Drugs Nephrotoxicity Flashcards
Drugs Causing Pre-Renal Azotemia
- Diuretics, alone or with other antihypertensive drugs
- Arterial vasodilators
- Immunosuppressant drugs
- NSAIDs
- Radiocontrast agents
- Anticoagulants and thrombolytic agents
Mechanism by which NASAIDs Cause
Pre-Renal Azotemia
NSAIDs inhibits prostaglandins causing vasoconstriction
of the afferent arterioles which lead to decrease
blood flow to the glomerulus.
Mechanism by which ACE inhibitors Cause
Pre-Renal Azotemia
ACE inhibitors causes vasodilation of the efferent
arterioles which lead to decrease intraglomerular pressure and decrease GFR.
Mechanism by which anticoagulants and
thrombolytics Cause Pre-Renal Azotemia
Anticoagulants and thrombolytic agent cause dissolution
of thrombus into small thrombi that can lead to
embolization of the renal arteries causing renal
ischemia, necrosis and infarction.
Drugs Causing Acute Interstitial Nephritis (AIN)
- Penicillins
- Cephalosporins
- Quinolones
- H2 receptors antagonists
- Proton Pump inhibitors
Renal (Intrinsic) Azotemia
Drugs that cause Acute Tubular Necrosis (ATN)
- Aminoglycosides
- Amphotericin
- Foscarnet
- Tenofovir
- Cisplatin
Renal (Intrinsic) Azotemia
Drugs that cause glomerular diseases and
rapidly progressive glomerulonephritis (RPGN)
- D-Penicillamine
- Hydralazine
- Propylthiouracil
Mechanism by which Aminoglycosides
Cause Acute Tubular Necrosis
Aminoglycosides accumulate in proximal tubular cell
lysozymes causing acute tubular necrosis
Post-Renal Azotemia
Drugs that cause intratubular obstruction
Crystal formation
- Acyclovir
- Indinavir
- Methotrexate
- Sulfonamides
Drugs that cause Rhabdomyolysis
- Statins and fibrates
- Zidovudine
- Antipsychotics
- Azathioprine
- Lithium
Types of Diuretics
- Thiazide Diuretics
- Loop Diuretics
- Osmotic Diuretics
- Carbonic Anhydrase inhibitors
- K+ sparing Diuretics
1.Thiazides Diuretics name(s)
2. Mechanism of Action
3. Adverse Effects
Chlorothiazide
Hydrochlorothiazide
Chlorthalidone
Indapamide
Metolazone
Mechanism of Action: Inhibit Na/Cl cotransport
Increase excretion: Na+, K+, Cl-, Mg++, HCO3
Decrease excretion: Ca++, Uric acid
Adverse Effects:
Hyponatremia, Hypokalemia, hypomagnesia, metabolic alkalosis,
Hypercalcemia and hyperuricemia
Thiazide diuretics increase plasma cholesterol and TGs (except indapamide)
Loop Diuretics
Name
MOA
A/E
Furosemide
Bumetanide
Torsemide
Ethacrynic acid
Mechanism of action: Inhibit the Na+/K+ dichloride cotransport system
Increase excretion: Na+, K+, Mg++, Cl-, HCO3, and Ca++
Adverse effects: Hyponatremia, hypokalemia, hypomagnesia
Metabolic alkalosis, hypocalcemia and Ototoxicity
Drug Interaction:
Loop diuretic + Antibiotic (aminoglycosides)
Increase risk for Ototoxicity
Osmotic Diuretics
Names
MOA
A/E
Mannitol
Glycerol
Mechanism of action: Increase the osmotic pressure in the proximal tubule which
Lead to inhibition of reabsorption of water and electrolytes
Indications:
Increase intracranial pressure (cerebral edema)
Increase intraocular pressure (acute glaucoma)
Acute renal failure
Adverse Effects:
Excessive plasma volume expansion which can lead to heart failure
Carbonic Andyddrase inhibitors
Names
MOA
A/E
Carbonic Anhydrase inhibitors
Acetazolamide
Dorzolamide
Mechanism of action: Increase excretion of Na+, K+, and HCO3
Indications:
High altitude sickness
Glaucoma
Overdose of acidic drugs (Alkalinize the urine)
Adverse effects
Drowsiness
Paresthesia
