Diuretants

Diuretants, commonly called diuretics, are substances or drugs that promote diuresis, an increase in urine production, and enhance sodium excretion. By reducing fluid retention, they are used to treat edema associated with conditions such as heart failure, liver cirrhosis, and kidney disease, and to manage hypertension. They may also be employed to lower intracranial or intraocular pressure in specific circumstances and to correct certain acid–base or electrolyte disturbances.

Most diuretics work by inhibiting sodium reabsorption at different segments of the nephron, so water follows osmotically and is eliminated in the urine. Major classes include:

- Loop diuretics (for example, furosemide, bumetanide) inhibit the Na-K-2Cl transporter in the thick ascending limb, producing potent diuresis and a tendency toward potassium loss.

- Thiazide diuretics (for example, hydrochlorothiazide, chlorthalidone) block the NaCl transporter in the distal convoluted tubule, providing moderate diuresis and are commonly used for hypertension.

- Potassium-sparing diuretics (such as spironolactone, eplerenone; amiloride, triamterene) reduce potassium loss by antagonizing aldosterone or by blocking epithelial sodium channels, useful in combination therapy but with a risk of hyperkalemia.

- Carbonic anhydrase inhibitors (acetazolamide) decrease bicarbonate reabsorption in the proximal tubule, yielding milder diuresis and potential metabolic acidosis.

- Osmotic diuretics (mannitol) increase filtrate osmolarity, used to reduce intracranial pressure and in certain renal settings, with possible dehydration.

Common adverse effects include electrolyte disturbances (hypokalemia or hyperkalemia depending on the agent), dehydration, hypotension, and, with thiazides and loop diuretics, hyperuricemia and gout. Kidney function and drug interactions influence the choice and dosing.