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)

Gram-negative bacterial infections were documented in 6 neonatal New World camelids (5 Ilamas and 1 alpaca). The organisms isolated from blood before death or from multiple organs after death were Escherichia coli (n = 3), Actinobacillus sp (n = 1), and Klebsiella pneumoniae (n = 1). Only 2 crias survived, and 1 became blind secondary to retinal detachment and ocular inflammation, which developed after treatment for bacterial infection. Abnormal events during the perinatal period (prematurity, dystocia, cesarean section, weak at birth) were reported in all 6 crias. Signs of depression, convulsions, and/or coma were observed in all animals. Diarrhea and respiratory distress were also noticed in the 3 crias that died shortly after admission. Serum immunoglobulins were assessed, but without the benefit of a stall-side test specific for Ilama immunoglobulins. All crias were suspected to have poor transfer of maternal immunoglobulins. Hemograms and serum biochemical values prior to the initiation of treatment were obtained on 5 of the 6 crias. Total nucleated cells ranged from 1,400 to 23,100 cells/microliter. Four of the 5 crias has a left shift, and 2 crias had toxic neutrophils. Serum glucose concentrations, measured in 5 of 6 crias, ranged from 83 to 293 mg/dl. Serum creatinine values were high in 2 of 5 crias, 1 of which had acute tubular necrosis. Three crias with high serum electrolyte (sodium, chloride, or potassium) values subsequently died. Arterial blood gas values were assessed in 3 crias, 1 of which had respiratory alkalosis and mild hypoxemia.
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PMID:Gram-negative bacterial infection in neonatal New World camelids: six cases (1985-1991). 142 94

To determine the effect of diabetes mellitus on gentamicin nephrotoxicity we treated male F344 rats with streptozotocin 22 mg/kg (DM rats). DM rats were compared to controls (C) and nondiabetic rats ingesting the osmotic diuretic isosorbide administered to simulate glycosuric diuresis (C/I). Base-line C/I renal function and histology did not differ from C. However, in DM rats base-line inulin clearance (CIN) was 20% lower, and renal cortical slice uptake of p-aminohippurate was reduced compared to C and C/I. DM rats also had foci of renal tubular epithelial dysplasia not seen in C or C/I. Gentamicin was administered at 40 mg/kg-day to C and C/I and 32 mg/kg-day to DM rats to adjust for base-line CIN. Acute tubular necrosis, associated with depression of CIN and renal cortical p-aminohippurate and N-methylnicotinamide uptake, developed in all three groups. There were no differences between C and C/I. However, the degree of acute tubular necrosis and dysfunction was less in DM rats than C and C/I. Renal cortical gentamicin accumulation was also slower in DM than either C or C/I, and changes in renal cortical gentamicin over time followed a different pattern in DM rats. These results indicate that 1) attenuation of gentamicin injury in DM rats may be related to reduced accumulation of gentamicin by the renal cortex, 2) this reduced accumulation may be due to subtle baseline tubular injury mediated by streptozotocin or the diabetic state, and 3) osmotic diuresis does not account for attenuation of renal injury in DM.
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PMID:Experimental gentamicin nephrotoxicity: effect of streptozotocin-induced diabetes. 315 84

A total of 39 Holstein cattle were grazed in tracts of wild grassland on account of shortage in pasture grass. Twenty-nine cattle were affected and 26 of them died during a 21-day period. The main signs were depression, anorexia, ascites, and oliguria. There was elevated serum urea nitrogen and sugar and protein in the urine. Pathological examination revealed turbid swelling of the kidney, an increase in the amount of fluid in the body cavity, edema in the perirenal adipose tissue and hemorrhage in various visceral organs and tissues. Histologically, acute tubular necrosis in the kidney, hypoplasia of the erythroblast series in the bone marrow, atrophy and degeneration of the lymphatic tissue and focal necrosis of the liver were observed in many of the cattle. Among cows experimentally fed Narthecium asiaticum Maxim., Polygonum sachalinense Fr. Schum., and Vitis coignetiae Pulliat which were presumed to have been ingested in large amounts by grazing cattle in the field, the cows fed N. asiaticum revealed the clinical, biochemical and pathological changes similar to those noticed in naturally affected cattle. Cows fed P. sachalinense and V. coignetiae showed no distinct systemic symptoms except transient anorexia and hypothermia.
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PMID:Narthecium asiaticum Maxim. Poisoning of grazing cattle: observations on spontaneous and experimental cases. 398 97

