Chloride-resistant (Urine chloride > 40 mEq/L)
Retention of bicarbonate – Retention of bicarbonate would lead to alkalosis. Shift of hydrogen ions into intracellular space – Seen in hypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells. In order to maintain electrical neutrality, hydrogen shifts into the    cells, raising blood pH. Hyperaldosteronism – Loss of hydrogen ions in the urine occurs when excess aldosterone (Conns syndrome) increases the activity of a sodium-hydrogen exchange protein in the kidney. This increases the retention of sodium ions whilst pumping hydrogen ions into the renal tubule. Excess sodium increases extracellular volume and the loss of hydrogen ions creates a metabolic alkalosis. Later, the kidney responds through the aldosterone escape to excrete sodium and chloride in urine. Excess glycyrrhizin consumption
Low levels of magnesium in the blood
Severely high levels of calcium in the blood
 Bartter syndrome and Gitelman syndrome – syndromes with presentations analogous to taking diuretics characterized with normotensive patients
Liddle syndrome – a gain of function mutation in the genes encoding the epithelial sodium channel (ENaC) which is characterized by hypertension and hypoaldosteronism. 11β-hydroxylase deficiency and 17α-hydroxylase deficiency – both characterized by hypertension
Aminoglycoside toxicity can induce a hypokalemic metabolic alkalosis via activating the calcium sensing receptor in the thick ascending limb of the nephron, inactivating the NKCC2 cotransporter, creating a Bartters syndrome like effect. Compensation
Compensation for metabolic alkalosis occurs mainly in the lungs, which retain carbon dioxide (CO2) through slower breathing, or hypoventilation (respiratory compensation).
Metabolic alkalosis is a metabolic condition in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations. The condition typically cannot last long if the kidneys are functioning properly. Signs and symptoms
Mild cases of metabolic alkalosis often cause no symptoms. Typical manifestations of moderate to severe metabolic alkalosis include abnormal sensations, neuromuscular irritability, tetany, abnormal heart rhythms (usually due to accompanying electrolyte abnormalities such as low levels of potassium in the blood), coma, seizures, and temporary waxing and waning confusion. Causes
The causes of metabolic alkalosis can be divided into two categories, depending upon urine chloride levels. Chloride-responsive (Urine chloride < 25 mEq/L)
Loss of hydrogen ions – Most often occurs via two mechanisms, either vomiting or via the kidney. Vomiting results in the loss of hydrochloric acid (hydrogen and chloride ions) with the stomach contents. In the hospital setting this can commonly occur from nasogastric suction tubes. Severe vomiting also causes loss of potassium (hypokalemia) and sodium (hyponatremia). The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions (sparing sodium/potassium pumps to prevent further loss of potassium), leading to metabolic alkalosis. Congenital chloride diarrhea – rare for being a diarrhea that causes alkalosis instead of acidosis. Contraction alkalosis – This results from a loss of water in the extracellular space, such as from dehydration.