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Anion gap can be classified as either high, normal or, in rare cases, low. Laboratory errors need to be ruled out whenever anion gap calculations lead to results that do not fit the clinical picture. Methods used to determine the concentrations of some of the ions used to calculate the anion gap may be susceptible to very specific errors.
Elevated protein (albumin, globulins) may theoretically increase the anion gap but high levels are not usually encountered clinically. Hypoalbuminaemia, which is frequently encountered clinically, will mask an anion gap. As a rule of thumb, a decrease in serum albumin by 1 G/L will decrease the anion gap by 0.25 mmol/L [citation needed]
Albumin is an acute negative phase respondent and not a reliable indicator of nutrition status. [10] Low albumin levels can also indicate chronic malnutrition from protein losing enteropathy. [3] This is often caused or exacerbated by ulcerative colitis, [11] but can also be seen in cardiac disease and systemic lupus erythematosus. [3]
Result 1: if there is a normal anion gap acidosis, the (AG – 12) part of the equation will be close to zero, the delta ratio will be close to zero and there is no mixed acid–base disorder. Your calculations can stop here. A normal anion gap acidosis (NAGMA) has more to do with a change in [Cl −] or [HCO − 3] concentrations.
The serum anion gap is useful for determining whether a base deficit is caused by addition of acid or loss of bicarbonate. Base deficit with elevated anion gap indicates addition of acid (e.g., ketoacidosis). Base deficit with normal anion gap indicates loss of bicarbonate (e.g., diarrhea).
Urine NH 4 + is difficult to measure directly, but its excretion is usually accompanied by the anion chloride. A negative urine anion gap can be used as evidence of increased NH 4 + excretion. In a metabolic acidosis without a serum anion gap: A positive urine anion gap suggests a low urinary NH 4 + (e.g. renal tubular acidosis).
Other causes [citation needed] Ingestion of ammonium chloride, hydrochloric acid, or other acidifying salts; The treatment and recovery phases of diabetic ketoacidosis; Volume resuscitation with 0.9% normal saline provides a chloride load, so that infusing more than 3–4L can cause acidosis; Hyperalimentation (i.e., total parenteral nutrition)
Hyperparathyroidism – can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis. Patients with hyperparathyroidism may have a lower than normal pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a normal anion gap. [3]