Within a certain range, the thyroid gland can adjust to variation in dietary iodine with changes in its clearance of iodide from plasma. However, either chronic dietary deficiency of iodine or conditions of severe iodine excess often exceed the capacity for regulation, resulting in disease states (see Chap. 37 and Chap. 38).

Virtually all of dietary iodine is reduced to iodide and absorbed in the small intestine. Circulating iodide is cleared from the blood principally by the kidney (80%) and by the thyroid (20%).1 Renal excretion, measured with a 24-hour collection, varies with filtered load and reflects 97% of dietary intake; only ˜3% is lost in the stool.1 Renal iodide is passively reabsorbed; thus, the renal clearance depends on glomerular filtration rate and is apparently unaffected by serum iodide concentration. Patients with end-stage renal disease (ESRD) have decreased renal iodide clearance and elevated serum iodide concentrations.3 Iodide excess is a proposed mechanism for the increased incidence of hypothyroidism, thyroid nodules, and goiter, whereas the mechanisms for increased thyroid cancer with ESRD are unknown.3 In contrast, thyroidal iodide clearance changes inversely with dietary intake and intrathyroidal iodine stores, increasing as much as fivefold under conditions of iodine deficiency.1