Purpose of reviewOsteoporosis is the most prevalent bone disorder in the general population, particularly in the middle and older age groups. Although more than half of the prevalent dialysis population is within these age groups, little concern has been given to the possible role of estrogen deficiency in the pathogenesis of bone disease in end-stage renal disease. The purpose of this review is to summarize the recent published evidence that supports a potential role of the postmenopausal state in the pathogenesis of bone disease in end-stage renal disease and their implications for treatment.Recent findingsRecent studies have shown that although the risk factors for fracture in end-stage renal disease are similar to the general population, the incidence is three to fourfold higher. The high prevalence of older population, the frequently observed premature amenorrhea and early menopause in dialysis patients may play a role. Similarly, the proportion of end-stage renal disease women receiving hormone replacement therapy is at least three times lower than the general population. Recent evidence on the risk of hormone replacement therapy should caution about its use in end-stage renal disease patients. New evidence suggests that selective estrogen receptor modulators may increase bone mass without significant secondary effects. Other alternatives, such as the use of bisphosphonates, should be considered with caution due to the risk of excessive suppression of bone turnover, worsening or favoring the development of adynamic bone disease.SummaryOsteoporosis should be recognized as an important entity that may modify the current conception of renal osteodystrophy in postmenopausal patients with end-stage renal disease. Further clinical studies are needed in order to propose strategies that may reduce the impact of postmenopausal osteoporosis in the dialysis population.