The Anion Gap

Oh, Man S.; Carroll, Hugh J.

doi:10.1056/nejm197710132971507

Cited by 266 publications

(68 citation statements)

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“…The first step is to rule out a wide anion gap type of metabolic acidosis that is masked by a process leading to a lower than normal baseline value for the plasma anion gap [2], The most common cause for an abnormally narrow plasma anion gap is hypoalbuminemia (albumin accounts for the vast major ity of the normal anion gap) [3]. Rarer causes are the presence of unmeasured cations (cationic proteins as in certain types of multiple myeloma) [4] or a lab problem that has led to an overestimation of the chloride concen tration (other halides or hyperlipemia confounding the turbidometric chloride analysis) [5,6].…”

mentioning

confidence: 99%

Urine Ammonium: The Key to the Diagnosis of Distal Renal Tubular Acidosis

Halperin

Richardson

Bear

et al. 1988

Nephron

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mentioning

confidence: 99%

Urine Ammonium: The Key to the Diagnosis of Distal Renal Tubular Acidosis

Halperin

Richardson

Bear

et al. 1988

Nephron

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“…As seen in table 1, for the patients with either normal or high serum tCO 2 , there was a virtually identical ratio of the change in anion gap (¢ anion gap) to the ¢ (albumin), 1.46 and 1.45, respectively. In contrast, for the low serum tCO 2 group this ratio was 1.89.…”

Section: Resultsmentioning

confidence: 79%

“…0.05). For these patients the anion gap was better correlated with the serum tCO 2 Comparison of the mean anion gaps in the patients in each tCO 2 group with the highest (13.5 g/dl) and lowest (!2.2 g/dl) quartiles for serum albumin levels ( fig. 1) shows a statistically significant difference in all three groups.…”

Section: Resultsmentioning

confidence: 90%

“…For patients with low serum tCO 2 , adding the r 2 values, which measure predictability, individually relating tCO 2 and ¢ (albumin) to anion gap nearly equals the r 2 for both parameters taken together: For tCO 2 versus anion gap r = 0.63; for ¢ (albumin) versus anion gap r = 0.26, and for both tCO 2 and ¢ (albumin) versus anion gap r = 0.71 (0.63) 2 + (0.26) 2 G (0.71) 2 , as 0.40 + 0.07 = 0.47, which is close to 0.50. This additive predictability suggests that in Fig.…”

Section: Discussionmentioning

confidence: 99%

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A Simple Estimate of the Effect of the Serum Albumin Level on the Anion Gap

Carvounis

Feinfeld²

2000

Am J Nephrol

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Background: The serum anion gap (serum [Na⁺]-Cl^-]-[CO₂]) is still the first-line approach to metabolic acidosis. However, while it is generally acknowledged that hypoalbuminemia mandates a downward adjustment of the expected anion gap, a specific correction factor for the anion gap in the face of low serum albumin has never been demonstrated. Methods: We reviewed initial laboratory data from 432 consecutive patients admitted or transferred to the medical intensive care unit at Nassau County Medical Center over a 6-month period and correlated the serum albumin with the anion gap and the serum [tCO₂] using multivariate analysis. We looked at the anion gap as a function of (albumin), the difference between normal and actual serum albumin, defined as 4.0 - measured serum albumin g/dl. We also assessed [tCO₂] as an independent variable. Results: For patients with normal or high serum tCO₂, the ratio of change in anion gap ( anion gap) to (albumin) was 1.46 and 1.45, respectively. For patients with serum tCO₂ <22 mEq/l this ratio was 1.89. In the latter group, anion gap was best predicted taking both (albumin) and serum tCO₂ into account: anion gap = 36.2 - serum tCO₂ - 2.3* (albumin) (r = 0.71, p < 0.0001). Conclusion: For intensive care patients with normal or high serum tCO₂ (>21 mEq/l) a simple bedside adjustment of the anion gap by subtracting 1.5 times the difference between measured serum albumin and the 'normal' level of 4.0 g/dl gives a close estimate of the actual anion gap. For intensive care patients with serum tCO₂ <22 mEq/l, correction of the anion gap is well predicted by adding about twice the (albumin) to the calculated gap.

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“…Little has been documented as for the degree of acidosis of those hyperchloremic patients, tansient or persistent, in comparison with the normochloremic patients in the similar clinical stage. If a possible mechanism of hyperchloremia were a great loss of bicarbonate as sodium bicarbonate followed by subsequent retention of sodium as sodium chloride (Oh and Carrol 1977) similar to the renal tubular acidosis even in an advanced stage of chronic renal failure, hyperchloremic patients would likely be more acidemic than normochloremic patients in a similar clinical stage. The present study was, therefore, undertaken to examine the electrolyte and acid base composition of the steady state hyperchloremic and normochloremic renal failure patients prospectively.…”

mentioning

confidence: 99%