Background Reduced kidney function is a common public health problem that increases risk for a wide variety of adverse outcomes, making the identification of potentially modifiable factors associated with the development of incident chronic kidney disease (CKD) important. Alterations in the hypothalamic-pituitary-thyroid axis have been linked to reduced kidney function, but the association of thyroid function with the development of incident CKD is largely uncharacterized. Methods Concentrations of thyroid stimulating hormone (TSH), free thyroxine (FT4), triiodothyronine (T3) and thyroid peroxidase antibody (TPOAb) were quantified in 12 785 black and white participants of the ongoing community-based prospective Atherosclerosis Risk in Communities study. Thyroid markers and clinical categories of thyroid dysfunction (euthyroidism, combined subclinical and overt hypothyroidism, combined subclinical and overt hyperthyroidism) were also evaluated for their association with reduced kidney function (estimated glomerular filtration rate <60 mL/min/1.73 m 2) at study baseline and with incident CKD over a median follow-up time of 19.6 years. Results Higher TSH and FT4 as well as lower T3 concentrations were strongly and independently associated with reduced kidney function at study baseline. The clinical entities hypothyroidism and hyperthyroidism were also associated with higher odds of baseline reduced kidney function, but this was not significant. However, none of the markers of thyroid function nor different clinical categories of thyroid dysfunction (hypothyroidism, hyperthyroidism or TPOAb positivity) were associated with incident CKD in adjusted analyses. Conclusions Elevated TSH, FT4 and reduced T3 concentrations were associated with reduced kidney function cross-sectionally. The lack of association with the development of incident CKD suggests that altered thyroid function in the general population is not causally related to CKD development, but screening for thyroidal status may be especially relevant in persons with reduced kidney function.
Bibliographical noteFunding Information:
The authors thank the staff and participants of the ARIC study for their important contributions. Reagents for the thyroid assays in the ARIC study were donated by Roche Diagnostics. U.T.S. and A.K. were funded by the Emmy Noether Programme of the German Research Foundation (DFG KO-3598/2-1) and by a grant from the Else Kröner-Fresenius-Stiftung (2013_Kolleg.03), Bad Homburg, Germany (U.T.S.). E.S. was supported by National Insitutues of Health (NIH)/National Institute of Diabetes and Digestive and Kidney Diseases grant R01DK089174. The ARIC study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201100005C, HSN268201100006C, HHSN268201100007C, HHSN 268201100008C, HSN268201100009C, HHSN268201100010C, HHSN268201100011C and HHSN268201100012C), R01HL087641, R01HL59367 and R01HL086694 and NIH contract HHSN268200625226C. Infrastructure was partly supported by grant number UL1RR025005, a component of the NIH and NIH Roadmap for Medical Research.
© The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
- chronic kidney disease
- cohort study
- thyroid disease
- thyroid hormones