1) Carbonic anhydrase inhibitors such as acetazolamide and dorzolamide work by inhibiting sodium bicarbonate reabsorption in the proximal tubule. They cause metabolic acidosis and decrease aqueous humor and CSF production. 2) Thiazide diuretics such as hydrochlorothiazide block the sodium-chloride symporter in the early distal convoluted tubule. They cause hypokalemia, hypercalcemia, and metabolic alkalosis. 3) Loop diuretics like furosemide block sodium, potassium, and chloride reabsorption in the thick ascending limb of the loop of Henle. They can cause hypokalemia, hypocalcemia

2. CA Inhibitors
Acetazolamide & Dorzolamide (topical
eye drop)
 MoA: Inhibits NaHCO3 reabsorption

 Location: PROXIMAL TUBULE
Sulfonamides = avoid in gout
 Actions:

 Causes metabolic acidosis (limits H+
excretion)
 Decreases aqueous humor & CSF
production

3. CA Inhibitors

Adverse
 Nephrolithiasis since CaPO4 precipitates in
alkaline urine
 Hypokalemia (adverse effect of all diuretics
except for K-sparring ones)
 Contra-indicated in gout and COPD (because of
effects of CA in lungs)

Therapeutic Uses
 Open angle glaucoma
 In combo with other diuretics to counter
alkalosis effects
 Edema from heart failure

4. Thiazides
Hydrochlorothiazide & Indapamide
 MoA: blocks the Na/Cl symport

 Location: Acts in early DCT (diluting capacity
is decreased)
Also are sulfonamides (contra for gout)
 Metabolic alkalosis (opposite of CA
Inhibitors)
 Calcium is retained 
HYPERCALCEMIA
 Only effective when GFR > 30 mL/min


5. Thiazides

Adverse
 Hypokalemia (more Na reaching collecting





tubule causes high K secretion)
Hypercalcemia (lower intracellular Na limits Ca
exchange; also limits Li excretion)
Metabolic alkalosis
Sexual dysfunction, postural hypotension
Not for pregnancy
Therapeutic Use
 1st choice for hypertension
 Used when there is any edema
 Ca Nephrolithiasis

6. Loop Diuretics


Furosemide & Ethacrynic acid (not a sulfonamide)
MoA: Blocks Na/K/Cl in the TAL of loop of henle
 Decreased lumen positive potential = dilution ability is
affected (Ca loss)
 Decreased hypertonicity of medulla = decreased
concentrating ability
 Inhibition of macula densa sensitivity (work even with
low GFR)


Osmolality is same as plasma due to loss of
concentration and dilution ability!!
Metabolic alkalosis; increased Ca and Mg
excretion

7. Loop Diuretics


Only diuretics which work with low GFR!!
(due to inhibition of macula densa sensitivity)
ADVERSE





Hypocalcemia, hypokalemia, hypochloremia
Tinnitus (due to alteration of endolymph)
Hyperglycemia in DM pts
Hypokalemia can increase digoxin and Li toxicity
Therapeutic Use
 Pulmonary edema, Heart failure
 Hypertension – only if renal insufficiency (allows
to work with low GFR)

8. K+ Sparring Diuretics


Triamterene; Amiloride; Spironolactone
MoA:
 Triamterene and Amiloride block Na channels directly
 Spironolactone blocks aldosterone receptors (which
prevents Na channels from even being produced)
 Location: late DCT & Cortical Collecting Tube



ONLY diuretics which do not cause increased K
excretion
Spironolactone takes 1-3 days to take effect
(blocks protein synthesis) and is metabolized to
its active metabolite – canrenone
Amiloride is excreted unchanged

9. K+ Sparring Diuretics

Adverse
 Hyperkalemia (may cause asystole)
 Sexual dysfunction (spironolactone)
 Mixing with b-blockers, ACE
inhibitors, NSAIDS (renin-angiotensin
system blunters) may increase hyperkalemia

Therapeutic Uses
 Prevention of hypokalemic states
 Spironolactone for primary hyperaldosteronism
(Conn syndrome), secondary
hyperaldosteronism (Cushing’s), and
hypertension with heart failure
 Amiloride for Li-Induced nephrogenic DI

10. Osmotic Diuretics


Mannitol
MoA: Increase the osmolarity of tubular fluid
 Location: proximal tubule & thick descending limb of loop
of Henle

Increases excretion of all ions
 Urine becomes acidic (but body is normal)
 Causes EXTRACELLULAR VOLUME EXPANSION
initially but then diuresis causes EXTRACELLULAR
VOLUME REDUCTION !!!!!!!
○ Can cause PULMONARY EDEMA

Therapeutic Use
 Reduces cerebral edema (neurosurgery)
 Reduces intraocular pressure in acute closed-angle
glaucoma

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