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 the sickle cell trait (SCT) is usually a benign and innocuous carrier state or condition rather than a disease, those with the trait are capable of developing any and all types of vascular occlusive lesions that have been observed in patients with sickle cell anemia. Obstructive vascular lesions in individuals with SCT occur infrequently, but when they do occur they are disabling and may be life-threatening. Disabilities attributed to in vivo sickling have the potential of seriously impeding the success of military missions. When selecting recruits to be trained and assigned to special operations, consideration should be given to hyposthenuria, the possibility of hematuria and to exercise-induced syndromes. Exertion to the point of exhaustion in previously healthy individuals with SCT may cause sudden death, rhabdomyolysis, and acute tubular necrosis. In vivo sickling of erythrocytes is a superimposed and late contributory and complicating factor of exertional syndromes.
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PMID:The sickle cell trait in relation to the training and assignment of duties in the armed forces: III. Hyposthenuria, hematuria, sudden death, rhabdomyolysis, and acute tubular necrosis. 673 89

Delayed graft function is an important medical problem after renal transplantation. It occurs in approximately 30% of cases, and is not only associated with more prolonged and complicated hospitalisation, but also with earlier graft loss on the long-term. Delayed graft function is the consequence of acute tubular necrosis caused by ischaemia-reperfusion injury, with insufficiently opposed toxic effects of reactive oxygen species and insufficient ATP regeneration. An optimal tissue thiamine status is pivotal for scavenging of reactive oxygen species and regeneration of ATP. There are several reasons to suppose that tissue thiamine availability is suboptimal in donor kidneys prior to reperfusion in transplantation. These reasons include a high prevalence of untreated thiamine deficiency at admission of donors to intensive care units, quick exhaustion of body thiamine stores during periods of non-feeding or inappropriate feeding during hospital stays of donors, and loss of the water-soluble vitamin into water-based organ preservation solutions. We therefore hypothesize that a suboptimal tissue thiamine status is a cause of delayed graft function after renal transplantation, and that it can be prevented with thiamine supplementation.
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PMID:Tissue thiamine deficiency as potential cause of delayed graft function after kidney transplantation: thiamine supplementation of kidney donors may improve transplantation outcome. 1737 23