TY - JOUR
T1 - Post-Transplant Osteodystrophy in the Era of the K/DOQI Guidelines
AU - Saab, George
AU - Mathew, Suresh
AU - Chaudhary, Lala R.
AU - Hruska, Keith A.
PY - 2003/11
Y1 - 2003/11
N2 - Despite normalization by renal transplantation of the various metabolic abnormalities associated with chronic kidney disease, a variety of bone abnormalities persist. Among these, both high turnover and low turnover states occur. In addition, a significant mineralization defect occurs out of proportion to bone turnover changes. This mineralization defect is manifested as decreased bone mineral density (BMD) on a DEXA scan. Risk factors for this decreased BMD include persistent hyperparathyroidism and the use of glucocorticoids. Other factors, such as post-transplant hypophosphatemia, appear to be associated with osteoblast apoptosis and decreased osteoblast number. Causes of post-transplant hypophosphatemia include persistent hyperparathyroidism, glucocorticoid use, and low vitamin D3 levels. In addition, recent evidence suggests the presence of a circulating phosphaturic factor, or phosphatonin, that may also play a role in post-transplant osteodystrophy and hypophosphatemia. Because of these abnormalities, the current National Kidney Foundation-Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines recommend frequent monitoring of calcium, phosphorus, iPTH, and BMD. The guidelines also recommend phosphorus supplementation for persistent hypophosphatemia and bisphosphonate treatment for significant pre-transplant osteopenia.
AB - Despite normalization by renal transplantation of the various metabolic abnormalities associated with chronic kidney disease, a variety of bone abnormalities persist. Among these, both high turnover and low turnover states occur. In addition, a significant mineralization defect occurs out of proportion to bone turnover changes. This mineralization defect is manifested as decreased bone mineral density (BMD) on a DEXA scan. Risk factors for this decreased BMD include persistent hyperparathyroidism and the use of glucocorticoids. Other factors, such as post-transplant hypophosphatemia, appear to be associated with osteoblast apoptosis and decreased osteoblast number. Causes of post-transplant hypophosphatemia include persistent hyperparathyroidism, glucocorticoid use, and low vitamin D3 levels. In addition, recent evidence suggests the presence of a circulating phosphaturic factor, or phosphatonin, that may also play a role in post-transplant osteodystrophy and hypophosphatemia. Because of these abnormalities, the current National Kidney Foundation-Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines recommend frequent monitoring of calcium, phosphorus, iPTH, and BMD. The guidelines also recommend phosphorus supplementation for persistent hypophosphatemia and bisphosphonate treatment for significant pre-transplant osteopenia.
UR - http://www.scopus.com/inward/record.url?scp=0242626113&partnerID=8YFLogxK
M3 - Review article
AN - SCOPUS:0242626113
SN - 0090-2934
VL - 32
SP - 651
EP - 663
JO - Dialysis and Transplantation
JF - Dialysis and Transplantation
IS - 11
ER -