Water Retention (Edema): Drug Therapy

Therapeutic target

Regression of edema

Therapy recommendations

• Because of the multiple possible causes of edema formation (hepatic, cardiac, and renal edema), drug therapy also varies widely and depends on the exact underlying pathomechanism:
  • For acute hepatic, cardiac, and renal edema: Loop diuretics (furosemide, torasemide).
  • For chronic hepatic, cardiac, or renal edema: Thiazide diuretics* (chlortalidone, hydrochlorothiazide, HCT).
  • Use for hepatic, cardiac, and renal edema: Potassium-sparing diuretics (amiloride, triampterene, each in combination with HCT).
  • For hepatic, cardiac, and renal edema unresponsive to other diuretics: Aldosterone antagonists (spironolactone).
• Idiopathic cyclic edema: aldosterone antagonists (spironolactone) if necessary – see under “Premenstrual syndrome (PMS)”.
• See also under “Further therapy“.

* Note: Thiazides can no longer be used if the glomerular filtration rate (GFR) is < 30-45 ml/min. This limit is considered waived when thiazide diuretics are combined with loop diuretics: Loop diuretics abolish the tubule-glomerular feedback mechanism.

Further notes

• All diuretics-except the aldosterone antagonist spironolactone-must be filtered into the tubule to be effective. In this process, the effect increases with increasing dose but reaches a maximum that does not change with further dose increase (ceiling effect). Note: If edema is present or if chronic kidney disease is present, the threshold of action for diuretics is higher and higher doses are needed to achieve the desired effects.
• When diuretics are not effective or renal insufficiency is advanced, sequential tubule blockade, for example with loop diuretics and thiazide diuretics, offers a solution. Another way to break diuretic resistance is to administer an ACE inhibitor or AT1 receptor blocker (angiotensin II receptor subtype 1 antagonists, AT1 antagonists, AT1 receptor antagonists, AT1 blockers, angiotensin receptor blockers, “sartans“). This is because the saline transporter in the proximal tubule is under the control of angiotensin-2. Furthermore, saline excretion increases under this comedication.