Thyroid Function and Clinical Outcomes in Kidney Failure

[摘要] Thyroid hormone synthesis is finely tuned to respond to the variable energy needs of the human body (1). This process is controlled by two fundamental mechanisms. The first, based on the thyroid-stimulating hormone (TSH)–thyroxine (T4) and triiodothyronine (T3) feed-back loop, constitutes a sensitive and efficient protection against alterations in thyroid secretion. The second, based on the extrathyroidal generation of T3 from T4, allows rapid adjustments in thyroid hormone availability at tissue level in response to stressful conditions such as nonthyroidal illness. This mechanism is of major relevance because about 80% of the T3 produced results from 5′-deiodination of T4 in peripheral tissues by two T4-5′-deiodinases (type I and type II) (2). Together with the liver, the kidney is the organ endowed with the most abundant deiodinase activity (type 1 4-5′ deiodinase) (2).

[学科分类] 泌尿医学

[关键词] Bone marrow necrosis;Sickle cell disease;Hyperhemolysis syndrome