Renal Drugs Flashcards
Mechanism: Mannitol
Osmotic diuretic:
Increases tubular fluid osmolarity → increase urine flow, decrease intracranial/intraocular pressure
Clinical use: Mannitol
Drug OD
Elevated intracranial/intraocular pressure
Adverse effects: Mannitol
Pulmonary edema
Dehydration
Contraindicated: Anuria, HF
Mechanism: Acetazolamide
Carbonic anhydrase inhibitor:
Causes self-limited NaHCO3 diuresis and decreases total body HCO3- stores
Clinical use: Acetazolamide
Glaucoma
Urinary alkalinization
Metabolic alkalosis
Altitude sickness
Pseudotumor cerebri
Adverse effects: Acetazolamide
Proximal renal tubular acidosis
Paresthesias
NH3 toxicity
Sulfa allergy
Hypokalemia
Mechanism: Loop diuretics
Furosemide
Bumetanide
Torsemide
Sulfonamide loop diuretic:
Inhibit 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 afferent arteriole); inhibited by NSAIDs
Increases Ca2+ excretion
Clinical use: Loop diuretics
Furosemide
Bumetanide
Torsemide
Edematous states
Hypertension
Hypercalcemia
Adverse effects: Loop diuretics
Furosemide
Bumetanide
Torsemide
Ototoxicity
Hyperkalemia
Pancreatitis
Hypomagnesemia
Dehydration
Allergy (sulfa)
Metabolic alkalosis
Interstitial nephritis
Mechanism: Ethacrynic acid
Nonsulfonamide inhibitor of cotransport sytem (Na+/K+/2Cl-) of thick ascending limb of loop of Henle
Clinical use: Ethacrynic acid
Diuresis in patients allergic to sulfa drugs
Adverse effects: Ethacrynic acid
Similar to fureosemide, but more ototoxic
Mechanism: Thiazide diuretics
Hydrochlorothiazide
Chlorhtalidone
Metolazone
Inhibit NaCl reabsorption in early DCT → decreasing diluting capacity of nephron
Decreases calcium excretion
Clinical use: Thiazide diuretics
Hydrochlorothiazide
Chlorhtalidone
Metolazone
Hypertension
HF
Idiopathic hypercalciuria
Nephrogenic DI
Osteoporosis
Adverse effects: Thiazide diuretics
Hydrochlorothiazide
Chlorhtalidone
Metolazone
Hypokalemic metabolic alkalosis
Hyponatremia
Hyperglycemia
Hyperlipidemia
Hyperuricemia
Hypercalcemia
Sulfa allergy
Pancreatitis
Mechanism: Potassium-sparing diuretics
Spironolacton
Eplerenone
Competitive aldosterone receptor antagonists in cortical collecting tubule
Mechanism: Potassium-sparing diuretics
Triamterene
Amiloride
Inhibit Na+ channels in cortical collecting tubule
Clinical use: Potassium-sparing diuretics
Spironolactone
Eplerenone
Triamterene
Amiloride
Hyperaldosteronism
K+ depletion
HF
Hepatic ascites (spironolactone)
Nephrogenic DI (amiloride)
Antiandrogen
Adverse
Adverse effects: Potassium-sparing diuretics
Spironolactone
Eplerenone
Triamterene
Amiloride
Hyperkalemia (can lead to arrhythmias)
Spironolactone: Endocrine effects
- Gynecomastia
- Antiandrogen effects
Mechanism: ACE inhibitors
Captopril
Enalapril
Lisinopril
Ramipril
(-pril)
Inhibit ACE → decrease AT II → decrease GFR by preventing constriction of efferent arterioles
Increases renin due to loss of negative feedback
Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator
Clinical use: ACE inhibitors
Captopril
Enalapril
Lisinopril
Ramipril
(-pril)
Hypertension
HF (decreases mortality)
Proteinuria
Diabetic nephropathy
Prevent unfavorable heart remodeling as a result of chronic hypertension
Adverse effects: ACE inhibitors
Captopril
Enalapril
Lisinopril
Ramipril
(-pril)
Cough
Angioedema (due to increased bradykinin); contraindicated in C1 esterase inhibitor deficiency
Teratogen (fetal renal malformations)
Increased creatinine (decreased GFR)
Hyperkalemia
Hypotension
Use with caution with bilateral renal artery stenosis becasue ACE inhibitors will further decrease GFR → renal failure
Clinical use: Angiotensin II receptor blockers
Losartan
Candesartan
Valsartan
Hypertension
HF
Proteinuria
Chronic kidney disease (diebetic neuropathy) with intolerance to ACE inhibitors (cough, angioedema)
Adverse effects: Angiotensin II receptor blockers
Losartan
Candesartan
Valsartan
Hyperkalemia
Decreased GFR
Hypotension
Teratogen
Mechanism: Aliskiren
Direct renin inhibitor → blocks conversion of angiotensinogen to angiotensin I
Clinical use: Aliskiren
Hypertension
Adverse effects: Aliskiren
Hyperkalemia
Decreased GFR
Hypotension
Angioedema
Relatively contraindicated: Patients already taking ACE inhibitors or ARBs