Several studies have indicated that bone alterations after
transplantation are heterogeneous. Short-term studies after
transplantation have shown that many patients exhibit a pattern consistent with adynamic
bone disease. In contrast, patients with long-term
renal transplantation show a more heterogeneous picture. Thus, while adynamic
bone disease has also been described in these patients, most studies show decreased bone formation and prolonged mineralization lag-time faced with persisting
bone resorption, and even clear evidence of generalized or focal
osteomalacia in many patients. Thus, the main alterations in bone remodeling are a decrease in bone formation and mineralization up against persistent
bone resorption, suggesting defective osteoblast function, decreased osteoblastogenesis, or increased osteoblast death rates. Indeed, recent studies from our laboratory have demonstrated that there is an early decrease in osteoblast number and surfaces, as well as in reduced bone formation rate and delayed mineralization after
transplantation. These alterations are associated with an early increase in osteoblast apoptosis that correlates with low levels of serum
phosphorus. These changes were more frequently observed in patients with low turnover bone disease. In contrast, PTH seemed to preserve osteoblast survival. The mechanisms of
hypophosphatemia in these patients appear to be independent of PTH, suggesting that other phosphaturic factors may play a role. However, further studies are needed to determine the nature of a phosphaturic factor and its relationship to the alterations of bone remodeling after
transplantation.