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mortality, especially in dialysis patients. The incidence of fractures was reported to be 1.8 to eight times higher in dialysis patients compared to the regional general population [1]. Dialysis patients with fracture showed a fourfold higher mortality and hospitalization rate compared to patients without fracture. Fractures are definitely related to osteoporosis in postmenopausal women and are also common in women undergoing chronic hemodialysis (HD). Older age, female sex, and low serum albumin concentration were all predictors for new fracture risk in the Dialysis Outcomes and Practice Patterns Study (DOPPS, 2002–2004) [2]. Vascular calcification (VC) is a good predictor for cardiovascular disease, morbidity, and mortality. VC is positively associated with vertebral fractures and is inversely correlated with bone mineral density (BMD) in populations without chronic kidney disease [3]. Lower serum fetuin-A level and presence of VC on thoracic and lumbar lateral views were independently linked to a higher risk of incident fracture in a Taiwanese prospective, observational cohort study of 685 dialysis patients [4]. Higher VC score was independently associated with increased risk of fracture in 341 HD patients. Elderly and female dialysis patients also had higher fracture risk based on a retrospective cohort study [5]. Therefore, VC is an important predictor of possible fracture, especially in postmenopausal women on dialysis. Estrogen deficiency after menopause induces a decrease in BMD by stimulating differentiation of osteoclast precursors and activating mature osteoclasts. Osteoporosis related to lower serum estradiol level is associated with high risk of fracture. Estrogen can prevent VC by inhibiting receptor activator of nuclear factor kappa B ligand (RANKL) signaling pathways. Estrogen replacement reduced bone morphogenetic protein-2, which is a calcification inducer, and increased the matrix gla protein, which is a calcification inhibitor, in both in vitro and in vivo studies. Endogenous estrogens consist of estrone, 17β-estradiol (E2), and estriol. E2 is the main and active form and works via estrogen receptor-alpha (ERα) and -beta. Growth arrest-specific gene 6, a member of the vitamin K-dependent protein family, is a regulatory target of E2/ER-α signaling in vascular smooth muscle cell calcification. Long-term E2 supplementation was associated with lower coronary artery calcium score in postmenopausal women aged 50 to 59 years compared to those who received placebo. Estradiol concentration is usually low in menopausal women treated with dialysis compared to the general population. Therefore, it is suspected that postmenopausal dialysis patients have high risk of VC and fracture. In this issue of Kidney Research and Clinical Practice, Nam et al [6] showed that the aortic calcification index (ACI) on abdominal computed tomography was independently associated with incident fracture in 593 dialysis patients (male, n = 328; female, n = 265). The fracture Sex hormones impact vascular calcification and fracture in dialysis patients