Metabolic Alkalosis: Causes

Pathogenesis

In metabolic (metabolic) alkalosis, the blood pH has risen above 7.45 because of an increase in bicarbonate (see below for addition alkalosis) or loss of hydrogen ions (see below for subtraction alkalosis). Possible causes of metabolic alkalosis are addition alkalosis and subtraction alkalosis: Metabolic alkalosis can result from either increased uptake or production of bases (bicarbonates) in the metabolism (addition alkalosis) or can be due to increased losses of acids (subtraction alkalosis). Addition alkalosis may be caused by the intake of alkaline-acting substances:

  • Citrate
  • Sodium bicarbonate
  • Lactate

Common causes of subtraction alkalosis are:

Etiology

Biographical causes

  • Genetic burden from parents, grandparents – among others that – or that.
  • Genetic diseases
    • Bartter syndrome – very rare genetic metabolic disorder with autosomal dominant or autosomal recessive or X-linked recessive inheritance; defect of tubular transport proteins; hyperaldosteronism (disease states associated with increased secretion of aldosterone), hypokalemia (potassium deficiency) and hypotension (low blood pressure).
    • Gitelman syndrome (GS; synonym: familial hypokalemia-hypomagnesemia) – genetic condition with autosomal recessive inheritance characterized by hypokalemic metabolic alkalosis (metabolic alkalosis with potassium deficiency) with marked hypomagnesemia (magnesium deficiency) and low urinary calcium excretion.

Behavioral causes

  • Increased alkali intake
  • Licorice
  • Chewing tobacco
  • Black cohosh (medicinal plant)

Causes related to disease

  • Drainage of gastric juice
  • Bartter syndrome – very rare metabolic disorder associated primarily with hyperaldosteronism and, as a result, hypokalemia (potassium deficiency)
  • Chronic vomiting – loss of acid gastric juice.
  • Endocrine disorders – e.g., hyperaldosteronism (consequently, hypokalemia (potassium deficiency))
  • Gitelman syndrome – genetic condition leading to increased loss of potassium and magnesium through the kidney.
  • Hypercalcemia (excess calcium).
  • Hyperparathyroidism (parathyroid hyperfunction).
  • Congenital chloridorrhea – diarrhea (diarrhea) caused by chloride malabsorption.
  • Liddle syndrome – very rare genetic disorder associated with hypertension (high blood pressure).
  • Gastric lavage
  • Malnutrition (malnutrition) → extrarenal potassium loss (“outside the kidneys”).
  • Milk-alkali syndrome (Burnett syndrome) – disease caused by an excess of alkalis such as milk and calcium carbonate; clinical picture: Nausea (nausea)/vomiting, vertigo (dizziness), and ataxia (gait disturbance); laboratory diagnosis: Alkalosis with hypercalcemia (excess potassium) without increased calcium excretion in the urine and without a drop in phosphate content in the blood; hypercalcemia leads to calcinosis (calcium salt deposits) of the conjunctiva, the cornea of the eyes (“band keratitis” of the palpebral fissure) and in the renal tubules with the risk of renal insufficiency (slowly progressive reduction in renal function).
  • Cushing’s disease – group of diseases leading to hypercortisolism (hypercortisolism) – excess of cortisol.
  • Adrenal enzyme defects such as hydroxylase deficiency.
  • Renal artery stenosis – narrowing of the renal artery(s) leading to hypertension (high blood pressure).
  • Edema – accumulation of water in the tissues
  • Primary aldosteronism (overproduction of aldosterone), which is due to a tumor or hyperplasia
  • Tumors that produce renin (enzyme that regulates blood pressure).
  • Villous adenoma – benign tumor.

Laboratory diagnoses – laboratory parameters that are considered independent risk factors.

  • Hypercalcemia (excess calcium).
  • Hypokalemia (potassium deficiency)
  • Hypomagnesemia (magnesium deficiency)

Medication