There are well-established interactions between the thyroid and the kidney. Thyroid hypofunction is associated with reduced renal plasma flow and hypothyroidism is highly prevalent in chronic kidney disease; however, less is known about the thyroid-kidney axis in the euthyroid state.
To study the association of thyroid function with renovascular parameters in a well phenotyped cohort of euthyroid normotensive and hypertensive individuals.
Cross sectional study, the HyperPATH Consortium.
Multi-center study in five US and European academic institutions.
789 individuals aged 18-65 years with serum TSH 0.4-5.5 mIU/L. Subjects with uncontrolled or secondary hypertension or on medication affecting the hypothalamus-pituitary-thyroid axis were excluded.
Hemodynamic parameters including renal plasma flow, thyroid function testing and the Thr92Ala deiodinase 2 polymorphism were assessed in the setting of liberal and restricted salt diet.
We searched for associations between thyroid function and renovascular parameters and accounted for confounding factors, such as older age, hypertension and diabetes.
Serum TSH was inversely associated with renal plasma flow assessed in the setting of both liberal and restricted salt diets. This association remained significant and independent when accounting for confounding factors, whereas free thyroxine index (fTI) and the Thr92Ala polymorphism, associated with lower deiodinase 2 catalytic activity and disrupted thyroid hormone tissue availability, were not independently associated with renal plasma flow. Serum TSH remained an independent predictor of renal plasma flow on a liberal salt diet when the analysis was restricted to healthy young individuals.
Serum TSH levels, but not fTI nor the Thr92Ala deiodinase 2 polymorphism, were independently inversely associated with renal plasma flow in individuals of the HyperPATH Consortium. These findings suggest a direct interconnection of TSH and renovascular dynamics even with TSH within reference range, warranting further investigation.

© The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.