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Renal > Drug-Induced Kidney Disease > Flashcards

Drug-Induced Kidney Disease Flashcards

1
Q

There are 5 general principles to prevent DIKD in patients, what are they?

A
  1. Avoid and limit exposure of nephrotoxic agents
  2. Avoid the concomitant use of nephrotoxic agents
  3. Avoid initiation of nephrotoxic drugs
  4. Adjust dosing according to kidney function
  5. Ensure adequate hydration
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2
Q

There are 3 general principles to manage DIKD in patients, what are they?

A
  1. Discontinue offending agent
  2. Hydration for volume depleted
  3. Supportive care (managing glucose, maintaining hemodynamics, nutritional support, consequence of AKI)
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3
Q

What medications cause damage in the prerenal area?

A
  • ACEi/ARBs
  • NSAIDs/COX-2 inhibitors
  • Calcineurin inhibitors
  • SGLT-2 inhibitors
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4
Q

Define prerenal

A

Before the kidneys OR perfusion of the kidneys

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5
Q

What conditions can be caused by intrinsic renal?

A

Acute tubular necrosis (ATN)
Tubular interstitial nephritis
- Acute allergic interstitial nephritis (AIN)
- Chronic allergic interstitial nephritis

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6
Q

What medications cause acuter tubular necrosis?

A
  • Aminoglycosides
  • Radiocontrast media
  • Amphotericin B
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7
Q

What medications cause acute, allergic interstitial nephritis (AIN)?

A
  • Beta lactams
  • NSAIDs
  • PPIs
  • Diuretics (loops and thiazides)
  • Immune checkpoint inhibitors (CTLA-4 and PD-1)
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8
Q

What medications cause chronic, allergic interstitial nephritis?

A
  • Calcineurin inhibitors (tacrolimus and cyclosporine)
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9
Q

Define intrinsic

A

Inside the structure of the kidneys (nephrons)

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10
Q

What conditions can be caused by post renal?

A
  • Nephrolithiasis

- Crystal nephropathy

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11
Q

What medications cause nephrolithiasis?

A
  • Sulfonamides
  • Antiretrovirals
  • Ciprofloxacin
  • Pseudoephedrine
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12
Q

What medications cause crystal nephropathy?

A
  • Sulfonamides
  • Acyclovir
  • Methotrexate
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13
Q

Define post renal

A

After the kidney OR involves blockage of filtrate

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14
Q

What is the presentation of ACEi/ARBs in prerenal activity?

A

SCr > 30% from 3-5 days of initiating therapy

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15
Q

What are the risk factors of ACEi/ARBs in prerenal activity?

A
  • Renal artery stenosis
  • HF
  • Sepsis
  • Preexisting renal disease
  • Hypovolemia
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16
Q

How can clinicians prevent DIKD with ACEi/ARBs?

A

Start at low doses and titrate as needed

17
Q

How can clinicians manage DIKD with ACEi/ARBs?

A

Monitor hyperkalemia

18
Q

What is the pathophysiologic mechanism of ACEi/ARBs?

A

Dilates efferent arteriole leading to a reduced GFR

19
Q

What is the presentation of NSAIDs/COXi in prerenal activity?

A

Low urine output, weight gain, edema within 2-7 days of initiating

20
Q

What are the risk factors of NSAIDs/COXi in prerenal activity?

A
  • Age > 65 yo
  • Concomitant use of ACEi/ARBs or diuretics
  • Heart failure
  • Hepatic disease/ascites present
  • Hypovolemia
  • SLE
21
Q

How can clinicians manage DIKD with NSAIDs/COXi?

A
  • Switch to APAP or analgesics with less prostaglandins inhibition
22
Q

What is pathophysiologic mechanism of NSAIDs/COXi?

A
  • Constrict afferent arteriole leading to a reduced GFR
23
Q

What is the presentation of calcineurin inhibitors (tacrolimus/cyclosporine) in prerenal activity?

A

SCr rises, oliguria, hyperkalemia, hypomagnesemia

24
Q

What are the risk factors of calcineurin inhibitors?

A
  • Age > 65 yo
  • Drug-drug interactions
  • High doses
  • Concomitant use w/ nephrotoxic drugs
  • Polymorphic P-gp expression
25
Q

How can clinicians prevent DIKD with calcineurin inhibitors?

A

Monitor serum trough levels

26
Q

What is the pathophysiologic mechanism of calcineurin inhibitors?

A

Reduce vasodilators synthesis and increase vasoconstrictors unbalancing the afferent and efferent arterioles leading to a reduced GFR

27
Q

What is the pathophysiologic mechanism of SGLT-2 inhibitors in prerenal activity?

A
  • Volume depletion occurs

- Afferent arteriole becomes constricted from tubuloglomerular feedback from macula densa

28
Q

What are the risk factors of SGLT-2 inhibitors?

A
  • Age > 65 yo
  • Volume depleted
  • Concomitant use of nephrotoxic agents
29
Q

How can clinicians prevent DIKD with SGLT-2 inhibitors?

A

If eGFR < 30 mL/min, avoid the use of SGLT-2 inhibitors

30
Q

What is the presentation of aminoglycosides in acute tubular necrosis?

A

Non-oliguria presents within 5-7 days of initiation

31
Q

What are the risk factors of aminoglycosides?

A
  • Aggressive dosing
  • Prolonged therapy
  • High trough levels exceeding 2 mcg/mL
  • Concomitant use of nephrotoxic drugs
32
Q

How can clinicians prevent DIKD with aminoglycosides?

A

Switch from conventional to high-dose extended interval dosing

33
Q

How can clinicians manage DIKD with aminoglycosides?

A

RRT may be needed in severe patients

34
Q

What is the pathophysiologic mechanism of aminoglycosides in acute tubular necrosis?

A
  • Accumulates in the PCT leading to generation of oxygen reactive species
  • Cell sloughing causes tubular obstruction and reduction in eGFR
35
Q

What is the presentation of radiocontrast media in acute tubular necrosis?

A

Non-oliguria within 24-48 hrs of initiation

36
Q

What are some risk factors of radiocontrast media?

A
  • Pre-existing renal disease
  • HF
  • Diabetic kidney disease
  • Concomitant use of nephrotoxic agents
  • Dehydration
37
Q

How can clinicians prevent DIKD with the use of radiocontrast media?

A
  • Minimizing contrast dose
  • Use low osmolar nonionic agents
  • Use alternative imaging techniques that do not require contrast
38
Q

What is the pathophysiologic mechanism of radiocontrast media in acute tubular necrosis?

A
  • Renal ischemia

- Direct cellular toxicity leads to ATN

Renal (4 decks)

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