Drug-Induced Kidney Disease Flashcards
(44 cards)
Causes for prerenal AKI
Volume Depletion
- Hemorrhagic
- GI losses
- Renal losses: Drug-induced, osmotic diuresis, diabetes insipidus
- Skin losses: Burns
- Third spacing (hypoalbuminemia)
Functional
- ACE-1, ARB
- NSAIDs
List causes for Acute tubular necrosis
Exogenous toxins:
- Nephrotoxic drugs
- Contrast
List causes for post renal AKI
Obstruction:
- BPH
- Tumor (malignancy)
- Anticholinergic drugs
- Displaced bladder catheter
What is the MC presentation of DIKD in hospitalized patients?
Acute Tubular Necrosis (ATN)
List the nephrotoxic agents that cause AKI
- Aminoglycosides
- Contrast
- Amphotericin B
- Osmotically active agents
Pathogenesis in hemodynamically mediated kidney injury
Decrease in glomerular capillary hydrostatic pressure
List the agents that cause hemodynamically mediated kidney injury
- ACE-1
2. NSAIDs
How many days after you initiated therapy would you see clinical manifestations of acute allergic interstitial nephritis (AIN)? Sx’s?
14 days
- Fever
- Maculopapular rash
- Eosinophilia
- Arthralgia
- Hematuria, proteniuria, oliguria
What is the most common electrolyte disorder?
Hyperkalemia
What other electrolyte disorders do we see in kidney disease?
- Hyperglycemia and insulin resistance
2. Hypertriglyceridemia
What is the pathogenesis of ATN with Aminoglycosides abx
Accumulation of high drug concentration in tubular epithelial cells leads:
- Tubular damage
- Kidney necrosis
How many days after initiation of Aminoglycosides do we see evidence of injury?
5-10 days
What is one of the main risk factors in ATN with the use of Aminoglycosides?
Pre-existing clinical condition
- Dehydration*
- CKD
- DM
What is the main preventative strategy in ATN with the use of Aminoglycosides?
Avoid volume depletion
Pathogenesis of Contrast-Induced Nephrotoxicity (CIN)
Renal ischemia from systemic hypotension and acute vasoconstriction (contrast is a vasoconstrictor) d/t disruption of normal RBF
Clinical presentation of Contrast-Induced Nephrotoxicity (CIN)
- Injury present w/in 24-48 hrs of administration
- Serum Cr peaks w/in 3-5 days
- Recovery in 7-10 days
Risk factors in Contrast-Induced Nephrotoxicity (CIN)
- Pre-existing kidney dz, GFR <60 mL/min
- Decreased RBF: CHF, dehydration
- Concurrent use of nephrotoxins: NSAIS, ACE-1
Prevention of Contrast-Induced Nephrotoxicity (CIN)
Use alternative imaging procedures
Pathogenesis of ATN with the use of Amphotericin B
- Increased permeability and necrosis
2. Decreased RBF exacerbates necrosis
What electrolytes will you see wasting with Amphotericin B?
- Potassium
- Sodium
- Magnesium
When does the dysfunction become apparent with the use of Amphotericin B? Lab findings?
1-2 weeks
Decrease in GFR
Increase in Serum Cr and BUN
What should you switch to for high risk patients in place of with the use of Amphotericin B?
Liposomal form
Amphotericin B prevention
- Increase infusion time
2. Alternative antifungals: Azoles, Caspofungin
What do patients take Cyclosporine for?
Prevent kidney graft rejection