Asymmetric dimethylarginine, vascular calcifications and parathyroid hormone serum levels in hemodialysis patients.

摘要

BACKGROUND: Asymmetric dimethylarginine (ADMA)is an endogenous amino acid similar to l-arginine and able to inhibit the enzyme endothelial nitric oxide synthase (eNOS). It is a factor of impaired nitric oxide (NO) synthesis. Serum levels of ADMA in chronic kidney disease (CKD) increase due to defective inactivation and excretion. High ADMA levels are associated with endothelial dysfunction and cardiovascular damage. A linkage between ADMA levels and vascular calcifications of CKD can therefore be hypothesized. This study explores also a possible relation between ADMA and parathyroid hormone (PTH) serum levels, which are known to be linked to increased rates of cardiovascular death. METHODS: The study was carried out in 79 patients on hemodialysis (HD), mean age 59.25 +/- 12 years. In all patients, serum ADMA, PTH, Ca, P, bone alkaline phosphatase (BALP), cholesterol and albumin were measured. In addition, the patients were subjected to multislice computed tomography for heart calcification evaluation. RESULTS: Correlation analysis of ADMA showed a significant relation with total and coronary calcium volumes, HD vintage, body mass index (BMI), cholesterol, serum albumin, PTH, natural logarithm of PTH (LnPTH) and BALP. Multiple regression analysis selected HD vintage, albumin and PTH as predictive variables for coronary calcium volume, while ADMA was excluded. With LnPTH as dependent variable, ADMA, serum calcium and BMI were predictive variables with R2 of 0.37. ADMA as dependent variable was also predicted by PTH, HD vintage, albumin and BMI. CONCLUSIONS: Despite the results of bivariate analysis showing a linkage between ADMA and cardiac and coronary calcifications, regression analysis showed only a spurious association. The strong positive correlation between ADMA and LnPTH, validated by the regression analysis, may suggesta link between ADMA and PTH-derived vascular damage. ADMA levels could be influenced by the severity of hyperparathyroidism and contribute to cardiovascular death linked to PTH of hemodialysis patients.