Low triiodothyronine alters flow-mediated vasodilatation in advanced nondiabetic kidney disease

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.

We investigated the relationship between flow-mediated vasodilatation (FMD) and thyroid hormones in a series of 217 nondiabetic patients with stage 3-4 CKD.

The plasma concentration of free T₃ (fT₃) was closely associated with FMD (r = 0.38; p < 0.001). fT₃ 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.

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.