Low triiodothyronine alters flow-mediated vasodilatation in advanced nondiabetic kidney disease
American Journal of Nephrology, cilt.33, sa.1, ss.25-32, 2011 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 33 Sayı: 1
- Basım Tarihi: 2011
- Doi Numarası: 10.1159/000322581
- Dergi Adı: American Journal of Nephrology
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.25-32
- Anahtar Kelimeler: Triiodothyronine, free, Chronic kidney disease, Endothelial dysfunction
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Background/Aims: Subclinical or frank hypothyroidism is causally implicated in endothelial dysfunction. Since the plasma concentration of the active form of thyroid hormone, triiodothyronine (T3), is reduced in chronic kidney disease (CKD), where endothelial function is frequently altered, low T3 may be a factor implicated in this disturbance in CKD patients. Methods: We investigated the relationship between flow-mediated vasodilatation (FMD) and thyroid hormones in a series of 217 nondiabetic patients with stage 3-4 CKD. Results: The plasma concentration of free T3 (fT 3) was closely associated with FMD (r = 0.38; p < 0.001). fT 3 was also inversely associated with hemoglobin (r = -0.41; p < 0.001), systolic pressure (r = -0.28; p < 0.001) and the plasma concentration of the endogenous inhibitor of NO synthase, asymmetric dimethylarginine (ADMA; r = -0.18; p = 0.007). However, adjustment for ADMA markedly attenuated the fT3-FMD link, a phenomenon suggesting that raised plasma ADMA, possibly driven by low fT3, at least in part mediates the adverse effects of low T3 on endothelial function in CKD. Conclusions: Low T3 in patients with moderate-to-severe CKD is a marker of endothelial dysfunction. This study sets a solid rationale for designing specific intervention studies aimed at clarifying the nature (causal or not causal) of the endothelial function-T3 link in CKD. Copyright © 2010 S. Karger AG, Basel.