Renal Pharmacology

Question 1

Renal Pharmacology

Mannitol

Answer 1

MOA: Osmotic diuretic. ↑ tubular fluid osmolarity → ↑ urine flow, ↓ intracranial/intraocular pressure’

Use: Drug overdose, elevated intracranial/intraocular pressure

Adverse Effects: Pulmonary edema, dehydration. Contraindicated in anuria, HF.

Question 2

Renal Pharmacology

Acetazolamide

Answer 2

MOA: Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and ↓ total body HCO3- stores.

Use: Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, psuedotumor cerebri.

Adverse Effects: Proximal renal tubular acidosis, paresthesias, NH3 toxicity, sulfa allergy, hypokalemia.

Question 3

Renal Pharmacology

Furosemide, bumetanide, torsemide

Answer 3

MOA: Sulfonamide loop diuretics. Inhibits cotransport system (Na+/K+/2Cl-) of thick ascending limb of loop of Henle. Abolish hypertonicity of medulla, preventing concentration of urine. Stimulate PGE release (vasodilatory effect on efferent arteriole); inhibited by NSAIDs. ↑ Ca2+ excretion.

Use: Edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia.

Adverse Effects: Ototoxicity, hypokalemia, dehydration, allergy (sulfa)/metabolic alkalosis, nephritis (interstitial), gout.

Question 4

Renal Pharmacology

Ethacrynic acid

Answer 4

MOA: Nonsulfonamide inhibitor of cotransport system (Na+/K+/2Cl-) of thick ascending loop of Henle.

Use: Diuresis in patients allergic to sulfa drugs

Adverse Effects: Similar to furosemide, but more ototoxic

Question 5

Renal Pharmacology

Hydrochlorothiazide, chlorthalidone, metolazone

Answer 5

MOA: Inhibit NaCl reabsorption in early DCT → ↓ diluting capacity of nephron. ↓ Ca2+ excretion

Use: Hypertension, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis.

Adverse Effects: Hypokalemic metabolic acidosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia. Sulfa allergy

Question 6

Renal Pharmacology

Spironolactone, eplerenone

Answer 6

MOA: Potassium-sparing diuretic. Competitive aldosterone receptor antagonists in cortical collecting tubule.

Use: Hyperaldosteronism, K+ depletion, HF, hepatic ascites (spironolactone)

Adverse Effects: Hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (gynecomastia, antiandrogen effects)

Question 7

Renal Pharmacology

Triamterene, amiloride

Answer 7

MOA: Potassium-sparing diuretic. Block Na+ channels in the cortical collecting tubule

Use: Hyperaldosteronism, K+ depletion, HF, nephrogenic DI

Adverse Effects: Hyperkalemia (can lead to arrhythmias)

Question 8

Renal Pharmacology

Captopril, enalapril, lisinopril, ramipril

Answer 8

MOA: Inhibit ACE → ↓ AT II → ↓ GFR by preventing constriction of efferent arterioles. ↑ renin due to loss of negative feedback. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator.

Use: Hypertension, HF (↓ mortality), proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a result of chronic hypertension.

Adverse Effects: Cough, angioedema (due to ↑ bradykinin; contraindicated in C1 esterase inhibitor deficiency), teratogen (fetal renal malformations), ↑ creatinine (↓ GFR), hyperkalemia, and hypotension. Used with caution in bilateral renal artery stenosis, because ACEIs will further ↓ GFR → renal failure

Question 9

Renal Pharmacology

Losartan, candesartan, valsartan

Answer 9

MOA: Selectively block binding of AT II to AT1 receptor. Effects similar to ACE inhibitors but do not ↑ bradykinin.

Use: Hypertension, HF, proteinuria, or diabetic nephropathy with intolerance to ACEIs.

Adverse Effects: hyperkalemia, ↓ GFR, hypotension; teratogen.

Question 10

Renal Pharmacology

Aliskiren

Answer 10

MOA: Direct renin inhibitor, blocks conversion of angiotensinogen to AT I.

Use: Hypertension

Adverse Effects: Hyperkalemia, ↓ GFR, hypotension. Relatively contraindicated in patients already taking ACEIs or ARBs.