Adynamic bone lesion in renal transplant recipients with normal renal function.

Adynamic bone lesion has been defined as low bone turnover, normal or low osteoid volume and decreased bone formation rate (BFR). A prospective cross-sectional study was performed in 16 asymptomatic post-transplant kidney patients with normal renal function, to evaluate low bone mineral density. The mean age of the nine women and seven men was 33.9 +/- 7.3 years, the mean serum creatinine was 1.1 +/- 0.2 mg/dl and the mean creatinine clearance 71.5 +/- 13.8 ml/min/1.73 m2. Six patients received triple immunosuppressive therapy for a period of 10.3 +/- 3.7 months and nine received double therapy. Eighty-four months after renal grafting, we carried out bone densitometry, biochemical markers and bone biopsy. Bone densitometry showed 78 +/- 8.7% and 80.4 +/- 8% for hip and lumbar spine, with a mean Z score of 1.79 +/- 0.72 and 1.88 +/- 0.78 (SD), significantly less than normal in the Hispanic young population for those two regions. Serum PTH (0.83 +/- 0.23 microgram/ml normal range 0.32-0.65), urine cAMP (4.1 +/- 1.3, normal range 0.5-4.7 nmol/mg Cr) and total and nephrogenic fraction (3.1 +/- 1.1, normal range 0.29-2.9 nmol/100 ml GFR) were significantly greater than normal (P < 0.01). The bone biopsy in 12/16 patients showed decreased percentage osteoid area (1.59 +/- 0.86% vs 3.19 +/- 0.82%), percentage mineralized area (13 +/- 4.7% vs 21.03 +/- 3.36%) and bone formation rate (505 +/- 237 vs 1275 +/- 168 microns2/mm2/day), with a P value < 0.05 compared with 10 normal bone biopsies. The remaining four patients exhibited low bone turnover image with normal bone formation rate (1442 +/- 206 microns2/mm2/ day). Iron deposits were demonstrated at the mineralization front in 10/16 patients. No aluminium or amyloid deposits were observed. The histomorphometric results showed the presence of adynamic bone lesion in 12 renal transplant recipients with normal renal function and osteopenia, which explains the low bone density. The long-term use of glucocorticoids and the presence of iron deposits may contribute to this bone lesion. The biochemical markers of bone remodelling showed abnormalities compatible with moderate increase in parathyroid function. The adynamic lesion in the presence of hyperparathyroid function may suggest down-regulation of PTH bone receptors, alterations of the bone microenvironment or both.