Mechanism: Carbonic anhydrase inhibitor that limits proton concentration for Na exchange and blocks sodium bicarbonate reabsorption at proximal tubule. Requires sulfonamide group for activity. Causes alkaline diuresis and hyperchloremic metabolic acidosis.

Treatment: glaucoma, acute mountain sickness, corrects metabolic alkalosis, anticonvulsant properties

Side effects: Paresthesias and somnolence, allergic reactions, renal stones from phosphaturia and hypercalcuria, renal K+ wasting

Contraindications: hepatic cirrhosis

Mechanism: osmotic diuretic acting in PT and descending limb of Henle's loop, increases urine volume and flow rates and reduces Na+ reabsorption, but resulting water loss is greater than sodium loss leading to hypernatremia

 Treatment: Reduces intracranial and intraocular pressure

Side effects: Extracellular volume expansion (hyponatremia) can complicate CHF and produce pulmonary edema, headache nausea and vomiting, dehydration and hypernatremia from excessive use

Mechanism: Loop diuretics that blocks Na+/K+/2Cl- cotransporter NKCC2 in thick ascending limb. Blocks electrical potential/driving force for reabsorption of Mg and Ca, act on luminal side

Treatment: acute pulmonary edema, other edematous conditions, and acute hypercalcemia.  Other indications: hyperkalemia, acute renal failure, anion overdose

Side effects: Hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesmia, allergic reactions (ethacrynic acid used if patient has sulfonamide allergy), impaired carbohydrate tolerance, dehydration, hyponatremia, hypercalcemia, gout

Mechanism: Blocks the electrically neutral Na+/Cl- cotransporter NCC in the DCT, enhances Ca+ reabsorption

Treatment: Hypertension, nephrolithiasis (idiopathic hypercalciuria), heart failure, nephrogenic diabetes insipidus (NDI)

Side effects: gout (competes with uric acid secretion), hypokalemia metabolic alkalosis and hyperuricemia, hyperglycemia, hyperlipidemia, hyponatremia, allergic reactions (to sulfonamide), weakness, fatigability, paresthesias, impotence

Mechanism: synthetic steroid, potassium-sparing diuretic that antagonizes effect of aldosterone, reduces Na+ absorption in collecting tubules and ducts

Treatment: Mineralcorticoid excess (primary hypersecretion: Conn's syndrome, ectopic ACTH production or secondary aldosteronism from heart failure, hepatic cirrhosis and nephrotic syndrome); eplerenone approved to treat hypertension

Side effects: hyperkalemia, hyperchloremic metabolic acidosis, gynecomastia

Mechanism: potassium-sparing diuretic that blocks ENaC ion channel in apical cells of the collecting tubule on luminal membrane

Treatment: mineralocorticoid excess

Side effects: hyperkalemia, hyperchloremic metabolic acidosis, gynecomastia, acute renal failure (triamterene + indomethacin), kidney stones 

Mechanism: ADH antagonists at V1 and V2 receptors, induces highly hyptonic diuresis, does not effect excretion of electrolyte; Li+ and demeclocycline reduces formation of cAMP in response to ADH

Treatment: euvolemic hyponatremia, SIADH

Side effects: hypernatremia and Nephrogenic diabetes insipidus

Li+can cause: renal failure, tremulousness, mental obtundation, cardiotixicity, thryoid dysfunction, and leukocytosis

Demeclocycline can cause: renal failure, should be avoided in patients with liver disease

Contraindications: patients with hypovolemic hyponatremia and pregnant women