Drugs acting on the renal system

Diuretics: You can classify diuretics by their site and mechanism of action as follows.

Loop diuretics (furosemide, ethacrynic acid, bumetanide and torsemide): These inhibit the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle and in the macula densa. They bind at the chloride-binding site of the cotransporter. Adverse effects include hypokalemic metabolic alkalosis, ototoxicity (hair cell damage), hyperuricemia, hypercalciuria, precipitation of gout, and sulfa allergy (furosemide, bumetanide and torsemide).
Thiazides (hydrochlorothiazide, chlorthalidone and chlorothiazide): These bind to and inhibit the NaCl transporter in the distal convoluted tubule, causing natriuresis and diuresis. They increase calcium reabsorption in the distal convoluted tubule, so they’re useful for preventing calcium stones. Thiazides are also used to treat nephrogenic diabetes insipidus. Adverse effects include hypokalemic metabolic alkalosis, hyperuricemia, precipitation of gout, hyperglycemia, and hyperlipidemia.
Potassium sparing diuretics: These act in the collecting ducts. They either block apical sodium channels (ENaC) (amiloride and triamterene) or act as aldosterone receptor antagonists (spironolactone and eplerenone). Spironolactone and eplerenone are used to treat hyperaldosteronism. Adverse effects include gynecomastia with spironolactone. Hyperkalemia can occur.
Carbonic anhydrase inhibitors (acetazolamide): This reversibly inhibits the enzyme carbonic anhydrase in the proximal tubule. This reduces hydrogen ion secretion in the renal tubule and increases renal excretion of sodium, potassium, bicarbonate, and water. Diuretic efficacy is low. These drugs tend to cause metabolic acidosis from bicarbonate loss and can also cause hypokalemia.
Osmotic diuretics (mannitol): This increases tubular fluid osmolarity, causing water loss (diuresis) by osmosis. Adverse effects include pulmonary edema and hypernatremia.

Diuretics: You can classify diuretics by their site and mechanism of action as follows.

Loop diuretics (furosemide, ethacrynic acid, bumetanide and torsemide): These inhibit the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle and in the macula densa. They bind at the chloride-binding site of the cotransporter. Adverse effects include hypokalemic metabolic alkalosis, ototoxicity (hair cell damage), hyperuricemia, hypercalciuria, precipitation of gout, and sulfa allergy (furosemide, bumetanide and torsemide).
Thiazides (hydrochlorothiazide, chlorthalidone and chlorothiazide): These bind to and inhibit the NaCl transporter in the distal convoluted tubule, causing natriuresis and diuresis. They increase calcium reabsorption in the distal convoluted tubule, so they’re useful for preventing calcium stones. Thiazides are also used to treat nephrogenic diabetes insipidus. Adverse effects include hypokalemic metabolic alkalosis, hyperuricemia, precipitation of gout, hyperglycemia, and hyperlipidemia.
Potassium sparing diuretics: These act in the collecting ducts. They either block apical sodium channels (ENaC) (amiloride and triamterene) or act as aldosterone receptor antagonists (spironolactone and eplerenone). Spironolactone and eplerenone are used to treat hyperaldosteronism. Adverse effects include gynecomastia with spironolactone. Hyperkalemia can occur.
Carbonic anhydrase inhibitors (acetazolamide): This reversibly inhibits the enzyme carbonic anhydrase in the proximal tubule. This reduces hydrogen ion secretion in the renal tubule and increases renal excretion of sodium, potassium, bicarbonate, and water. Diuretic efficacy is low. These drugs tend to cause metabolic acidosis from bicarbonate loss and can also cause hypokalemia.
Osmotic diuretics (mannitol): This increases tubular fluid osmolarity, causing water loss (diuresis) by osmosis. Adverse effects include pulmonary edema and hypernatremia.