Thyroxine-binding by Serum

The occurrence of hypercholesterolemia, lowered basal metabolic rate and depressed serum proteinbound iodine in the nephrotic syndrome has directed attention to the thyroid gland in this disorder. Although hypothyroidism has been suspected, these patients are usually considered, on clinical grounds, to be euthyroid, and they fail to respond in a specific manner to even large doses of thyroid hormone (1-3). Since the thyroid gland itself appears to be functioning normally, or even excessively, with respect to iodine accumulation (4), and responds in a normal fashion to thyrotropin and exogenous thyroxine (5), possible disorders in the peripheral metabolism of thyroid hormone have been investigated. Recant and Riggs (5) have suggested that the loss of hormonal iodine in the urine, although considerable, is insufficient to explain the low serum iodine concentration. These investigators demonstrated a normal degradation rate for exogenous thyroxine, whereas Rasmussen (6) found a lower than normal amount degraded each day. Inasmuch as the circulating thyroid hormone is almost entirely bound to serum protein (7), and since the protein components of serum are extensively altered in nephrosis, a possible defect in this aspect of thyroid physiology has been suspected (5). A preliminary report from our laboratory (8), as well as one by Recant (9), has suggested the presence of a qualitatively abnormal thyroxine-protein complex in nephrotic serum. The data presented in this report, however, indicate that in the nephrotic state, the serum proteins which interact with thyroxine are normal from a physical standpoint.