Diuretics increase renal sodium and water excretion through nephron-site-specific mechanisms. Their clinical effect depends on delivered drug, kidney function and compensatory sodium retention.

Major groups include carbonic-anhydrase inhibitors in the proximal tubule, loop diuretics in the thick ascending limb, thiazides in the distal convoluted tubule, and potassium-sparing agents in the collecting nephron; osmotic agents act where water permeability permits.

Major groups include carbonic-anhydrase inhibitors, loop diuretics, thiazide and thiazide-like drugs, potassium-sparing agents and osmotic diuretics.

Common roles include relief of fluid overload and oedema, blood-pressure control, selected electrolyte disorders, raised intracranial or intraocular pressure, and other class-specific indications.

Volume depletion, hypotension, kidney-function deterioration and sodium, potassium, magnesium, calcium or acid–base disturbances vary by class.

Assess volume status, blood pressure, kidney function, serum electrolytes and indication-specific response. Review NSAIDs and other medicines that alter renal perfusion or electrolytes.