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Flashcards in Renal Drugs Deck (12):

Carbonic acid anhydrase inhibitors

inhibits carbonic anhydrase in the PT; prevents breakdown of carbonic acid and subsequent reabsorption of bicarbonate, and relatedly NaCl reabsorption (via NaH antiporter); result is increased excretion of water, bicarb, and mild increased Na and K excretion


Osmotic diuretics

Mannitol; Glucose (when SGLT is saturated)
molecules that are freely filtered but not reabsorbed, take water out with it; this also prevents NaCl reabsorption so they are potent


Loop diuretics

block NKCC and thereby 20% of NaCl reabsorption; increase Na, K, Cl, and H2O excretion; but must be secreted into the tubule to act on the luminal transporter


Thiazide diuretics

Class I: Hydrochlorothiazide; use when GFR is adequate
Class II: Metolazone, Indapamide; newer and more potent, use when GFR is 30
block NaCl (electroneutral transporter) in early DCT, thereby preventing about 5% of Na reabsorption; increase Na, K, Cl, and H2O excretion - risk of hypo-electrolytes and dilutional hypoNa



binds receptors in medullary CD and increases IC cGMP which decreases Na reabsorption, and water follows Na out; no change in K excretion


Diuretics acting in CD

block ENaC: Amiloride, Triamterene
ALD-R antagonist: Spironolactone/Eplerenone
These all increase Na excretion, and lumen is less negative so both K and H secretion are reduced; thus these are K-sparing diuretics


Which diuretics increase potassium excretion?

PT - acetezolamide
LOH - furosemide
DCT - thiazide
Osmotic diuretics
Because they all increase the Na delivered to the CD, and attempts to reabsorb more means more K secretion (recall that hypoK is also related to alkalosis when protons are secreted to try and reabsorb the secreted K)



aka AVP/ADH; an anti-diuretic
Binds both V1 and V2 receptors - V1 causes vascular smooth muscle contraction; V2 (in PCs in CD) causes more AQPs and urea transporters to be put into the membrane


Selective V2R agonists

Desmopressin (DDAVP)
Used to treat central DI (kidneys waste water) because it will stimulate the V2R which says to put more AQPs into membrane


Selective V1R agonists

Increase constriction of GI and vascular smooth muscle; used to treat bleeding



[highly selective] V2R antagonists (so also vasopressin/ADH antagonists)
used to treat hypervolemia, SIADH, and hyponatremia; CYP3 metabolism



a class of drugs that increases blood flow to the kidney without increasing reabsorption of NaCl reabsorption; result is water loss without loss of electrolyte concentration; Examples: vasopressin antagonists (vaptans)