Flashcards in Drug-Induced Kidney Disease Deck (44)
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1
Causes for prerenal AKI
Volume Depletion
1. Hemorrhagic
2. GI losses
3. Renal losses: Drug-induced, osmotic diuresis, diabetes insipidus
4. Skin losses: Burns
5. Third spacing (hypoalbuminemia)
Functional
1. ACE-1, ARB
2. NSAIDs
2
List causes for Acute tubular necrosis
Exogenous toxins:
1. Nephrotoxic drugs
2. Contrast
3
List causes for post renal AKI
Obstruction:
1. BPH
2. Tumor (malignancy)
3. Anticholinergic drugs
4. Displaced bladder catheter
4
What is the MC presentation of DIKD in hospitalized patients?
Acute Tubular Necrosis (ATN)
5
List the nephrotoxic agents that cause AKI
1. Aminoglycosides
2. Contrast
3. Amphotericin B
4. Osmotically active agents
6
Pathogenesis in hemodynamically mediated kidney injury
Decrease in glomerular capillary hydrostatic pressure
7
List the agents that cause hemodynamically mediated kidney injury
1. ACE-1
2. NSAIDs
8
How many days after you initiated therapy would you see clinical manifestations of acute allergic interstitial nephritis (AIN)? Sx's?
14 days
1. Fever
2. Maculopapular rash
3. Eosinophilia
4. Arthralgia
5. Hematuria, proteniuria, oliguria
9
What is the most common electrolyte disorder?
Hyperkalemia
10
What other electrolyte disorders do we see in kidney disease?
1. Hyperglycemia and insulin resistance
2. Hypertriglyceridemia
11
What is the pathogenesis of ATN with Aminoglycosides abx
Accumulation of high drug concentration in tubular epithelial cells leads:
1. Tubular damage
2. Kidney necrosis
12
How many days after initiation of Aminoglycosides do we see evidence of injury?
5-10 days
13
What is one of the main risk factors in ATN with the use of Aminoglycosides?
Pre-existing clinical condition
1. Dehydration*
2. CKD
3. DM
14
What is the main preventative strategy in ATN with the use of Aminoglycosides?
Avoid volume depletion
15
Pathogenesis of Contrast-Induced Nephrotoxicity (CIN)
Renal ischemia from systemic hypotension and acute vasoconstriction (contrast is a vasoconstrictor) d/t disruption of normal RBF
16
Clinical presentation of Contrast-Induced Nephrotoxicity (CIN)
1. Injury present w/in 24-48 hrs of administration
2. Serum Cr peaks w/in 3-5 days
3. Recovery in 7-10 days
17
Risk factors in Contrast-Induced Nephrotoxicity (CIN)
1. Pre-existing kidney dz, GFR <60 mL/min
2. Decreased RBF: CHF, dehydration
3. Concurrent use of nephrotoxins: NSAIS, ACE-1
18
Prevention of Contrast-Induced Nephrotoxicity (CIN)
Use alternative imaging procedures
19
Pathogenesis of ATN with the use of Amphotericin B
1. Increased permeability and necrosis
2. Decreased RBF exacerbates necrosis
20
What electrolytes will you see wasting with Amphotericin B?
1. Potassium
2. Sodium
3. Magnesium
21
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
22
What should you switch to for high risk patients in place of with the use of Amphotericin B?
Liposomal form
23
Amphotericin B prevention
1. Increase infusion time
2. Alternative antifungals: Azoles, Caspofungin
24
What do patients take Cyclosporine for?
Prevent kidney graft rejection
25
What is unique about Cyclosporine toxicity?
Dose-Dependent
26
Presentation of nephrotoxicity with use of ACE-1 and ARBs
1. Decrease in UO
2. Acutely reduces GFR
3. Rise in Serum Cr up to 30% in 3-5 days
27
How long after discontinuing the ACE-1 or ARB do you stabilize?
1-2 weeks
28
Risk factors for nephrotoxicity with the use of an ACE-1 or ARB
1. Renal artery stenosis
2. Decrease arterial blood flow: CHF, volume depletion
29
When should you discontinue an ACE-1 or ARB?
SCr increases >30% in 1-2 weeks
30
Pathogenesis of NSAIDs and COX-2 in pre-renal AKI
Inhibits synthesis of vasodilatory prostoglandins=unopposed vasoconstriction of afferent arteriole
31
Presentation of NSAIDs and COX-2 in pre-renal AKI
1. Decreased UO
2. Weiht gain/edema
3. HTN
4. Elevated SCr, BUN, K+
32
What is a a potent compound you should avoid in high risk patients with NSAIDs/COX-2 pre-renal AKI
Indomethacin
33
What NSAID can you consider that has a shorter half life for prevention management in pre-renal AKI?
Sulindac
34
What is Methicillin-induced AIN associated with? When do you see injury after initiation of these drugs?
Beta-lactacm abx
14 days after initiation
35
Clinical presentation of Methicillin-induced AIN
1. Fever
2, Maculopapular rash
3 Eosinophila
4. Arthralgia
5. Oliguria
36
How do you treat/manage Methicillin-induced AIN
Immediate corticosteroids
37
List the cause for chronic interstitial nephritis
1. Cyclosporine
38
List the cause for papillary necrosis
NSAIDs
39
What drugs can cause intratubular obstruction (obstructive nephropathy)?
1. Acyclovir
2. Sulfonamides
40
what conditions can cause intratubular obstruction (obstructive nephropathy)?
1. Hyperuricemia
2. Rhabdomyolysis
41
What drugs increases your risk for Rhabdomyolysis?
1. HMG-CoA reductase inhibitors (statins)
2. Concurrent CYP3A4 drugs
42
What drugs cause renal vasculitis and thrombosis
1. Hydralazine
2. Methamphetamine
43
What drugs cause a cholesterol emboli
1. Warfarin
2. Thrombolytic agents
44
