title: Rapid loss of vertebral mineral density after renal transplantation.
abstract: BACKGROUND
  Osteopenia is a major complication of renal transplantation. Immunosuppressive regimens including cyclosporine, which permit the use of lower doses of glucocorticoids, may reduce glucocorticoid-induced osteopenia.
  
  
  METHODS
  We prospectively studied the magnitude, distribution, and mechanism of bone loss in 20 adults who received renal allografts from living related donors, who had good renal function, and who were treated with azathioprine, cyclosporine, and low doses of prednisone. We measured serum biochemical markers of bone metabolism, determined the bone mineral density of the second, third, and fourth lumbar vertebrae and the shaft of the radius, and analyzed the histomorphometric features of iliac bone at the time of transplantation and six months later. Measurements of vertebral mineral density were repeated 18 months after transplantation in 17 of the patients.
  
  
  RESULTS
  After transplantation, the mean serum concentrations of parathyroid hormone, phosphorus, and alkaline phosphatase decreased and the serum calcitriol concentration increased. The mean (+/- SD) bone mineral density of the vertebrae had decreased 6.8 +/- 5.6 percent 6 months after transplantation (P less than 0.05) and 8.8 +/- 7.0 percent 18 months after transplantation. In contrast, the bone mineral density of the radius had increased six months after transplantation (P less than 0.05). The histomorphometric studies showed that the rate of bone formation decreased from 50.5 +/- 44.8 to 23.1 +/- 13.8 microns3 per square micrometer per year (P less than 0.05), and the formation period lengthened from 70 +/- 42 to 146 +/- 144 days (P less than 0.05). Consequently, the amount of bone replaced during a remodeling cycle diminished.
  
  
  CONCLUSIONS
  Osteopenia associated with renal transplantation remains a problem in the cyclosporine era. The loss of vertebral bone in our subjects was due to an imbalance in bone remodeling consistent with a toxic effect of glucocorticoids.
authors.affiliation: Department of Medicine, University of Alabama, Birmingham 35294.
authors.forename: B A
authors.initials: BA
authors.lastname: Julian
authors.forename: D A
authors.initials: DA
authors.lastname: Laskow
authors.forename: J
authors.initials: J
authors.lastname: Dubovsky
authors.forename: E V
authors.initials: EV
authors.lastname: Dubovsky
authors.forename: J J
authors.initials: JJ
authors.lastname: Curtis
authors.forename: L D
authors.initials: LD
authors.lastname: Quarles
mesh_terms: D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D015519:Bone Density / Q000187:drug effects / Q000502:physiology*; D001851:Bone Diseases, Metabolic / Q000209:etiology; D002117:Calcitriol / Q000097:blood; D005260:Female; D006801:Humans; D007085:Ilium / Q000473:pathology; D007165:Immunosuppression Therapy / Q000009:adverse effects; D016030:Kidney Transplantation / Q000009:adverse effects*; D008159:Lumbar Vertebrae / Q000737:chemistry; D008297:Male; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000097:blood; D011183:Postoperative Complications / Q000209:etiology; D011241:Prednisone / Q000009:adverse effects; D011446:Prospective Studies; D011884:Radius / Q000737:chemistry; D013997:Time Factors
chemical_list: D010281:Parathyroid Hormone; D010758:Phosphorus; D000469:Alkaline Phosphatase; D002117:Calcitriol; D011241:Prednisone