Suppression of thyroid profile during roxadustat treatment in chronic kidney disease patients.

Renal anaemia is a common complication of chronic kidney disease (CKD) and the severity of anaemia increases with the deterioration of renal function [1]. Anaemia is known to be associated with increased morbidity and mortality of cardiovascular disease [2]. Roxadustat is a new oral prolyl hydroxylase domain (PHD) protein inhibitor that is extensively used for the treatment of anaemia in CKD patients [3–7]. The most common side effects reported in clinical trials are high blood pressure, myocardial infarction, heart failure, infections and thrombosis. So far, only two case reports of Roxadustat-induced suppression of thyrotropin secretion in haemodialysis (HD) patients with comorbidity of primary hypothyroidism have been described [8, 9]. Moreover, low thyroid hormones in patients with CKD have been related to a higher risk of cardiovascular disease and all-cause mortality [10–14]. However, whether suppression of the thyroid profile is caused by roxadustat treatment itself remains unclear. Our objective was to evaluate the effects of roxadustat/erythropoietin (EPO) on thyroid stimulating hormone (TSH) and thyroid hormone levels in CKD patients without primary hypothyroidism.