Table 1.

Principal pharmacological properties of drugs with diuretic effects

	Natriuretic effect when used in monotherapy (FENa%)	Time to peak efficacy	Half‐life	Bioavailability	Side effects
Loop diuretics	25%–30%	PO: 0.5–1 h IV: 5–10 min	3 h	Highly variable for oral furosemide 90% for bumetanide/torsemide	Important RAAS activation
Diuretic resistance induced by compensatory DCT hypertrophy
Hypokalaemia
Hypomagnesaemia
Hyperuricaemia
Gout
Thiazide‐like diuretics	10% Loop diuretics potentializing ++++	PO: 1–6 h IV: only chlorothiazide with onset of 30 min	HCTZ: 6–15 h Metolazone: 6–20 h Chlortalidone: 45–60 h	HCTZ: 65%–75% Metolazone: 60%–65% Chlortalidone: NA	RAAS activation
Hypokalaemia
Hyponatraemia
Hyperuricaemia
Gout
Hypercalcaemia
Hypomagnesaemia
MRAs	2%	PO: 48–72 h IV: potassium canreonate: 2.5 h	Eplerenone: 3–6 h Canrenone: 17 h	Spironolactone: 90% Eplerenone: 70%	Hyperkalaemia
Average increase in serum potassium: 0.4 mmol/L
SGLT2i	3% Loop diuretics potentializing ++	PO: 1.5–2 h	12 h	80%–90%	Keto‐acidosis (in patients treated with insulin)
Acetazolamide	Heavily depends on subsequent tubular segments	PO: 2 h	6 h	>90%	Hypokalaemia
Metabolic acidosis
Hyponatraemia
Amiloride	2%	PO: 6 h	6–9 h	50%	Hyperkalaemia
Hyponatraemia

DCT, distal convoluted tubule; FENa, fractional excretion of sodium; HCTZ, hydrochlorothiazide; IV, intravenous; MRA, mineralocorticoid receptor antagonist; NA, not available; PO, per os; RAAS, renin–angiotensin–aldosterone system; SGLT2i, sodium–glucose cotransporter 2 inhibitor.

Adapted from Mullens et al. ¹⁶