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)

Experimental animal work has shown that thyroid hormone levels become undetectable 9 hours after brain death. It is unknown whether such an acutely hypothyroid state contributes to the hemodynamic instability of brain-dead donors or whether these donors should be resuscitated with thyroid hormone. No previous clinical study has examined thyroid hormone levels in human brain-dead organ donors. We retrospectively examined the thyroid hormone levels as measured by triiodothyronine and thyroxine in 22 human cadaver donors. Eight donors provided heart and kidney allografts, and the remaining 12 were kidney donors only. No donor had a normal triiodothyronine level and 10 were below normal, with undetectable levels in 12. Thyroxine levels were normal in 10 and below normal in 12. In comparing donors with below normal to undetectable triiodothyronine levels and donors with normal to below normal thyroxine levels, no statistically significant differences were found regarding blood pressure during harvest, duration of harvest, or dopamine requirements during harvest. Donors with a closed-head injury plus multiple injuries had statistically lower thyroxine values than donors with only a closed-head injury. For the heart donors, no correlation was found between thyroid hormone levels and the duration or dose of dopamine required for the heart allograft recipients after transplant. The incidence of acute tubular necrosis in the kidney transplants did not correlate with the donor thyroid hormone levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thyroid hormone levels in heart and kidney cadaver donors. 330 71

Delayed graft function (DGF) in cadaver kidney transplants is a common problem and is often due to acute tubular necrosis (ATN). DGF in transplants may have a deleterious effect on long-term graft survival. Since thyroid hormone has been shown to hasten recovery from ATN in experimental models, we designed a trial to determine if a defined course of triiodothyronine (T3) would improve the short- or long-term outcome of patients with DGF in cadaveric transplants. A prospective, randomized, placebo controlled, double blind trial of T3 was carried out in patients with DGF in cadaveric renal transplants. End-points were percentage requiring dialysis, percentage recovering function, time to recovery and length of hospital stay. Long-term outcomes were percentage grafts functioning at 1 year and mean serum creatinine at 1 year. Forty-four patients were randomized to receive either T3 or placebo. Three patients were dropped from each group when early biopsies disclosed that DGF was due to rejection. The groups were well matched by age, cold ischemia time of the graft, and percentage reactivity to a random panel of antigens. Baseline thyroid function studies, including T3, reverse T3 (rT3), and thyroid stimulating hormone (TSH) levels, were similar between the two groups and typical of 'euthyroid-sick syndrome'. T3 had no effect on percentage requiring dialysis, time to recovery, percentage recovering function, or length of stay. At 1 year follow-up, graft function was similar in both groups and significantly lower than that seen in patients with good initial function. Thyroid hormone, given early in the course of DGF in cadaver kidney recipients, had no effect on the course of DGF. Long-term graft function is impaired in patients who experience post-transplant DGF compared to those who have good initial function.
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PMID:Thyroid hormone in the treatment of post-transplant acute tubular necrosis (ATN). 1209 57