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)

Although relatively rare in the United States, acute liver failure (ALF) is associated with very high rates of morbidity and mortality. A leading cause of morbidity and mortality is cerebral edema and intracranial hypertension. Hypothermia, osmotic diuretics, and hyperosmolar therapy are commonly used to manage these complications; however, when these are ineffective, renal replacement therapy may be needed for volume management. Acute kidney injury is a common complication of ALF and may arise from a number of etiologies, including hepatorenal syndrome and acute tubular necrosis. Acute kidney injury is most common in patients who develop ALF because of acetaminophen toxicity or ischemia. With regard to renal replacement therapy, we will review specific considerations relevant to the management of the patient with ALF.
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PMID:What a Nephrologist Needs to Know About Acute Liver Failure. 2631 99

The Food and Drug Administration Animal Rule requires evaluation of cardiovascular and central nervous system (CNS) effects of new therapeutics. To characterize an adult and juvenile mouse model, neurobehavioral and cardiovascular effects and pathology of a single sublethal but toxic, 8 mg/kg, oral dose of potassium cyanide (KCN) for up to 41 days postdosing were investigated. This study describes the short- and long-term sensory, motor, cognitive, and behavioral changes associated with oral dosing of a sublethal but toxic dose of KCN utilizing functional observation battery and Tier II CNS testing in adult and juvenile mice of both sexes. Selected tissues (histopathology) were evaluated for changes associated with KCN exposure with special attention to brain regions. Telemetry (adult mice only) was used to evaluate cardiovascular and temperature changes. Neurobehavioral capacity, sensorimotor responsivity or spontaneous locomotor activity, and rectal temperature were significantly reduced in adult and juvenile mice at 30 minutes post-8 mg/kg KCN dose. Immediate effects of cyanide included bradycardia, adverse electrocardiogram arrhythmic events, hypotension, and hypothermia with recovery by approximately 1 hour for blood pressure and heart rate effects and by 2 hours for body temperature. Lesions consistent with hypoxia, such as mild acute tubular necrosis in the kidneys corticomedullary junction, were the only histopathological findings and occurred at a very low incidence. The mouse KCN intoxication model indicates rapid and completely reversible effects in adult and juvenile mice following a single oral 8 mg/kg dose. Neurobehavioral and cardiovascular measurements can be used in this animal model as a trigger for treatment.
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PMID:Neurobehavioral and Cardiovascular Effects of Potassium Cyanide Administered Orally to Mice. 2717 Jun 81


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