Diuretics

Sites of action

Diuretics act at distinct nephron segments - loop diuretics (thick ascending limb, most potent), thiazides (distal convoluted tubule), and potassium-sparing agents (collecting duct, including mineralocorticoid receptor antagonists) - segment of action determines both diuretic potency and characteristic electrolyte disturbance pattern
Loop diuretics inhibit the Na-K-2Cl cotransporter, producing the most potent natriuresis/diuresis given the thick ascending limb's large sodium reabsorption capacity - but also causing potassium and magnesium wasting given increased distal sodium delivery driving compensatory potassium/hydrogen secretion
Thiazides inhibit the Na-Cl cotransporter in the distal tubule - less potent diuresis but also cause hypokalaemia, plus a distinct tendency to hyponatraemia (particularly in older patients) and hypercalcaemia (reduced distal calcium excretion, in contrast to loop diuretics' calcium-wasting effect)
Potassium-sparing diuretics/mineralocorticoid receptor antagonists block aldosterone-driven sodium reabsorption/potassium secretion, causing the opposite electrolyte risk - hyperkalaemia, particularly with renal impairment or concurrent ACE inhibitor/ARB use

Amongst the most widely prescribed medication classes given their central role in heart failure, hypertension, and oedema management

Electrolyte monitoring (potassium, sodium, magnesium) matched to the specific diuretic class's characteristic disturbance pattern, particularly important at initiation and dose changes
Renal function monitoring given volume depletion risk with aggressive diuresis, particularly relevant in combination diuretic regimens for resistant oedema

Sequential nephron blockade (combining a loop diuretic with a thiazide or potassium-sparing agent acting at a different nephron segment) overcomes compensatory sodium reabsorption at downstream segments, used for diuretic-resistant oedema when a single agent alone is inadequate
Electrolyte replacement (potassium, magnesium) or dose reduction guided by monitoring results, rather than routine empirical supplementation regardless of measured levels

Loop diuretic-associated hypokalaemia/hypomagnesaemia (arrhythmia risk), thiazide-associated hyponatraemia (particularly in older adults) and hypercalcaemia, mineralocorticoid receptor antagonist-associated hyperkalaemia (particularly with concurrent ACE inhibitor/ARB)

Thiazide and loop diuretics have opposite effects on calcium handling - thiazides reduce urinary calcium excretion (potentially causing hypercalcaemia, and used therapeutically for calcium-containing kidney stone prevention), while loop diuretics increase calcium excretion (potentially causing hypocalcaemia) - this is a frequently tested, easily confused distinction given both classes cause hypokalaemia similarly

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