We read with great interest the article by Carmen Sánchez-Perales et al., recently published in Nefrología.1 In this study, the authors analysed the presence of valvular calcification in patients starting dialysis and its relationship to cardiovascular events and cardiovascular death. We would like to offer some comments on the study.

Valvular calcification may occur in the presence or absence of renal disease. In individuals without renal disease, calcification is usually a result of a pro-inflammatory state caused by other comorbidities such as diabetes, dyslipidaemia, and hypertension. In individuals with chronic kidney disease (CKD), often it cannot be established with certainty whether calcification is due to changes in bone mineral metabolism, inflammation caused by comorbidities, or both.2

In the “methods” section of the study, the authors stated that they measured serum levels of phosphorus, calcium, and parathyroid hormone (PTH). However, calcium and PTH were not included in the univariate analysis. We think that the statistical analysis of these two variables would be relevant, because the studies performed by Streja et al.3 and Floege et al.,4 found that patients with serum values of intact PTH, calcium, and phosphate outside the ranges recommended by the Kidney Disease Outcomes Quality Initiative (KDOQI™)5 (iPTH, 150–300pg/mL; calcium, 2.10–2.37mmol/L; and phosphate, 1.13–1.78mmol/L) had a higher mortality risk than patients with values within these ranges.

In the multivariate analysis by Sánchez-Perales et al., the authors state that the model was adjusted for factors with statistical significance in the univariate analysis and for other factors that were potentially involved in the valvular calcification process. However, it was not clear why variables associated with valvular calcification in patients with CKD (PTH, calcium, and phosphate) were not included.

Finally, whilst the study demonstrates that the presence of valvular calcification is a predictor of mortality, the analysis performed does not establish whether calcification is secondary to atherogenic comorbidities or to an imbalance of bone mineral metabolism. Future studies could further explore this association.