triiodothyronine--reverse and Nephrotic-Syndrome

Topics: Acute Kidney Injury; Humans; Kidney Diseases; Nephrotic Syndrome; Thyroid Hormones; Thyroxine; Thyroxine-Binding Proteins; Triiodothyronine; Triiodothyronine, Reverse

To evaluate reverse 3,3',5'-triiodothyronine (rT3) metabolism in nephrotic syndrome, serum rT3 kinetic studies from 10 nephrotics (mean urinary protein losses 7.0 g/day) with normal glomerular filtration rates (GFR; creatinine clearance 107 ml/min) were compared with 9 normal healthy subjects. Serum disappearance data were analyzed in a three-pool model, including rapidly (liver and kidney) and slowly (muscle, skin, and brain) equilibrating pools exchanging with serum, with all losses from the rapidly equilibrating pool. Serum free thyroxine (T4), determined by equilibrium dialysis, and parathyroid hormone levels were unaltered; total T4, T3, and rT3, and free rT3, albumin, and transferrin levels were significantly decreased; and free fractions of T4 and rT3 and thyroid-stimulating hormone (TSH) levels were increased. Despite reduced rT3 binding in serum, fractional transfer rates from serum to extravascular sites and serum clearance rates of total rT3 were unaltered. Free hormone clearance, serum appearance, and maximum hormone production rates were decreased. Total hormone transfer rates between serum and tissue pools and rT3 mass in serum and both tissue pools were reduced. Binding in the slowly equilibrating pool was decreased, and binding in both rapidly and slowly equilibrating pools was correlated with the free fraction of rT3 (r = -0.79, P = 0.007, and r = -0.70, P less than 0.025, respectively), with a shift of rT3 from the slow to the rapid pool. These findings suggest that binding of rT3 and T4 to serum carrier proteins is reduced, the transfer process for rT3 from serum to extravascular sites is decreased by factors in addition to reduced serum binding, degradation of rT3 is impaired, and decreased slow-pool binding may reflect reduced rT3 binding to serum-derived proteins in interstitial fluid. Furthermore, rT3 production rates are reduced, despite normal serum free T4 levels, accounting for low serum free rT3 concentrations. Total rT3 levels are decreased because of decrements in both serum binding and production rates.

Topics: Adult; Female; Glomerular Filtration Rate; Humans; Kinetics; Male; Models, Biological; Nephrotic Syndrome; Reference Values; Thyroid Gland; Thyroxine; Time Factors; Triiodothyronine; Triiodothyronine, Reverse

Effects of Prednison therapy on serum levels of T4, T3, rT3, TBC, basal TSH and TSH response to TRH in 10 children (7 with nephrotic syndrome, 3 with trombocytopenia) were studied. It has been found out that corticotherapy (Prednison 1--2 mg/kg/24 h; 2--4 weeks) causes a significant decrease of total T3 concentration together with a considerable rise of reverse T3 and lower T3-binding capacity. Basal TSH level was increased about twice; TSH response to TRH between both groups (without and with Prednison therapy) did not differ significantly. The observations suggest the presence of hypothyroidism during chronic corticotherapy in children.

Topics: Child; Child, Preschool; Female; Humans; Hypothyroidism; Male; Nephrotic Syndrome; Prednisone; Thrombocytopenia; Thyrotropin; Thyrotropin-Releasing Hormone; Thyroxine; Triiodothyronine; Triiodothyronine, Reverse

The thyroid function of 13 patients with proteinuria and normal serum creatinine level (Group 1) and 15 patients with proteinuria and increased creatinine level (Group 2) was investigated. The daily urinary T41- and T3 excretion was much higher in Group 1 patients than in Group 2 patients (37.1 +/- 25.9 nmol T4 vs 17.5 +/- 8.7 nmol T4, 3.3 +/- 1.6 nmol T3 vs 1.1 +/- 0.8 nmol T3, respectively) and correlated in both groups with the protein loss. None of the patients suffered from hypothyroidism as a consequence of this hormone loss. Although the mean serum T4-, T3-, FT4-, FT3-, TBG- and TBPA concentrations in both groups of patients were within the normal range, the urinary hormone loss appeared to influence these values considerably. It was striking that the rT3 concentration in the patients with the highest hormone loss was frequently less than 0.08 nmol/l, the lower limit of detectability. The basal TSH levels in serum of the nephrotic patients were similar to those of normal individuals. The thyroid function of patients with proteinuria accompanied by retention of creatinine due to renal failure was more difficult to assess because different pathological mechanisms may exert their influence on the thyroidal hormone secretion as well as on the peripheral hormone metabolism.

Topics: Aged; Creatinine; Female; Humans; Male; Middle Aged; Nephrotic Syndrome; Proteinuria; Thyroid Function Tests; Thyroid Gland; Thyrotropin; Thyrotropin-Releasing Hormone; Thyroxine; Thyroxine-Binding Proteins; Triiodothyronine; Triiodothyronine, Reverse