Abnormal vitamin D metabolism and loss of bone mass after renal transplantation.

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Osteoporosis is a major complication after renal transplantation. The most important causative factor is the use of corticosteroids, but abnormalities in vitamin D metabolism and persisting hyperparathyroidism could also be involved. The present study examines changes in vitamin D metabolites, intact parathyroid hormone, and bone mineral density (BMD) during the first 2 years after renal transplantation.

Related collections

Most cited references 6

Record: found
Abstract: found
Article: not found

Prevention of corticosteroid osteoporosis. A comparison of calcium, calcitriol, and calcitonin.

N Pocock, Daniel J Birmingham, Tiffany Nguyen … (1993)

Prolonged corticosteroid therapy increases the risk of osteoporosis and fracture. We studied whether corticosteroid-induced osteoporosis could be prevented by treatment with calcium, calcitriol (1,25-dihydroxyvitamin D3), and calcitonin. One hundred three patients starting long-term corticosteroid therapy were randomly assigned to receive 1000 mg of calcium per day orally and either calcitriol (0.5 to 1.0 microgram per day orally) plus salmon calcitonin (400 IU per day intranasally), calcitriol plus a placebo nasal spray, or double placebo for one year. Data on treatment efficacy were available for 92 of these patients. Bone density was measured every four months for two years by photon absorptiometry. There were no significant differences between groups with respect to age, underlying disease, initial bone density, or corticosteroid dose during the first year. Calcitriol (mean dose, 0.6 microgram per day), with or without calcitonin, prevented more bone loss from the lumbar spine (mean rates of change, -0.2 and -1.3 percent per year, respectively) than calcium alone (-4.3 percent per year, P = 0.0035). Bone loss at the femoral neck and distal radius was not significantly affected by any treatment. In the second year, lumbar bone loss did not occur in the group previously treated with calcitonin plus calcitriol (+0.7 percent per year), but it did occur in the group given calcium alone (-2.3 percent per year). The calcitriol group also lost lumbar bone (-3.6 percent per year) but received more corticosteroid in the second year than the other two groups. Calcitriol and calcium, used prophylactically with or without calcitonin, prevent corticosteroid-induced bone loss in the lumbar spine.

0 comments Cited 27 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Cyclosporine bone remodeling effect prevents steroid osteopenia after kidney transplantation.

F Westeel, H Mazouz, F Ezaitouni … (2000)

It is well established that prednisone above 7.5 mg/day may induce osteopenia in association with decreased bone formation. In contrast, the effect of cyclosporine on bone remodeling and bone mineral density (BMD) is controversial. Multiple confounding factors explain this controversy, especially after renal transplantation. Fifty-two renal transplanted patients never exposed to aluminum while on dialysis were selected because they had no rejection and no hypercalcemia for 24 months while being treated with low dose prednisone/cyclosporine A (daily dose at 10 mg and 4.8 mg/kg, respectively, beyond 3 months). Bone remodeling markers (BRMs; plasma osteocalcin, bone and total alkaline phosphatases for formation, and urinary pyridinolines for resorption) were sequentially measured together with plasma creatinine, intact parathyroid hormone (PTH) and 25 OH vitamin D and cyclosporine from day 0 to 24 months. BMD was measured at 3, 6, 12, and 24 months by quantitative computerized tomography (QCT) at the lumbar spine and by double-energy x-ray absorptiometry (DEXA) at this site, as well as at the femoral neck, radius shaft, and ultradistal (UD) radius. Plasma concentrations of creatinine, PTH, and 25 OH vitamin D initially decreased and stabilized beyond three months at 137 micromol/L, 1.5 the upper limit of normal (ULN) and 11 ng/mL, respectively. All BRM increased significantly above the ULN at six months and then decreased. The BMD Z score at three months was low at all sites measured by DEXA and QCT. Follow-up measurements showed stability of absolute value and of Z score at all sites measured by DEXA. A comparison of the lumbar QCT Z score, which was available in 42 patients at 3 and 24 months, showed an increase in 28 and a decrease in 14, so that the increase for the whole group was significant (P < 0.04). Compared with patients with a decreased Z score, those with an increased Z score had significantly higher cyclosporine and lower prednisone dosages and a greater BRM increase at six months, whereas age, sex ratio, and plasma creatinine, PTH and 25 OH vitamin D were comparable and stable from months 3 through 24. The mean trough level of cyclosporine for the first six months was positively correlated to osteocalcin and total alkaline phosphatase increase at six months, and both bone formation and resorption marker increases were significantly correlated to the lumbar QCT Z score increase at 24 months. Combined low-dose prednisone and cyclosporine immunosuppression are associated with a stabilization of BMD measured at all sites with DEXA 3 to 24 months after renal transplantation and with a prevention of age-related loss of vertebral trabecular bone, as shown by the significant increase in lumbar spine QCT Z score. It is suggested that cyclosporine, together with the decrease of prednisone dosage but independent of renal function, PTH, and vitamin D status, contributes to a transient stimulation of bone remodeling at six months, which counterbalances the deleterious effect of prednisone on bone formation and BMD.