Renal function changes in patients with subclinical hyperthyroidism: a novel postulated mechanism.

BACKGROUND

Subclinical hyperthyroidism (SCH) is found to be associated with renal dysfunction. Hyperthyroidism is a well-known cause of secondary systolic hypertension. However, the effect of SCH on the kidney and its vasculature is still unknown.

AIM

To assess the presence of renal function changes and renal vasodysfunction in SCH patients and their relation to hypertension.

METHODS

The study included 321 patients with SCH and 80 healthy matched controls. Laboratory investigations included thyroid function tests, anti-TSH receptor antibody (TRAb), creatinine, estimated glomerular filtration rate (eGFR), serum osmolarity (S. Osmol), urine osmolarity (U. Osmol), Fractional Excretion of Sodium (FeNa), Fractional Excretion of Potassium (FeK), copeptin (CPP), and aldosterone/renin ratio (ARR). Ultrasound for the thyroid gland, echocardiography, total peripheral resistance (TPR), flow-mediated dilatation (FMD), and Renal Arterial distensibility (RAD) was also done.

RESULTS

Serum creatinine was significantly lower while eGFR was significantly higher in SCH patients compared to euthyroid subjects (mean 0.59 ± 0.11 mg/dl Vs mean 0.8 ± 0.1 mg/dl, p = 0.001 and mean 128.28 ± 14.69 ml/min/1.73m2 Vs mean 100.49 ± 14.9 ml/min/1.73m2, p = 0.013, respectively). The TPR and FMD showed a significant decrease in SCH group compared to controls (mean 975.85 ± 159.33 mmHg.min/L Vs mean 1120.24 ± 135.15 mmHg.min/L, p = 0.045 and mean 7.03 ± 4.02% Vs mean 13.48 ± 4.57%, p = 0.003, respectively). RAD was significantly higher in hypertensive SCH patients compared to normotensive SCH patients (mean 17.82 ± 2.46 mmHg Vs mean 11.98 ± 3.21 mmHg, p = 0.001).

CONCLUSION

SCH patients showed vascular resistance reduction. Alterations in thyroid hormones and blood pressure could be the driving mechanisms for the change in renal functions in patients with SCH.