Chronic renal failure affects the secretion of pituitary glycoprotein hormones by mechanism(s) that are still unknown. In this study, we evaluated serum concentrations of TSH, free thyroid hormones (FT4, FT3), LH, FSH, testosterone (T), and α-subunit (α-SU) in 25 uremic patients (19 males and 6 females), both in basal conditions and after stimulatory and inhibitory tests. Basal TSH levels were in the normal range, while FT4 and FT3 were significantly lower than in controls. Basal LH and FSH levels were clearly elevated. The LH levels measured by RIA were significantly higher than those measured by a “two-site” IRMA (48.9±16.5 vs 18.0±8.6 U/L) due to α-SU cross-reactivity in RIA. FSH bioactivity was normal in all patients. Serum T was normal in all but 3 males, without any correlation with LH and FSH levels. Serum α-SU concentrations were significantly elevated (5.5±3.0 vs 0.4±0.2 μg/L). Of 17 patients, the TSH response to TRH was normal in 9 and impaired in 8, whereas α-SU response was normal in 5 and impaired in 12. In 8 male patients, TRH plus GnRH caused a normal LH and FSH response in 4 patients, while the increase of α-SU was normal in only one patient and significantly lower than expected in subjects with comparable basal α-SU levels in the remaining 7. In 2 patients, the combined suppression test with T undecanoate and T3 completely blocked TSH secretion and reduced both LH and FSH release by 30%, while serum α-SU levels did not change. The present data 1) confirm that pituitary glycoprotein hormone secretion in patients with chronic renal failure is altered, 2) demonstrate the existence of an uncontrolled hypersecretion of α-SU and, finally, 3) show that circulating FSH molecules posses normal bioactivity.
- Chronic renal failure
- FSH bioactivity.
- immunometric assays for gonadotropin measurement
- pituitary glycoprotein hormones
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism