Type of diuretic and where it works

CA inhibitors = proximal tubule

Osmotic = entire tubule

Loops = ascending limb

Thiazides = early distal

K+ sparing = early collecting

Aldosterone antagonists = early collecting

Hypokalemia and Alkalosis

K+ secretion is coupled w/ H+ secretion in the kidney

So diuretics that block Na+ reabsorption at segments above the collecting ducts will increase Na+ load downstream leading to increased loss of K+ and H+ (both the Loops and thiazide diuretics)

Osmotic diuretics

Mannitol inhibits H2O reabsorption throughout tubule and increases urine volume

Uses: decrease IOP in glaucoma

decreases intracerebral pressure

anuric states

rhabdomyolysis

SE: acute hypovolemia

Carbonic anhydrase inhibitors

Acetazolamide & Dorzolamide

MOA: decreased H+ formation inside the proximal convoluted tubule cell --> dec. Na+/H+ antiport (so Na+ stays in the urine along w/ bicarb) --> diuresis

Uses: glaucoma, acute mountain sickness, metabolic alkalosis

SE: bicarbonaturia, acidosis, hypokalemia, hyperchloremia, paresthesias, renal stones, sulfonamide hypersensitivity

Urinary electrolytes = inc in Na+/K+/HCO3-

Blood pH = acidosis

Loop diuretics

Ethacrynic acid & furosemide>torsemide>bumetanide

MOA: works in ascending loop, inhibiting the Na/K/2Cl transporter --> dec. intracellular K+ (plus Na & Cl) which inhibits the paracellular spaces from opening and reabsorbing Ca2+/Mg2+ (both lost) --> diuresis

Uses: DOC for acute pulmonary edema

Heart failure, HTN, refractory edema, acute renal failure, anion overdose, hypercalcemic states

SE: sulfonamide hypersensitivity, hypokalemia, alkalosis, hypocalcemia, hypomagnesemia, hyperuricemia, ototoxicity

DI:Aminogylcosides (enhanced ototoxicity), Lithium, Digoxin    

Urinary electrolytes = inc. in Na+/K+/Ca2+/Mg2+/ Cl-

Blood pH = alkalosis

Thiazides

HCTZ & Indapamide

MOA: on distal convoluted tubule inhibits Na/Cl transporter --> increased Na/Cl in urine --> diuresis

Uses: HTN, CHF, Nephrolithiasis (b/c you increase the activity of Ca2+ reabsorption)

Nephrogenic diabetes insipidus

SE: sulfonamide hypersensitivity, hypokalemia, alkalosis, hypercalcemia, hypocalciuria, hyperglycemia, hyperlipidemia

don't use in diabetics

Urinary electrolytes = inc. in Na+/K+/Cl- and dec. in Ca2+

Blood pH = alkalosis

K+ Sparing Drugs

Spironolactone & Eplerenone: action at the collecting duct

MOA: aldosterone receptor antagonist

Uses: hyperaldosteronic state, adjunct to K+ wasting diuretics, female hirsutism, CHF (proven to reduce remodeling when given w/ ACEI's

SE: Hyperkalemia, acidosis, antiandrogen

Amiloride & Triamterene: action at collecting duct

MOA: Na+ channel blockers

Uses: adjunct to K+ wasting diuretics, Li+ induced nephrogenic diabetes insipidus

SE: hyperkalemia/acidosis

Effect on urine electrolytes = small inc in Na+ and dec. in K+, blood pH = acidotic