Metabolic complications associated with use of diuretics

Semin Nephrol. 2011 Nov;31(6):542-52. doi: 10.1016/j.semnephrol.2011.09.009.


Diuretics are commonly used therapeutic agents that act to inhibit sodium transport systems along the length of the renal tubule. The most effective diuretics are inhibitors of sodium chloride transport in the thick ascending limb of Henle. Loop diuretics mobilize large amounts of sodium chloride and water and produce a copious diuresis with a sharp reduction of extracellular fluid volume. As the site of action of diuretics moves downstream (thiazide and potassium-sparing diuretics), their effectiveness declines because the transport systems they inhibit have low transport capacity. Depending on the site of action diuretics can influence the renal handling of electrolyte-free water, calcium, potassium, protons, sodium bicarbonate, and uric acid. As a result, electrolyte and acid-base disorders commonly accompany diuretic use. Glucose and lipid abnormalities also can occur, particularly with the use of thiazide diuretics. This review focuses on the biochemical complications associated with the use of diuretics. The development of these complications can be minimized with careful monitoring, dosage adjustment, and replacement of electrolyte losses.

Publication types

  • Review

MeSH terms

  • Acid-Base Imbalance / chemically induced
  • Acidosis / chemically induced
  • Diuretics / adverse effects*
  • Dyslipidemias / chemically induced
  • Humans
  • Hyperglycemia / chemically induced
  • Hyperkalemia / chemically induced
  • Hyperuricemia / chemically induced
  • Hypokalemia / chemically induced
  • Metabolic Diseases / chemically induced*
  • Sodium Chloride Symporter Inhibitors / adverse effects
  • Sodium Potassium Chloride Symporter Inhibitors / adverse effects


  • Diuretics
  • Sodium Chloride Symporter Inhibitors
  • Sodium Potassium Chloride Symporter Inhibitors