1. Investigación

Introduction. Renal function and thyroid metabolism are tightly related. However, evidence about subclinical hypothyroidism prevalence in patients with chronic kidney disease and its related factors is scarce. Objectives. Our aim is to analyze subclinical hypothyroidism prevalence and its related factors in patients with advanced chronic kidney disease. Materials and methods. Nondialysis-dependent patients with chronic kidney disease at stages 3 to 5 were included. Other inclusion criteria were age above 18 years and clinical stability. Patients with diagnosed thyroid illnesses were excluded. Subclinical hypothyroidism was de ned as thyroid stimulating hormone (TSH) > 5.3 mU/L, with free thyroxine 4 (FT4) between 0.54 and 1.24 ng/dl. Filiation data, comorbidities, and routine blood and urine test results were registered. Results. A total of 299 patients were included. Of them, 184 (61.5%) were men. The mean age was 71 ± 13 years old. The mean glomerular fltration rate (CKD-EPI) was 22 ± 9 ml/min/ 1.73m2. According to chronic kidney disease stages, global distribution of patients was as follows: Stage 3, 67 patients (22.4%); Stage 4, 155 patients (51.8%); and Stage 5, 77 patients (25.8%). We found subclinical hypothyroidism in 54 (18.1%) patients. According to chronic kidney disease stages, distribution of affected patients was as follows: Stage 3, 9 patients (13%); Stage 4, 25 patients (16.1%); and Stage 5, 20 patients (26%). Di¤erences among stages were statistically signifcant. By univariate analysis, factors related with subclinical hypothyroidism were as follows: age RR 1.048 (95% CI 1.019–1.078; p = 0.001), hypertension RR 2.705 (95% CI 1.026–7.130; p = 0.04), glomerular fltration rate RR 0.962 (95% CI 0.929–0.996; p = 0.03), and proteinuria higher than 1 gram/day RR 2.387 (95% CI 1.303–4.374; p = 0.005). By multivariate analysis adjusted by age, hypertension, glomerular fltration rate, proteinuria, diabetes, and cardiovascular disease history, only age RR 1.016 (95% CI 1.009–1.028; p = 0.04) and glomerular fltration rate RR 0.963 (95% CI 0.930–0.997; p = 0.03) preserved their independent association with subclinical hypothyroidism. Conclusions. Subclinical hypothyroidism prevalence in patients with chronic kidney disease is high and increases with renal disease severity. Factors independently related to subclinical hypothyroidism are age and glomerular fltration rate.

To determine adipose tissue cellularity in hypo- and hyperthyroidism, male rats were thyroidectomized after weaning (T) and injected daily with either 0, 0.1, 1. 8, or 25 µg of L-thyroxine/100 g body weight for 40 days. They were compared with intact controls (C). Both epididymal fat-pad weight and adipocyte diameter were reduced in T+0, T+0.1 and T+25 animals. When corrected per unit of body weight, the diameters of adipocytes from T+0 and T+0. l animals were larger than in the other groups. Those same animals have reduced absolute adipocyte number but not when corrected per unit of body weight. The fat-pad protein concentration varied conversely with the fat cell diameter. These findings indicate that thyroid hormone deficiency reduces thf proliferation of fat cells in parallel with body growth while hyperthyroidism causes reduction in the size, but not the number, of fat cells which corresponds to its depletion of fat storage.

Plasma amino acid concentrations, together with other metabolic parameters were determined in thyroidectomized rats treated with daily injections of sal ins (hypothyroid), and 250 ,ug/kg L-T4 {hypothyroid). Data were compared with sham-operated controls. TherP. is a genera! incre'!SE> in plasma amino acid concentrations in hyperthyroidism, a limited in· crease only in several amino acid r.oncentrations in hypothyroid rats as compared with controls, and a considerable difference between the plasma aminograms of both groups. Amino acid homeostasis seems to be subject to greater modification in hyperthyroidism than in hypothyroidism.

1) Thyoridectomized rats were fed with a low iodine diet, injected daily with 0, 0.1, 1.8 or 25 µg of L-thyroxine/100 g body wt., and compared with intact controls. 2) Plasma protein-bound iodine was decreased in the rats given the 0 and 0.1 µg doses, unchanged in those given the 1.8 µg doses, unchanged in those given the 1.8 µg dose increased in those given the 25 µg one. 3) The liver content of DNA-P, phospholipid-P, proteins and fatty acids was decreased in the rats that did not receive thyr.oxine, practically recuperated in those receiving 0.1 µg and normal in those given 1.8 or 25 µg of thyroxine. 4) 3 h of starvation produced a reduction in the liver content of total fatty acids that disappeared after 24 h. 5) When fod, liver glycogen concentration was low in the rats given 25 µg of thyroxine. 6) With starvation, the fall in liver glycogen and blood glucose, and the rise in liver acetylCoA and citrate and blood glycerol concentrations were faster in the thyroidectomized rats that did not receive thyroxine than in the other groups. 7) The rise in plasma free fatty acid and blood ketone bodies concentrations were similar in all the groups, the greater level of the first parameter being observed after 6 h of starvation in the rats given 25 µg of thyroxine and in the second one after 24 h in the rats given either 0.1, 1.8 or 25 µg of thyroxine. 8) The rapid decrease in the availability of carbohydrate stores with starvation in the thyroidcctomized rats could be responsible for their fast call for lipid utilization. The slower response to fasting in the hyperthyroid animals is probably a consequence of their reduced amount of endogenous substrates to be mobilized.