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)

Rhabdomyolysis is a serious and potentially life threatening condition. Although consensus criteria for rhabdomyolysis is lacking, a reasonable definition is elevation of serum creatine kinase activity of at least 10 times the upper limit of normal followed by a rapid decrease of the sCK level to (near) normal values. The clinical presentation can vary widely, classical features are myalgia, weakness and pigmenturia. However, this classic triad is seen in less than 10% of patients. Acute renal failure due to acute tubular necrosis as a result of mechanical obstruction by myoglobin is the most common complication, in particular if sCK is >16.000 IU/l, which may be as high as 100,000 IU/l. Mortality rate is approximately 10% and significantly higher in patients with acute renal failure. Timely recognition of rhabdomyolysis is key for treatment. In the acute phase, treatment should be aimed at preserving renal function, resolving compartment syndrome, restoring metabolic derangements, and volume replacement. Most patients experience only one episode of rhabdomyolysis, mostly by substance abuse, medication, trauma or epileptic seizures. In case of recurrent rhabdomyolysis, a history of exercise intolerance or a positive family history for neuromuscular disorders, further investigations are needed to identify the underlying, often genetic, disorder. We propose a diagnostic algorithm for use in clinical practice.
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PMID:Rhabdomyolysis: review of the literature. 2494 98

In February 2012, 100% mortality was reported in a herd with 79 local sheep that were kept around of Abhar, Northwest of Iran. The ration for adult sheep was daily mixed (40 kg straw, 25 kg wheat and 2 kg Vit-C premix) and accidentally 1 500 g of salinomycin (Salinomycin 12% Premix; Aras Bazar Laboratories, Iran) had been added to the ration (22388 mg/kg = 22388 ppm) and overnight was fed to herd. At the morning, 78 sheep were founded dead and one of them showed convulsive seizures. Postmortem examination revealed pulmonary congestion and edema, hemorrhages in abomasum, large pale kidney and white streak lines in myocardium. Main histopathologic lesions were extensive subepicardial and intercardiomyofibers hemorrhages, extensive cardiomyolysis and myocarditis in heart, severe hyperemia and extensive acute tubular necrosis (ATN) in kidneys and focal necrosis and retention of bile cholangitis in the liver. In this study, on the basis of the history, observation of the ionophore remnant in the ration, clinical signs, gross and histopathological findings, acute salinomycin intoxication is definitely diagnosed.
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PMID:High mortality due to accidental salinomycin intoxication in sheep. 2610 96

Seizures and neurologic involvement have been reported in patients infected with Shiga toxin (Stx) producing E. coli, and hemolytic uremic syndrome (HUS) with neurologic involvement is associated with more severe outcome. We investigated the extent of renal and neurologic damage in mice following injection of the highly potent form of Stx, Stx2a, and less potent Stx1. As observed in previous studies, Stx2a brought about moderate to acute tubular necrosis of proximal and distal tubules in the kidneys. Brain sections stained with hematoxylin and eosin (H&E) appeared normal, although some red blood cell congestion was observed. Microglial cell responses to neural injury include up-regulation of surface-marker expression (e.g., Iba1) and stereotypical morphological changes. Mice injected with Stx2a showed increased Iba1 staining, mild morphological changes associated with microglial activation (thickening of processes), and increased microglial staining per unit area. Microglial changes were observed in the cortex, hippocampus, and amygdala regions, but not the nucleus. Magnetic resonance imaging (MRI) of Stx2a-treated mice revealed no hyper-intensities in the brain, although magnetic resonance spectroscopy (MRS) revealed significantly decreased levels of phosphocreatine in the thalamus. Less dramatic changes were observed following Stx1 challenge. Neither immortalized microvascular endothelial cells from the cerebral cortex of mice (bEnd.3) nor primary human brain microvascular endothelial cells were found to be susceptible to Stx1 or Stx2a. The lack of susceptibility to Stx for both cell types correlated with an absence of receptor expression. These studies indicate Stx causes subtle, but identifiable changes in the mouse brain.
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PMID:Shiga Toxin Mediated Neurologic Changes in Murine Model of Disease. 2774 96

Lilies are considered nephrotoxic only to domestic cats, which belong to the family Felidae of the suborder Feliformia. However, a 7-month-old female meerkat, belonging to the family Herpestidae of the suborder Feliformia, presented with oliguria, seizure, tachypnea, self-biting, and nystagmus after it ingested lilies. The meerkat died approximately 40 hr after lily ingestion. Gross and histopathologic lesions consistent with acute renal failure were conspicuous in the animal. The renal lesions were acute tubular necrosis, corresponding to the typical pathological changes of lily toxicosis in cats. In addition, massive hepatocyte necrosis and pulmonary congestion/edema were observed. These findings suggest that lily toxicosis in meerkats is characterized by pulmonary and hepatic failure, in addition to the renal failure observed in domestic cats.
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PMID:Suspected lily toxicosis in a meerkat (Suricata suricatta): a case report. 2931 34

The star fruit (Averrhoa carambola) is consumed in high amounts in Asia and Central/South America. It contains oxalic acid and caramboxin. In some individuals, its ingestion may lead to nephrotoxicity and neurotoxicity. The nephrotoxic effect is due to oxalate deposition in renal tubules resulting in acute tubular necrosis and interstitial nephritis. Although uraemic encephalopathy secondary to acute kidney injury may play a role, a shift to an excitatory state of the central nervous system (CNS) by caramboxin through activation of excitatory neuroreceptors and inhibition of GABA receptors leads to mental confusion, seizures and status epilepticus seen with star fruit intoxication. In this mini-review, we discuss the mechanisms of star fruit-related toxicity.
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PMID:Mechanisms of star fruit (Averrhoa carambola) toxicity: A mini-review. 3296 29


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