Dear Editor, We read with interest the article by Lindner et al. [1], where it is suggested that hypernatremia can lead to an increase in standard base excess (SBE). In this study, base excess caused by changes in sodium is 4.1 mmol/L when peak sodium is achieved. At the same time, no change in base excess due to chloride changes is seen from last normal to peak sodium levels. These variations in base excess were calculated taking into account normal values for sodium and chloride. While sodium has a wide normal range of values (135–145 mmol/L), the authors choose 140 mmol/L as a normal value. It is more difficult to determine a normal value for chloride levels, mainly in patients with hypernatremia. The authors choose to correct chloride using the Nanormal ? /Na ratio, taking the assumption that the Cl/ Na ratio remains constant in sodium disorders. However, other studies [2, 3], have demonstrated that the sodium–chloride difference is more accurate than the Cl/Na ratio to identify acid–base disorders. This approach can hide the effect of chloride in SBE changes. The physicochemical approach states that an apparent strong ion difference (SIDa) is a determinant of acid base status and not the variation of an isolated ion. Using this principle, another interpretation of the findings presented by Lindner et al. can be that a failure by chloride to augment in the same proportion of sodium level can lead to metabolic alkalosis in patients with hypernatremia, maintaining what has been proposed by Luke and Galla when they suggested the term chloride depletion alkalosis [4]. To investigate which ion is associated with SBE, we analyzed partial data from a prospective study with patients admitted at emergency department. We obtained signed informed consent from the patients, and the protocol was approved by the local ethics committee. We included 312 patients (61.8 % males) with a mean age of 58.2 ± 12.1 years. Arterial blood samples were collected at emergency department. Overall, 38 (12.2 %) patients had hypernatremia and only 5 hypernatremic patients had had a positive SBE. Mean SBE in hypernatremic patients was not higher than in those with normal sodium levels (-7.58 ± 4.68 vs. -6.82 ± 4.06 mmol/L, p = 0.556). On the other hand, when patients were divided according to chloride levels, patients with absolute hypochloremia and no hypernatremia (serum chloride \95 mmol/L, n = 39) had a higher SBE than others (-4.5 ± 7.29 vs. -7.38 ± 4.60 mmol/L, p = 0.02). When all patients were analyzed regarding the association of physicochemical determinants of acid base status with SBE (Table 1), there was no association between sodium levels and SBE, while chloride level is associated with SBE even after controlling for other determinants of acid base status. Hypernatremia at emergency department is generally due water deficit, while hypertonic solutions can be the main responsible in ICU patients. Although not explored by Lindner et al., expansion solutions are generally rich in chloride with a SID near zero, favoring a state of acidosis