Renal Pharm

• Drug: mannitol
• Location: Proximal tubule
• Mechanism: inhibits water reabsorption thru tubules, increases urinary vol
• Use: decrease IOP in glaucoma, decreases intracerebral pressure, oliguric states (ie rhabdomyolysis), shock, drug OD
• Side effects: acute hypovolemia pulmonary edema, contraindicated in anuria and CHF

• Drug: acetazolamide, dorzolamide
• Location: Proximal tubule
• Mechanism: CA inhibition results in:
• decreased H formation in PCT
• decreased Na/H antiport
• Increased Na and HCO3- in lumen
• increased diuresis and reduction in total body bicarb
• Use: glaucoma, acute mountain sickness (>1000 ft, you likely hyperventilate, so give CAI to cause a metabolic acidosis prior), metabolic alkalosis,
• Side effects: biocarbonaturia & acidosis, hypokalemia, hyperchloremia, paresthesia, renal stones (due to hi pH), sulfonamide hypersensitivity

ACIDazolamide causes ACIDosis

• Drug: furosamide
• Location: Thick ascending loop
• Mechanism: Na/K/2Cl- transporter inhibition causes:
• decreased intracellular K, decreased back diffusion, decreased reabsorption of Ca and Mg, inreased diuresis
• Use: DOC for acute pulmonary edema, CHF that causes pulmonary edema, htn, refractory edemas, acute renal failure, anion OD, hypercalcemic states
• Side effects: sulfonamide hypersensitivity, hypokalemia and alkalosis, hypocalcemia, hypomagnesemia, hyperuricemia, OTOXOCITY (MC tested question)
• Drug interactions: aminoglycosides, lithium clearance decreased, increased toxicity of digoxin due to elyte disturbances

• Loops Loose Ca
• OH DANG toxicity = Ototoxicity, Hypokalemia, Dehydration, Allergery (sulfa), Nephritis (interstitial), Gout

• Drug: ethacrynic acid
• Location: Thick ascending loop
• Mechanism: same as furosamide (inhibition of Na/K/2Cl-)
• Derivative: phenoxyacetic acid
• Clinical Use: diuresis in pts allergic to sulfa drugs
• Toxicity: similar to furosamide (OH DANG) can be used in hyperuricemia and acute gout (not used to treat gout!)

• Carbonic anhydrase inhibitors
• All loop diuretics (except ethacrynic acid)
• Thiazides
• Sulfa abx
• Celecoxib

• Loop diuretcis (mostly ehtacrynic acid)
• Aminoglycoside abx
• Quinidine (cinchonism)

• Drugs: Hydrochlorothiazide, indapamide, metolozone
• Location: early distal tubule
• Mechanism: Na/Cl transporter inhibition, results in: more Na, Cl in DCT, diuresis
• Use: htn, CHF, nephrolithiasis, nephrogenic diabetes insipidis
• Side effects: sulfa hypersensitivity, hypokalemia, alkalosis, hypercalemia, hyperuricemia, hyperglycemia (lessK = inhibits insulin release = increased BG), hyperlipidemia (except indapmide), sulfa allergy
• Drug interactions/cautions: digoxin has increased toxicity bc of elyte disturbances), avoid in pts w/ DM
• Ineffective w/ GFR < 30 (should use a loop)

• Pathology of NDI: uncoupled V2 receptors in the kidney = can't respond to ADH
• tx: is hydrochlorothiazide
• Mechanism: initially the thiazide causes loss of Na and water, then starts to absorbe more Na and lose less water

1. Loops: Oxotoxicity and hypocalcemia 2. Thiazides: Hypercalcemia, hyperglycemia, hyperlipidemia, sexual dysfunction

• Mechanism: aldosterone receptor antagonist
• Use: hyperaldosteronic state, adjuct to K wasting diurectics, antiandrogenic use (female hirsuitism bc it blocks androgen receptors), CHF (inhibits remodeling)
• Side Effects: Hyperkalemia, acidosis, antiandrogen (gynecomastia = spironolactating :) ) Example: pt starts on a new drug for CHF and starts developing breasts what is the drug?

the K STAys: Spironolactone, Triamterene, Amiloride, eplerenone

• Mechanism: aldosterone receptor antagonist
• Similar to spironolactone but does not have the antiandrogenic effect

the K STAys: Spironolactone, Triamterene, Amiloride, eplerenone

• Mechanism: Na channel blockers
• Use: adjunct to K wasting diuretics, Li induced nephrogenic diabetes isipidis (amiloride)
• Side Effects: hyperkalemia, acidosis

the K STAys: Spironolactone, Triamterene, Amiloride, eplerenone

Loops and thiazides

renal failure

acidosis

alkalosis

alkalosis

acidosis

• Drugs: Captopril, enlalpril, lisinopril
• Mechanism: inhibits angio-converting enzyme, preventing inactivation of bradykinin ( produces VD, angioedema, cough), increases renin release due to loss of FB inhibition
• clinical use: CHF, diabetic renal dz (nephroprotective)
• Toxicity: CAPTOPRIL
• Cough
• Angioedema
• Proteinuria
• Taste changes
• hypOtension
• Pregnancy problems (fetal renal damage)
• Rash
• Increased renin
• Lowers angioII
• Also....hyperkalemia
• avoid use w/ renal stenosis :)

A little encouragement :)