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Flashcards in Renal Deck (13):


MoA: osmotic diuretic. increases tubular fluid osmolarity--> increased urine flow & decreased intracranial/ intraocular pressure.

Use: Tx of drug overdose, elevated intracranial/ intraocular pressure.

Toxicity: pulmonary edema, dehydration. Contraindicated in anuria, CHF.



MoA: carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis & reduction in total-body HCO3- stores.

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

Toxicity: hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy.

Mnemonic: ACIDazolamide -> ACIDosis


(Loop Diuretic)

MoA: sulfonamide loop diuretic. Inhibits cotransport system (Na+, K+, 2Cl-) of thick ascending limb of loop of Henle. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs. Increases Ca+2 excretion.

Use: edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia.

Toxicity: Ototoxicity, Hypokalemia, Dehydration, Allergy (sulfa), Nephritis (interstitial), Gout. Mnemonic: OH DANG!


Ethacrynic acid
(Loop Diuretic)

MoA: phenoxyacetic acid derivative (not a sulfonamide). Essentially same action as furosemide.

Use: diuresis in pts allergic to sulfa drugs.

Toxicity: similar to furosemide; can cause hyperuricemia; never use to treat gout.



MoA: thiazide diuretic. Inhibits NaCl reabsorpn in early distal tubule, reducing diluting capacity of nephron. Decreases Ca+2 excretion.

Use: HTN, CHF, idiopathic hypercalciuria, nephrogenic DI

Toxicity: hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, & hyperCalcemia. Sulfa allergy.
Mnemonic: hyperGLUC


K+ sparing diuretics

Drugs: spironolactone & eplerenone; triamterene & amiloride

Spironolactone & eplerenone- competitive aldosterone receptor antagonists in cortical collecting tubule.
Triamterene & amiloride- act at cortical collecting tubule by blocking Na+ channels.

Use: hyperaldosteronism, K+ depletion, CHF.

Toxicity: hyperkalemia (can lead to arrhythmias), endocrine effects w/ spironolactone (e.g. gynecomastia, anti androgen effects).


Diuretics: electrolyte changes
(Urine NaCl)

Increased (all diuretics. Serum NaCl may decrease as a result.


Diuretics: electrolyte changes
(Urine K+)

Increased (all except K+-sparing diuretics). Serum K+ may decrease as a result.


Diuretics: electrolyte changes
(Blood pH- acidemia)

Decreased (acidemia):

carbonic anhydrase inhibitors- decreased HCO3- reabsorption.
K+ sparing- aldosterone blockade prevents K+ secretion and H+ secretion.
Hyperkalemia leads to K+ entering all cells (via H+/ K+ exchanger) in exchange for H+ exiting cells.


Diuretics: electrolyte changes
(Blood pH-alkalemia)

Increased (alkalemia): loop diuretics & thiazides cause alkalemia thru several mechanisms:
1. Volume contraction-> increased AT II-> Na+/H+ exchange in prox tubule-> increased HCO3- reabsorption ("contraction alkalosis")
2. K+ loss -> K+ exiting all cells (via H+/ K+ exchanger) in exchange for H+ entering cells
3. In low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule -> to alkalosis and "paradoxical acuduria"


Diuretics: electrolyte changes
(Urine Ca+2)

Increased w/ loop diuretics: decreased paracellular Ca+2 reabsorption-> hypocalcemia

Decreased w/ thiazides: enhanced paracellular Ca+2 reabsorption in prox tubule & loop of Henle


ACE inhibitors

Drugs: captopril, enalapril, lisinopril

MoA: inhibit ACE-> decreased angiotensin II-> decreased GFR by preventing constriction of efferent arterioles. Levels of renin increase as a result of loss of feedback inhibition. Inhibition of ACE prevents ACE from inhibiting bradykinin activation.

Use: HTN, CHF, proteinuria, diabetic renal disease. Prevent unfavorable heart remodeling as a result of chronic HTN.

Toxicity: Cough (b/c of bradykinin), Angioedema, Teratogen (fetal renal malformations), Creatinine increase (decreased GFR), Hyperkalemia, And Hypotension. Avoid in bilateral renal artery stenosis, because ACE inhibitors will further decrease GFR-> renal failure.

Mnemonic: captopril's CATCHH (acronym for toxicities)


(Angiotensin II receptor blockers)

Drugs: sartans

have effects similar to ACE inhibitors but do not increase bradykinin-> no cough or angioedema