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A serum test called T50 assesses the overall propensity for calcification of the blood and is associated with cardiovascular outcomes. We aimed to examine T50 over time in kidney transplant recipients and also address any effects of ibandronate. Serum samples taken from kidney transplant patients included in a prospective, randomized placebo controlled study of ibandronate were analyzed in retrospect. Adequate analyses were performed at baseline (approximately 3 weeks after transplantation) in 129 patients, at 10 weeks in 127 patients and at 1 year in 123 patients. There were no statistical differences between ibandronate and placebo treatment in terms of T50 at 10 weeks ( P = .094) or at 1 year ( P = .116). Baseline T50 was a significant covariate ( P < .0001) for T50 scores at 10 weeks and 1 year. In the total cohort, there was a highly significant ( P < .0001) increase in T50 of 26.6% after 10 weeks and T50 remained stable after 1 year. T50 change was inversely correlated to phosphate of −0.515 ( P < .0001) and to change in serum albumin ( P < .03). We found that T50 increased from baseline to 10 weeks after transplantation with no further change after 1 year. Ibandronate had no effect on T50. [ABSTRACT FROM AUTHOR]

Body composition after kidney transplantation is linked to glucose metabolism, and impaired glucose metabolism is associated with increased risk of cardiovascular events and death. One year after transplantation, we examined 150 patients for post-transplant diabetes performing oral glucose tolerance tests and body composition measurements including visceral adipose tissue ( VAT) content from dual-energy X-ray absorptiometry scans. We found that glucose metabolism was generally improved over the first year post-transplant, and that the levels of VAT and percentage VAT of total body fat mass ( VAT%tot BFM) were lowest in those with normal glucose tolerance and highest in those with post-transplant diabetes mellitus. In a multivariable linear regression analysis, 87.4% of the variability in fasting glucose concentration was explained by insulin resistance ( P<.001, HOMA- IR index), beta cell function ( P<.001, HOMA-beta), VAT%tot BFM ( P=.007), and body mass index ( BMI; P=.015; total model P<.001), while insulin resistance ( P<.001) and beta cell function ( P<.001) explained 31.9% of the variability in 2-hour glucose concentration in a multivariable model (total model P<.001). VAT was associated with glucose metabolism to a larger degree than BMI. In conclusion, VAT is associated with hyperglycemia one year after kidney transplantation, and insulin resistance and beta cell function estimates are the most robust markers of glucose metabolism. [ABSTRACT FROM AUTHOR]