Endocrine Abstracts

The aim of this study was to investigate the contribution of thyroid and parathyroid glands dysphunction to the arterial hypertension ethiology in elderly patients suffering from hronic renal failure.

In 34 patients, average age of 67 years (range: 65–68), with glomerular filtration rate (GFR, ^99mTcDTPA) <60 ml/min, as well as the creatinine clearence (Cockcroft) values between 60 and 30 ml/min, thyroid gland function was analysed by thyrotropin releasing hormone (TRH, 200 μg/ml iv).

In 18 out of 34 patients (53%) stimulated TSH response in 20th and 60th minutes were elevated (28 mU/l±8 and 56 mU/l±12 respectively), that characterize the primary hypothyroidism, with peak of free thyroxine serum value in 60th minute of 11.8±2.6 pM/l as typical quality of lower fast thyroid gland reserve.

Elevated inorganic phosphates (1.72±0.8, range: 1.56–1.88 mM/l) were confirmed in 28 out of 34 (82%) patients, lower 25OHD₃ (42±8.4 (X±S.E.), range: 34–58 nM per litre) and secondary hyperparathyroidism (PTH: 132 pg/ml±12, range: 102–186). In 11/28 (39%) suffering from hyperparathyroidism, the primary hypothyroidism was established.

Elevated ionized serum calcium (28/34 patients: 1.36±0.12 mM per litre, range: 1.32–1.52), followed lower serum magnesium (0.82 mM/l±0.12, X±S.E.).

In 76% (26/34) people suffering from secondary hyperparathyroidism as well as in 67% (12/18) those with primary hypothyroidism arterial hypertension have been confirmed (TA 160/100, range 145–180 for systolic and 90–110 for dyastolic value respectively).

Chronic, progressive renal failure influence both the thyroid and parathyroid glands function, contributing to hypothyroidism, secondary hyperparathyroidism and arterial hypertension, as well as to the blood vessels atheromatosis and calcifications.