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Chloride is the major extracellular anion; it is not actively regulated normally. It reflects changes in sodium; if it changes independent of sodium, this is usually due to an acid–base disorder.
Normal range: 97–110 mmol/L.
With sodium, potassium, and carbon dioxide to assess electrolyte, acid–base, and water balance. Chloride usually changes in the same direction as sodium except in metabolic acidosis with bicarbonate depletion and metabolic alkalosis with bicarbonate excess, when serum sodium levels may be normal.
Metabolic acidosis associated with prolonged diarrhea with loss of sodium bicarbonate
Renal tubular diseases with decreased excretion of hydrogen ions and decreased reabsorption of bicarbonate (“hyperchloremic metabolic acidosis”)
Respiratory alkalosis (e.g., hyperventilation, severe CNS damage)
Excessive administration of certain drugs (e.g., ammonium chloride, IV saline, salicylate intoxication, acetazolamide therapy)
False (methodologic) increase due to bromides or other halogens
Retention of salt and water (e.g., corticosteroids, guanethidine, phenylbutazone)
Some cases of hyperparathyroidism
Diabetes insipidus, dehydration
Sodium loss > chloride loss (e.g., diarrhea, intestinal fistulas)
Prolonged vomiting or suction (loss of hydrochloric acid)
Metabolic acidosis with accumulation of organic anions
Chronic respiratory acidosis
Salt-losing renal diseases
Expansion of extracellular fluid (e.g., SIADH, hyponatremia, water intoxication, CHF)
Alkalosis (e.g., bicarbonates, aldosterone, corticosteroids)
Diuretic effect (e.g., ethacrynic acid, furosemide, thiazides)
Other loss (e.g., chronic laxative abuse)
Direct ISE (ion-selective electrode) measurements do not give the volume displacement error in specimens with high lipid or protein content, as indirect ISE and flame measurements do.
May be slightly decreased after meals; fasting specimen collection is recommended.