THYROXINE METABOLISM IN THE NEPHROTIC SYNDROME1

The presence of hypometabolism and hypercho-lesterolemia in nephrosis suggests decreased thy-roid function. Because of these abnormalities Epstein (1) treated a number of nephrotic pa-tients with large doses of thyroid, and found that hypermetabolism could not be produced with daily doses of 4 to 5 grams of desiccated thyroid.3 Leiter, therefore, suggested (2) that the low basal metabolic rates and high concentrations of serum cholesterol in this disease were due to some cause other than hypothyroidism. The demonstration of low concentrations of protein-bound iodine in the serum of nephrotic patients (3) led Recant and Riggs to reinvestigate this problem (4). They found subnormal concentrations of serum PBI127, normal to high uptakes of I181 by the thyroid gland, low basal metabolic rates and high serum choles-terols in their nephrotic subjects. They also noted amounts of PB1127 in the urine as high as 36 pg. per day; a decrease in the thyroidal uptake of I1l1 fol-lowing thyroid therapy; and the ability of the thy-roid gland to respond to thyrotropic hormone as measured by a rise in the concentration of serum PBI127. On the basis of these findings, they postu-lated that in nephrosis the thyroid gland functions normally, that a deficiency of thyrotropic activity is unlikely, that the thyroxine-binding capacity of the plasma proteins is reduced, but that a nor-mal supply of thyroid hormone is delivered to the peripheral tissues (i.e., presumably a normal amount is degraded each day). The low basal metabolic rate and high concentration of serum cholesterol were attributed to some factor other than decreased thyroid function. Although they found protein-bound iodine in the urine, they fel