Stabilization of bone mass after renal transplant with preemptive care

OSTEODYSTROPHY is a well-known complication of renal insufficiency and failure. The loss of nephron mass and the resultant decreased excretory function leads to an increased retention of toxic metabolites, hyperphosphatemia, and metabolic acidosis. In addition, the loss of nephron mass leads to decreased renal synthesis of 1,25dihydroxy vitamin D3, which causes decreased calcium absorption from the gastrointestinal tract. While transplantation corrects many of these metabolic complications leading to osteodystrophy, the addition of corticosteroids, and preexisting hyperparathyroidism may nullify the benefits of a well-functioning graft on bone metabolism. A prospective approach was undertaken at our institution to provide therapy aimed at decreasing the rate of bone loss after transplantation. Preemptive therapy included: goal of tapering steroids to less than 10 mg per day by the second year post-transplant; routine calcium and vitamin D supplementation; surgical parathyroidectomy when indicated; and hormone replacement in post-menopausal females. Routine bone densitometry by dual energy x-ray absorptiometry (DEXA) and markers of bone metabolism were measured at 1, 6, 12, and 24 months after renal transplant.