Recombinant Human Thyrotropin Worsens Renal Cortical Perfusion and Renal Function in Patients After Total Thyroidectomy Due to Differentiated Thyroid Cancer.

Abstract

Background: Although thyrotropin (TSH) receptors are found in many nonthyroid tissues, we know little about the direct action of TSH on these receptors. Patients after total thyroidectomy for differentiated thyroid cancer (DTC) provide an interesting model for studying this issue. The administration of exogenous TSH in patients with an established thyroid state on levothyroxine (LT4) treatment allows us to study the effect of elevated TSH concentrations independent of thyroid status on the function of various organs, including the kidneys. The aim of this study was to assess the effects of the administration of recombinant human TSH (rhTSH) on renal perfusion and glomerular filtration in this group of patients. Methods: The study included 24 patients after total thyroidectomy due to DTC, without concomitant diseases, receiving only LT4 who qualified for radioiodine treatment (RIT). For two consecutive days, the patients received rhTSH and subsequently the RIT. Clinical and biochemical evaluation of thyroid and renal function was carried out before and 24 hours after the second dose of rhTSH and before the RIT. On the sixth day of hospitalization, the patients' glomerular filtration rate was re-evaluated. Kidney perfusion was assessed using color Doppler ultrasound imaging before and 24 hours after the second dose of rhTSH and before the RIT. Results: The administration of rhTSH to patients after total thyroidectomy due to DTC caused significant deterioration of renal perfusion after the second dose of rhTSH before the RIT, which was followed by a significant reduction in glomerular filtration. Furthermore, rhTSH did not significantly affect the hemodynamic parameters that could worsen renal function. Conclusions: This study indicates that TSH alone, independent of thyroid hormone concentrations, can influence renal perfusion and renal function.