Metabolic Alkalosis - Urinary Chloride Algorithm
Cl- responsive metabolic alkalosis
• Kidney loss of Cl-
- Remote use of loop or thiazide diuretics
- Post-hypercapneic metabolic alkalosis
• Loss of Cl- outside the kidneys
- Gastrointestinal: Vomiting/nasogastric suction, Congenital chloride diarrhea
- Sweat: Cystic fibrosis
Cl- resistant metabolic alkalosis
• Normal/low blood pressure: Active diuretic use, Bartter syndrome, Gitelman syndrome, Hypomagnesemia
• Hypertension: Increased mineralocorticoid or mineralocorticoid-like effect
Normal gap metabolic acidosis
• Chronic diarrhea
• Kidney tubular acidosis
Anion gap metabolic acidosis
• Diabetic ketoacidosis
• Starvation ketoacidosis
• Alcoholic ketoacidosis
• D-lactic acidosis
• Chronic salicylate poisoning
Normal acid-base status
• LiCl use
The urine chloride concentration can be used to distinguish between a chloride responsive and resistant metabolic alkalosis. In a normal gap metabolic acidosis due to diarrhea, a high urine chloride isthe result of increased excretion of NH4Cl. Urine chloride is high in kidney tubular acidosis due to acidosis-induced decreased reabsorption of NaCl in the proximal tubule. In the indicated causes of anion gap metabolic acidosis, a high urine chloride is the result of increased excretion of NH4Cl. In these settings, the urine sodium is typically higher than the chloride due to the excretion of sodium and potassium acid salts.
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