Background: Persisting disturbances in acid/base homeostasis may have an impact on several metabolic aspects of individuals with a kidney graft, specifically with regard to mineral metabolism and bone.
Methods: We undertook a cross-sectional analysis among 823 unselected patients being transplanted with a functioning renal allograft who had at least one measurement of venous serum bicarbonate available within a 4-year period before May 1, 2005. As a determinate of metabolic acidosis bicarbonate was measured along with serum calcium, phosphate, parathyroid hormone, and other routine serological and epidemiological parameters. Data were assessed according to quartiles of serum bicarbonate and by univariate analysis. A multivariate regression model examined the effects of potential predictors of acidosis.
Results: Mean serum bicarbonate was 22.5+/-4 mmol/L, with 58.1% of the examined renal transplant patients having metabolic acidosis as defined by a venous bicarbonate of <24 mmol/L. Bicarbonatemia was highly associated with serum parathyroid hormone, phosphate, and calcium but also with renal graft function (determined as calculated glomerular filtration rate). Multiple stepwise regression analysis revealed age, glomerular filtration rate, parathyroid hormone, and albumin to be the strongest predictors of serum bicarbonate concentration. Therapy with any calcineurin inhibitor was not associated with an increased likelihood of acidosis (odds ratio 1.04), but a significant difference was found between cyclosporine A and tacrolimus, which had an attributed odds ratio for acidosis of 0.6 and 1.8, respectively.
Conclusions: Metabolic acidosis is highly prevalent among an unselected cohort of renal transplant patients. A clear association exists between the severity of acidosis and disturbances of mineral metabolism. Thus, persisting acid/base disorders may accentuate bone disease in a setting with other factors predisposing for posttransplant osteopathy.