Sodium diethyldithiocarbamate (DDTC) administered following cis-diamminedichloroplatinum(II) (DDP) has been reported to attenuate structural renal damage and elevation of blood urea nitrogen in rats. Since DDP damages primarily proximal tubular epithelium in this species, we compared proximal tubular function, glomerular function, and histology in male Sprague-Dawley rats treated with DDP followed by either DDTC or 0.9% NaCl solution (NS) rescue. Male Sprague-Dawley rats received a single i.p. injection of DDP (7.5 mg/kg)-mannitol (75 mg/kg)-NaCl (67.5 mg/kg). Forty-five min later, rats were given i.p. injections of either DDTC (750 mg/kg) dissolved in 0.5 ml of NS (DDP + DDTC group; ten rats) or 0.5 ml NS (DDP + NS group; nine rats); additional rats received either DDTC only (DDTC group; six rats) or no treatment (untreated control group; six rats). All groups were sacrificed 5 days later by ether anesthesia and exsanguination. Compared to the untreated control group, the DDTC group had slightly lower mean blood urea nitrogen at sacrifice [12.5 +/- 0.5 (S.E.) versus 15.4 +/- 0.8 mg/dl; p less than 0.025 by unpaired Student's t test]; there was no difference in serum creatinine. The DDP + DDTC group had no diarrhea and no presacrifice deaths in contrast to diarrhea and three presacrifice deaths in the DDP + NS group. Blood urea nitrogen was also lower in the DDP + DDTC group at sacrifice (187 +/- 30 versus 383 +/- 39 mg/dl; p less than 0.005). However, weight loss and serum creatinine were not different. Structural acute tubular necrosis was marked in both DDP groups but was less severe in the DDP + DDTC group than in the DDP + NS group. Proximal tubular function was indexed by the uptake of the organic base N-[14C]methyl nicotinamide (NMN) and the organic acid p-aminohippurate in renal cortical slices incubated 90 min in Cross and Taggart medium. NMN uptake (expressed as slice to medium ratio) was slightly lower in the DDTC group than in untreated controls (4.1 +/- 0.2 versus 5.0 +/- 0.2; p less than 0.025). Marked depression of p-aminohippurate and NMN uptake occurred in both DDP + DDTC and DDP + NS groups. There was no difference in NMN uptake, but depression of p-aminohippurate uptake was slightly less severe in the DDP + DDTC group (5.3 +/- 0.7 versus 3.1 +/- 0.3; p less than 0.005). We conclude that DDTC rescue attenuates structural DDP injury in this animal model. DDP-mediated proximal tubular dysfunction was only marginally attenuated by DDTC; glomerular filtration rate, as indexed by serum creatinine, was not protected. DDTC attenuation of DDP toxicity may be mediated in part via reducing volume depletion due to DDP-associated diarrhea.
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PMID:cis-diamminedichloroplatinum(II) nephrotoxicity: tubular function after rescue with sodium diethyldithiocarbamate in rats. 630 93

The early use of gold in medicine and dentistry dates back to the ancient Chinese and Egyptians. The discovery in 1890 that gold salts were toxic in vitro to tubercle bacilli led to the extensive treatment of tuberculosis with gold salts in the first three decades of this century. Eventually, gold therapy was extended to arthritis and lupus erythematosus, because of the belief that these diseases were forms of tuberculosis. Because of its beneficial effect particularly on active rheumatoid arthritis, chrysotherapy has remained one of the most widely used treatments of rheumatoid arthritis for the past half century. Toxicity of gold salts includes hypersensitivity reaction of skin and mucous membranes, bone marrow depression, and nephrotoxicity. The nephrotoxic clinical manifestations are renal insufficiency, proteinuria and hematuria, and the nephrotic syndrome. The pathologic changes are tubular degeneration, acute tubular necrosis or immune complex glomerulonephritis. The justification that any of these possible changes are the result of gold therapy rests clinically upon the time relationship of gold therapy and the renal symptoms, and pathologically upon the presence of gold inclusions (aurosomes) in proximal tubular epithelial cells. Aurosomes can at times be visualized by light microscopy, are usually seen by electron microscopy, and can be identified by microprobe analysis. Their pathology will be illustrated and pathogenic mechanisms discussed.
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PMID:Gold nephropathy. 703 39

