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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, hyperphosphatemla, and metabolic acidosis. In addition, the loss of nephron mass leads to decreased synthesis of 1,25 dihydroxy vitamin D, which results in decreased calcium absorption from the gastrointestinal tract While transplantation corrects many of these metabolic complications leading to asteodystrophy, the addition of corticosteroids, and preexisting hyperparathyroidism may nullify the benefits of a well functioning graft on bone density. A retrospective review of bone density and markers of bone metabolism was undertaken in 46 kidney transplant patients, transplanted between December 1994 and November 1996. In the patients studied 19 (41%), and 26 (57%) were black. The cause of end stage renal disease, as chronic hypertensive glomerulosclerosis in 31 (67%), polycystic kidney disease in 6 (13%), IgA nephropathy in 2 (4%), pyelonephritis in 2 (4%), chronic reflux in 2 (4%). FSGS in 2 (4%), CYA toxicity secondary to a previous heart transplant in 1 (2%), and Lupus in 1 (2%). Twenty-six (57%) required long term pre-transplant HD 8 (17%) were treated with CAPD, 3 (7%) received both, and 9 (20%) required no dialysis before transplantation, and 39 (85%) received cadaveric kidneys.
Immunosuppression consisted of CYA or FK, AZA or MMF, all patients were taking prednisone. Patients were routinely started on elemental calcium (mean dose 1081 + 107 mg/day) and vitamin D (584 + 72 units/day) supplementation immediately post-transplant. Bone density did not change significantly 6 months post-transplant, but there was a significant decrease at the level of the lumbar spine 12 months post-transplant. The mean bone density of the lumbar spine decreased from 1.26 to 1.22 gm/cm2 (p=O.28), Z score 0.51, to -0.28 (p=O.O3); femoral neck decreased from 0.99 to 0.92 gm/cm2 (p=O.17), Z score -0.2 to -0.70 (p=O.O9), ward's triangle decreased from 0.88 to 0.86 gm/cm2 (p=O.48), Z-score -0.04 to -0.47 (p=O.17) The mean pyridinoline crosslinks decreased from 69.0 to 49.7 pmoles/umole-creatinine (p=O.O03), deoxypyridinoline crosslinks decreased from 18.5 to 13.7 pmoles/umole-creatine (p=O.O4), intact parathyroid hormone decreased from 117.6 to 78.9 pgm/ml (p=O.OO2) and bone specific alkaline phosphatase increased from 12.05 to 13.9 microgm/L (p=O.35) twelve months post-transplant. There were no reported fractures during the study period. In conclusion, a well functioning kidney resulted in B decrease of intact-PTH to recommended levels, and normalization of bone metabolytes pyridinoline and deoxypyridinoline crosslinks at twelve months post-transplant. However, there was still a significant loss of bone density at 1 year after transplantation. Only 3 patients had bone densities below the fracture threshold of 1.O gm/cm2 at the level of the lumbar spine, and bone loss was less than previously reported in kidney transplant patients. More aggressive and/ or specific interventions to attempt to normalize bone density are warranted.
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