Abstract

ABSTRACT Abnormalities of thyroid and pituitary function are well recognized in patients with end-stage renal failure. We have investigated the influence of varying degrees of renal insufficiency on serum thyroid (total thyroxine, TT4; total 3,5,3′-triiodothyronine, TT3, and 3′,5′,3′-triiodothyronine, reverse T3) and pituitary (thyrotrophin, TSH; growth hormone, GH; prolactin, PRL) hormone levels before and after 200 μg thyrotrophin releasing hormone (TRH) iv administration. Patients with mild renal insufficiency (= group 1, plasma creatinine (Cr) > 1.3 mg% but < 3.0 mg%) had normal basal and TRH-stimulated hormone concentrations. In patients at a more advanced stage of the disease (= group 2; Cr > 3.0 mg % but < 7.0 mg %) basal hormone concentrations were also normal. In contrast to the normal group, where no GH reaction to TRH could be detected, GH serum concentrations increased in these patients after TRH. The TT3 and PRL response to TRH remained normal. The TSH reaction to TRH was blunted in four, normal in two and exaggerated in one patient. Patients with end-stage renal failure (= group 3; Cr > 7.0 mg%) had significantly decreased basal TT3 concentrations but a normal TT3 response to TRH. Basal TT4, TT3 and TSH concentrations were normal. The TSH reaction was blunted in four and normal in three patients. The mean basal GH was elevated, albeit not significantly different from the control mean value. The GH increase after TRH was even more pronounced than in group 2. Basal PRL concentrations were significantly increased, but maximal differences between basal and TRH-stimulated concentrations were not significantly different from control. Our data suggest that changes in the pituitary and hypothalamic control of GH are an early consequence of renal insufficiency. Alterations in thyroid function occur simultaneously on the pituitary – hypothalamic and peripheral level at a more advanced stage of the disease. PRL basal levels increase with decreasing renal function. In contrast to other studies we could not observe any significant influence of uraemia on the TRH-stimulated PRL reserve of the pituitary.

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