Post-Transplant Osteodystrophy in the Era of the K/DOQI Guidelines

George Saab, Suresh Mathew, Lala R. Chaudhary, Keith A. Hruska

Research output: Contribution to journalReview articlepeer-review


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.

Original languageEnglish
Pages (from-to)651-663
Number of pages13
JournalDialysis and Transplantation
Issue number11
StatePublished - Nov 2003


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