Background: While early bone loss after renal transplantation (RT) is well-described, factors affecting the long-term fate of bone have received less attention. Methods: Whole body (WB), lumbar spine (LS) and femoral neck (FN) bone mineral density (BMD) was measured using dual energy X-ray absorptiometry in 132 stable RT patients and repeated in 114 patient after three years. BMD was compared to normal values for age and gender and percentage change/year was calculated. Results: The whole body, lumbar spine and femoral neck BMD% (Z score) was 93.9 ± 8.9 (-0.90 SD), 91.6 ± 14.9 (-0.98 SD) and 87 ± 15.3 (-1.0 SD)%, respectively. Low BMD was associated with low creatinine clearance, repeated graft loss, long dialysis duration, acidosis, hyperparathyroidism, raised alkaline phosphatase, osteocalcin and urinary deoxypyridoline, low 25-OH-vitamin D, and high cyclosporine concentration. Patients with clinical atherosclerosis, hypoalbuminemia, renovascular disease and diabetic nephropathy had lower bone mass, possibly secondary to malnutrition or low physical activity. High bone mass was associated with previous dialysis alfacalcidol therapy. Low bone mass was a marker of increased subsequent mortality. Percentage change/ year was: WB-0.7 ± 1.5**, LS-0.3 ± 2.6, FN 1.0 ± 3.0**, and, corrected for expected loss for age and sex: WB -0.5**, LS 0.0, FN -0.8*. Factors associated with increased loss rates were short RT duration, high prednisone dose, high cyclosporine trough concentration, high PTH, high alkaline phosphatase and high osteocalcin. Marginal detrimental effects of uremia, hypoalbuminemia and hyperphosphatemia were noted. Thiazide treatment seemed to protect against, and furosemide to exacerbate, bone loss, but this may have been related to associated uremia. Patients treated with vitamin D gained bone, while untreated patients with low initial 1,25-vitamin D lost bone. The prevalence of hyperparathyroidism (52%) and hypercalcemia (22%) remained unchanged. Conclusion: While LS BMD stabilizes after RT, there is a continuing loss of WB and FN BMD. The major causes of bone loss are steroid therapy and continous hyperparathyroidism, with no tendency towards spontaneous resolution. Other factors include malnutrition and hypovitaminosis D. Increased vitamin D and calcium therapy should be considered for this patient group, and more aggressive therapy, e.g. parathyroidectomy given for patients with resistant hyperparathyroidism of > 150 ng/1 (* = p < 0.05, ** = p < 0.01).
|Tidsskrift||Nieren- und Hochdruckkrankheiten|
|Status||Udgivet - 1 maj 2005|