Elevated serum parathyroid hormone (PTH) is an important complicated phenomenon in patients with chronic kidney disease (CKD). Emerging evidence indicates the involvement of PTH in organ fibrosis, and suppression of PTH by cinacalcet (CINA) ameliorates the progression of fibrotic disorders. However, the underlying mechanisms are largely unknown. The endothelial-to-mesenchymal transition (EndMT) has been shown to be an important mechanism involved in renal fibrosis. The present study aimed to investigate whether CINA treatment attenuated renal EndMT in rats with adenine-induced chronic renal failure (CRF). Compared with the control group, serum PTH was significantly higher in the CRF group and was suppressed after CINA treatment. The serum calcium, phosphorus and calciumxphosphorus product levels were similar in the CRF group and the CINA-treated CRF group. Renal collagen accumulation was significantly increased in the CRF group which was markedly ameliorated by CINA treatment. The expression of the endothelial marker, CD31 was significantly downregulated in rats with CRF, while the expression of the mesenchymal markers, fibroblast specific-protein (FSP1) and α-smooth muscle actin (α-SMA) was markedly upregulated. These changes were inhibited by CINA treatment. The protein levels of these EndMT-related markers were strongly correlated with serum PTH concentrations. Furthermore, in vitro study showed that PTH could significantly increase the expression of FSP1 and α-SMA and decrease CD31 in mRNA and protein levels in a concentration- and time- dependent manner. In conclusion, our study suggested that reducing serum PTH by CINA treatment could attenuate renal fibrosis via suppression of EndMT in the adenine-induced CRF rat model.