Article ID Journal Published Year Pages File Type
3482226 Journal of Laboratory and Clinical Medicine 2006 5 Pages PDF
Abstract

Although “unmeasured” anions contribute to metabolic acidosis in a variety of disease states, they are generally not measured directly but estimated from the calculation of “gaps.” Among the most commonly used method, the anion gap (AG) is not only a function of “unmeasured” anions, but also it is a function of plasma non-carbonate buffers (albumin and phosphate), the plasma pH, and the method of measurement. To clarify the contribution of non-carbonate buffers to the AG, the Figge–Fencl–Waston model of human plasma was applied to laboratory values obtained from two novel populations, patients with nephrotic syndrome and patients with diabetic ketoacidosis (DKA). The model performed adequately, justifying the common clinical practice of correcting the AG for the net protein charge.

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