Chloride, but not unmeasured anions, is correlated with renal bone disease markers

Many factors are involved in the progression of secondary hyperparathyroidism, including acidosis. Stewart's approach has made it possible to identify real determinants of acid-base status, making chloride a real etiological factor of acid-base disturbances. In addition, it has allowed the quantification of the components of these disturbances, especially the unmeasured anions. We performed a cross-sectional study to quantify each component of acidosis in hemodialysis patients and correlate them with renal bone disease biochemical markers.

Sixty maintenance hemodialysis patients and 14 controls were enrolled in this study. Each acid-base determinant was quantified and correlated in multivariate regression with intact serum parathormone and bone-specific alkaline phosphatase, adjusting to other variables.

Hemodialysis patients were more acidotic than controls, mainly due to the retention of unmeasured anions, hyperchloremia and hyperphosphatemia. In multivariate regression analysis, the only acid-base determinants independently correlated with bone markers were chloride, calcium and phosphorus (beta=0.537, beta=-0.256 and beta=-0.242, respectively). Although unmeasured anions were a major component of acidosis, they had no correlation with these markers.

Although unmeasured anions are considered the main component of acidosis in hemodialysis patients, serum chloride was the only acid-base determinant correlated with bone markers.