The Authors Reply

Abstract

We respectfully disagree with the comments made by Dr Berend.1.Berend K. Assessing acid–base disorders. Letter to the editor.Kidney Int. 2010; 77: 744Abstract Full Text Full Text PDF PubMed Scopus (1) Google Scholar The study he quoted to counter our ‘assumption that the chloride level is normal in high anion gap acidosis’ failed to detect absolute hypochloremia in patients with this condition.2.Durward A. Skellett S. Mayer A. et al.The value of the chloride: sodium ratio in differentiating the aetiology of metabolic acidosis.Intensive Care Med. 2001; 27: 828-835Crossref PubMed Scopus (86) Google Scholar Thus, normochloremic acidosis is an appropriate and standard term for high anion gap acidosis. This term allows differentiation of high anion gap acidosis from the normal anion gap acidosis that features hyperchloremia. The need to adjust the plasma anion gap for the anionic charge of plasma albumin, a simple computation performed routinely by clinicians, is unrelated to the proposed effect of albumin itself on acid–base status. As stated in our paper,3.Adrogué H.J. Gennari F.J. Galla J.H. et al.Assessing acid–base disorders.Kidney Int. 2009; 76: 1239-1247Abstract Full Text Full Text PDF PubMed Scopus (75) Google Scholar there is no evidence that the body, and in particular, the liver, regulates albumin to maintain acid–base balance. A role of albumin itself in the regulation of acid–base status is accepted by neither the physiological nor the base-excess approach. Dr Berend claims that our assessment of example 2 is probably incorrect because we did not consider that a decrease in plasma albumin by 1 g/dl results in an increase in bicarbonate by 2.8 mmol/l. As this claim is based on a simple associative relationship,4.Omron E.M. Comparative quantitative acid-base analysis in coronary artery bypass, severe sepsis, and diabetic ketoacidosis.J Intensive Care Med. 2005; 20: 317-326Crossref PubMed Scopus (6) Google Scholar it provides no support for a cause-and-effect relationship of albumin to plasma bicarbonate. Finally, the lack of definition of the secondary ventilatory response to metabolic acid–base disorders is indeed one of the limitations of the physicochemical approach, but certainly not its most serious drawback, as Dr Berend asserts.