Metabolic alkalosis is a common clinical problem encountered by the nephrologist. An understanding of the pathogenesis of this electrolyte disorder, which includes a generative and a maintenance phase, is essential to elucidating the etiology and deciding on the appropriate treatment. Metabolic alkalosis is characterized by an increase in pH, a decrease in [H+], and an increase in [HCO3–]. The generative phase of metabolic alkalosis involves either loss of acid (e.g., gastrointestinal losses), gain of bicarbonate (e.g., antacids), or cellular shift (e.g., hypokalemia). The maintenance phase involves impairment of the renal handling of bicarbonate (decreased glomerular filtration, increased bicarbonate tubular reabsorption). We discuss the different etiologies, such as chloride depletion (e.g., vomiting), potassium depletion (e.g., primary hyperaldosteronism), and hypercalcemic states (e.g., milk-alkali syndrome). This review also discusses the symptoms, diagnosis, and prognosis of metabolic alkalosis. A diagnostic algorithm based on volume status and urine electrolytes will help differentiate the different etiologies. Treatment options are summarized based on chloride-sensitive or chloride-resistant metabolic alkalosis. This review contains 5 figures, 3 tables and 12 references Key words: chloride resistance, chloride sensitivity, generative phase, maintenance phase, metabolic alkalosis, syndromes with metabolic alkalosis