Abnormal thyroid function in peritoneal dialysis patients: lots of smoke but no fire.

Thyroid disorders are the second most common endocrine condition following diabetes mellitus. It is not difficult for physicians to diagnose and treat patients with overt hypothyroidism or hyperthyroidism presenting significant biochemical derangements and clinical symptoms. In the spectrum of subclinical thyroid dysfunction and nonthyroidal illness syndrome (i.e., alterations in thyroid hormones without any underlying intrinsic thyroid disorder), however, it is not always an easy task. The interpretation of thyroid functions in patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD) is even more complicated by the declination in glomerular filtration rate (GFR), the difference in dialysis modalities, and comorbidities. CKD is a well-known cause of nonthyroidal illness syndrome and affects all levels of the hypothalamus-pituitary-thyroid axis. Serum TSH levels are usually normal or elevated in CKD patients with normal or low free and total T3 and T4 levels. Low T3 syndrome is the most frequently observed thyroid alteration in CKD patients. An epidemiological study using data from NHANES III, indicated a higher prevalence of hypothyroidism in predialysis CKD patients; it is mainly subclinical among these patients. Furthermore, there was a graded and increased likelihood of hypothyroidism with progressively lower GFR. These disarrangements are similar in ESRD patients after the commencement of peritoneal dialysis (PD) treatment. The major thyroid dysfunctions in PD patients include subclinical hypothyroidism and low T3 syndrome. The clearance of iodide is primarily by glomerular filtration. Thus, iodide excretion is diminished in advanced CKD, with subsequent elevation in plasma inorganic iodide concentration. Increases in total body inorganic iodide can block thyroid hormone production (the Wolff-Chaikoff effect), which may explain the high incidence of subclinical hypothyroidism in CKD patients. Low T3 levels reflect a diminished conversion of T4 to T3 in the periphery. Its physiological significance has been interpreted as an adaptive compensatory attempt to conserve energy stores by reducing metabolic rate in diseased states. Increasing evidence supports the association of subclinical hypothyroidism with cardiovascular diseases (CVD) and mortality. Because of the known effects of thyroid hormone, including modulating heart rate, cardiac contractility, arterial peripheral resistance and cholesterol metabolism, it is