Although the same contents of pentavalent arsenic and hexavalent chromium were injected in treated animals with CCA and with the prepared solutions of As2O5 and CrO3, the arsenic concentration on kidneys of CCA-exposed animals was much higher than those in animals exposed to As2O5 (32- and 28-fold higher at 14 and 24h, respectively). However, the elimination of chromium seems to occur similarly in the kidneys of animals treated with CCA and CrO(3)per se. Interactions among the components of CCA result in a marked decrease of the ability of kidney to eliminate simultaneously both analytes. The nephrotoxicity of CCA was higher than its components per se, evidencing a possible synergetic effect.
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PMID:Nephrotoxicity effects of the wood preservative chromium copper arsenate on mice: histopathological and quantitative approaches. 1948 32