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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Thyroid hormone metabolism and thyroid diseases in chronic renal failure.

Patients with ESRD have multiple alterations of thyroid hormone metabolism in the absence of concurrent thyroid disease. These may include elevated basal TSH values, which may transiently increase to greater than 10 mU/liter, blunted TSH response to TRH, diminished or absent TSH diurnal rhythm, altered TSH glycosylation, and impaired TSH and TRH clearance rates. In addition, serum total and free T3 and T4 values may be reduced, free rT3 levels are elevated while total values are normal, serum binding protein concentrations may be altered, and disease-specific inhibitors reduce serum T4 binding. Changes in T4 and T3 transfer, distribution, and metabolism resemble those of other nonthyroidal illnesses, while changes in rT3 metabolism are disease specific. Dialysis therapy minimally affects thyroid hormone metabolism, while zinc and erythropoietin administration may partially reverse thyroid hormone abnormalities. Thyroid hormone metabolism normalizes with renal transplantation; however, glucocorticoid therapy may induce additional changes. ESRD patients may have an increased frequency of goiter, thyroid nodules, thyroid carcinoma, and hypothyroidism. Goiter and hypothyroidism may be induced by iodide excess, due to reduced renal iodide excretion, and may be reversed with iodide restriction in some patients. The increased frequency of thyroid nodules and malignancies in ESRD may relate to secondary hyperparathyroidism. After renal transplantation, the higher frequency of thyroid malignancies may relate to the immunosuppressed state. Clinical symptoms and signs and biochemical features of hypothyroidism and hyperthyroidism may be altered by concurrent ESRD. ESRD patients with hyperthyroidism or follicular neoplasms require reduced dosages of Na 131-I depending upon type, frequency, and duration of dialysis therapy.[1]


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