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Flashcards in Renal: Drugs Deck (12)
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  • Works at the Proximal Convoluted Tubule
  • Mechanism:
    • Carbonic anhydrase inhibitor
    • Causes self limited NaHCO3 diuresis and ↓ total-body HCO3- stores
  • Tx: Glaucoma, Urinary alkalinization, Metabolic alkalosis, Altitude sickness (↓ CSF), Pseudotumor cerebri
  • SEx: Hyperchloremic metabolic acidosis after several days of admin., Renal Stones, Potassium loss, Parasthesias, NH3 toxicity, Sulfa allergy
  • Contra: Hepatic cirrhosis (NH4+ accumulation)
  • ACID azolamide causes ACIDosis



  • Works at the Thin Descending Tubule
  • metabolically inert hexose sugar
  • Mechanism:
    • Osmotic diuretic, ↑ Tubular fluid osmolarity, Producing ↑ urine flow (lowers resistance)
    • ↓ Intracranial / Intraocular pressure
    • ↑ RPF
  • Tx: Acute renal failure, Drug overdose, ↑Intracranial / Intraocular pressure
  • SEx: Pulmonary edema, Dehydration, Hypernatremia, Extracellular volume expansion
  • Contraindicated in Anuria, CHF



  • Works on the Thick Ascending Limb
  • Mechanism:
    • Sulfonamide loop diuretic.  Inhibits cotransport system (Na+/K+/2Cl-) - Limb of Henle
    • Abolishes Hypertonicity of Medulla, preventing concentration of Urine
    • Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs ↑ Ca2+ excretion.  Loops Lose calcium
  • Tx: Edematous states (CHF, Cirrhosis, Nephrotic syndrome, Pulmonary edema), HTN, Hypercalcemia
  • SEx: Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout - OH DANG!

Loop Diuretics


  • Works on the Thick Ascending Limb
  • Mechanism:
    • Phenoxyacetic acid derivative (Not a Sulfonamide)
    • Essentially same action as Furosemide
  • Tx: Diuresis in patients allergic to Sulfa Drugs
  • SEx:  Similar to Furosimide; can cause Hyperuricemia, NEVER use to treat Gout

Ethacrynic Acid


  • Works on the Distal Convoluted Tubule
  • Mechanism:  Thiazide diuretic.  Inhibits NaCl reabsorption in early Distal Tubule.  ↓ Diluting capacity of the Nephron.  ↓ Ca2+ excretion
  • Tx:  Hypertension, CHF, Idiopathic Hypercalciuria, Nephrogenic Diabetes insipidus, Osteoporosis
  • SEx: HyperGLUCs
    • Hypokalemic metabolic alkalosis, Hyponatremia, HyperGlycemia, HyperLipidemia, HyperUricemia, and HyperCalcemia, Sulfa drugs



  • Works on the Collecting Tubule
  • Mechanism:
    • Spironolactone and Eplerenone are competitive Aldoserone receptor antagonsits in the Cortical collecting tubule
    • Triamterene and Amiloride act at the same part of the Tubule by blocking Na+ channels in the CCT
  • Tx:  Hyperaldosteronism, K+ depletion, CHF
  • SEx: Hyperkalemia (can lead to arrhythmias) Endocrine effects w/ Spironolactone (e.g. Gyncomastia, Antiandrogen effects)

K+ - Sparing Diuretics


Electrolyte changes due to Urine NaCl?

  • ↑ all diuretics except Acetazolamide
  • Serum Nacl may ↓ as a result


Diuretic electrolyte changed due to Urine K+?

  • ↑ w/ Loop and Thiazide diuretics
  • Serum K+ may ↓ as a result


Diuretic electrolye changes due to ↓ Blood pH?

  • ↓ Acidemia
  • Carbonic anhydrase inhibitors - ↓ HCO3- reabsorption
  • K+ sparing - Aldosterone blockade prevents K+ secretion and H+ secretion
  • Additionally, Hyperkalemia leads to K+ entering all cells (via H+/K+ exchanger) in exchange for H+ exiting cells


Diuretic electrolyte changes due to ↑ Blood pH?

  • ↑ Alkalemia
  • Loop diuretics and Thiazides cause Alkalemia through several mechanisms
  • Volume contraction -> ↑ AT II -> ↑ Na+/H+ exchange in Proximal tubule -> ↑ HCO3- reabsorption ("contraction alkalosis")
  • K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells
  • In Low K+ state, H+ (Rather than K+) is exchanged for Na+ in Cortical Collecting Tubule -> Alkalosis and "paradoxical aciduria"


Diuretic electrolyte changes due to Ca2+?

  • ↑ w/ Loop Diuretics:
    • ↓ Paracellular Ca2+ reabsorption -> Hypocalcemia​
  • ↓ w/ Thiazides:
    • Enhanced paracellular Ca2+ reabsorption in Distal Convoluted Tubule


  • Mechanism:
    • Inhibit ACE -> ↓ Angiotensin II -> ↓ GFR by preventing constriction of efferent arterioles
    • Levels of Renin ↑ as a result of loss of Feedback inhibition
    • Inhibition of ACE also prevents inactivation of Bradykinin, a potent vasodilator
  • Tx:  Hypertension, CHF, Proteinuria, Diabetic nephropathy.  Prevent unfavorable heart remodeling as a result of Chronic Hypertension
  • SEx:  Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), ↑ Creatinine (↓ GFR), Hyperkalemia, and Hypotension - CATCHH
    • Avoid in bilateral Renal artery stenosis, because ACE inhibitors will further ↓ GFR -> Renal Failure

ACE Inhibitors

  • Captopril
  • Enalapril
  • Lisinopril
  • Angiotensin II receptor blockers (-sartans) have effects similar to ACE inhibitors but do not ↑ Bradykinin -> ↓ Risk of cough or Angioedema