Suppression of thyroid profile during roxadustat treatment in chronic kidney disease patients
Yuan Cheng, Qiong Xiang, Tao Cao, Fei Tang, Jia Chen, Dongli Qi, Haofei Hu, Haiying Song, Zheyi Chang, Ming Ku, Xinglin Chen, Chi Chen, Qijun Wan
Abstract
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.