Poisonings with industrial products represent approximately 7% of the cases reported to the poison centres. Ingestion of petroleum distillates induces irritation of the gastrointestinal tract, central nervous system depression and aspiration pneumonitis which may be severe; treatment is mainly supportive. Ethylene and diethylene glycol poisonings produce central nervous system depression, anion gap metabolic acidosis, osmolar gap and acute tubular necrosis; in severe cases, hypocalcaemia, cerebral oedema and heart failure may be observed; treatment often associates supportive measures, haemodialysis and administration of competitive inhibitors of alcohol dehydrogenase (ethanol or 4-methylpyrazole). Glycol ethers induce central nervous system depression and metabolic acidosis; in addition, ethylene glycol monobutyl ether produces haemolysis; monomethyl and monoethyl ethers are responsible for bone marrow and lymphoid organ toxicity, they adversely affect spermatogenesis and are teratogens.
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PMID:[Acute poisoning with industrial products]. 1074 68

Clostridium perfringens type D isolates cause enterotoxemia in sheep, goats, and probably cattle. While the major disease signs and lesions of type D animal disease are usually attributed to epsilon toxin, a class B select agent, these bacteria typically produce several lethal toxins. Understanding of disease pathogenesis and development of improved vaccines are hindered by the lack of a small-animal model mimicking natural disease caused by type D isolates. Addressing this need, we developed an oral challenge mouse model of C. perfringens type D enterotoxemia. When BALB/c mice with a sealed anus were inoculated by intragastric gavage with type D isolates, 7 of 10 type D isolates were lethal, as defined by spontaneous death or severe clinical signs necessitating euthanasia. The lethalities of the seven type D isolates varied between 14 and 100%. Clinical signs in the lethally challenged mice included seizures, convulsions, hyperexcitability, and/or depression. Mild intestinal gas distention and brain edema were observed at necropsy in a few mice, while histology showed multifocal acute tubular necrosis of the kidney and edema in the lungs of most challenged mice that developed a clinical response. When the lethality of type D isolates in this model was compared with in vitro toxin production, only a limited correlation was observed. However, mice could be protected against lethality by intravenous passive immunization with an epsilon toxin antibody prior to oral challenge. This study provides an economical new model for studying the pathogenesis of C. perfringens type D infections.
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PMID:Development and application of an oral challenge mouse model for studying Clostridium perfringens type D infection. 1756 65

The aim of this experimental study was to investigate the pathological effects of gentamicin in birds. Broiler chicks at 1 day of age were intramuscularly administered gentamicin at dose levels varying from 0 to 180 mg/kg. Clinical signs comprising of depression, decreased feed consumption, increased water intake, loose watery droppings and reduced body weights appeared in a dose-related manner in chicks administered 30 mg/kg or higher dose levels. Mortality was 0% and 20% in chicks given 40 mg and 50 mg/kg gentamicin. It increased in a dose-related manner and was 100% in 100mg/kg or higher dose groups. The LD50 calculated at total deaths in 5 weeks duration was 77.56 mg/kg. Kidneys and livers of chicks given 50mg/kg or higher doses of gentamicin were congested, enlarged and had hemorrhages on the surfaces. Microscopically kidneys exhibited acute tubular necrosis. Livers showed fatty change, vacuolar degeneration, necrotic areas and cellular infiltration around portal triads. Serum total proteins and albumin decreased while creatinine and ALT increased in chicks given 20mg/kg and higher doses. The no observable effect level (NOEL) of a single intramuscular administration of gentamicin in day-old broiler chicks was 10mg/kg body weight.
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PMID:Pathological effects of gentamicin administered intramuscularly to day-old broiler chicks. 1904 12