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830 > Drug-Induced Kidney Disease > Flashcards

Drug-Induced Kidney Disease Flashcards

1
Q

Reasons Kidneys are Susceptible to Drug Toxicity

A

Drug Exposure

  • Kidneys get 20-25% cardiac
  • Water reabsorption increases solute concentration in tubules

High Energy Requirements of Renal Tubular Cells

  • Metabolic enzymes in kidneys
  • Transporters in tubule cells
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2
Q

Drug-Induced Kidney Disease

A
  • > 1 type of renal injury may be present
  • Drugs can cause damage by more than one mechanism
  • 4 main histological components
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3
Q

4 Histological Components

A
  1. Blood Vessels
  2. Glomerulus
  3. Tubules
  4. Interstitium
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4
Q

Types of Drug-Induced Kidney Disease

A
  1. Hemodynamically Mediated Renal Failure
  2. Glomerulonephritis
  3. Acute Tubular Necrosis
  4. Acute Allergic Interstitial Nephritis
  5. Chronic Interstitial Nephritis
  6. Obstructive Nephropathy
  7. Acute Phosphate Nephropathy
  8. Pseudo-Renal Failure
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5
Q

Pseudo-Renal Failure

A
  • NO renal structures affects
  • Patho: increased production or decreased clearance of renal function markers
  • Presentation: Increased SCr OR BUN from baseline without actual decreases in GFR/kidney function
  • Outcome: SCr and BUN return to baseline when drug is stopped
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6
Q

Pseudo-Renal Failure Examples

A
  1. Increased protein catabolism - increases BUN (corticosteroid, tetracycline)
  2. Competitively inhibits renal tubule secretion of Cr which increases SCr (trimethoprim, fenofibrate)
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7
Q

Hemodynamically Mediated Renal Failure

A
  • Glomerulus blood vessels affected
  • Patho: decreased blood flo though glomerulus via AFFerent arteriole constriction OR EFFerent arteriole vasodilation
  • Presentation: Increased SCr and decreased GFR within days of drug initiation
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8
Q

NSAIDs & SGLT2i

A

Causes afferent arteriole vasoconstriction

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9
Q

ACEIs & ARBs

A
  • Causes efferent arteriole vasodilation

- Discontinue if SCr increases >50% or GFR decreases by >50% from baseline

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10
Q

Other Factors that Predispose ACEI Patients to DNI/AKI

A
  1. Na/H2O depletion: dehydration, poor fluid intake, low sodium diet
  2. ACEI dramatically decreases systemic blood pressure such that renal perfusion cannot be sustained
  3. Concomitant administration with drugs that cause affection afferent arteriole vasoconstriction
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11
Q

GN

A
  • Glomerulonephritis
  • Damage/inflammation to glomerular filtration surface
  • Patho: immune-mediated patho more common than direct toxicity
  • Presentation: proteinuria +/- decreased GFR, also dysmorphic RBCs in urine
  • EX: NSAIDs, ampicillin
  • Outcome: reversible depending on cause/length of insult
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12
Q

ATN

A
  • Acute Tubular Necrosis
  • Tubular epithelium damaged
  • Patho: caused by renally eliminated drugs, dose related partly, drugs/metabolites directly toxic or cause ischemia, cells die and slough off
  • Presentation: granular and epithelial casts (muddy and brown) with free epithelial cells in urine; also increased urinary sodium
  • Outcome: reversible if identified early; depends on drug/exposure/damage, PROLONGED recovery
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13
Q

ATN Examples

A
  1. Aminoglycoside
  2. Radiographic contrast dye
  3. Amphotericin B
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14
Q

Aminoglycoside-Induced Nephropathy - Patho

A

Patho: accumulates aminoglycoside in renal tubular cells => dysfunction and death

  • Dose dependent risk
  • Increased risk with prolonged therapy, large total cumulative doses, high trough concentrations
  • Presentation: increased SCr and decreased CrCl after 5-10 days of therapy, also cause hypo-osmolar, nonoliguria (>500 mL/day)
  • Outcome: usually reversible if caught early
  • Preventable: alternative agent, extend drug interval (once a day), monitor drug levels and kidney function
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15
Q

Radiographic Contrast Dye Nephropathy

A
  • Patho: direct tubular toxicity and/or renal ischemia
  • Risk Factors: diabetes, CKD, decreased blood flow patients (CHF, dehydration)
  • Risk increases as risk factors increase
  • Presentation: injury evident within 24 hours, SCr peaks in 2-5 days
  • Outcome: usually reversible, recovery after 4-10 days, irreversible oliguric kidney injury requiring dialysis reported in high-risk patients
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16
Q

Radiographic Contrast Dye Nephropathy Prevention

A
  • Use alternative imaging procedure that requires no contrast contrast agent
  • Administer smallest dose possible
  • Use low or iso-osmolar contrast dye
  • Hydration with IV
  • Avoid using with other nephrotoxic agents like aminoglycosides
  • Hold metformin before contrast and for 48 hours afterwards
17
Q

AIN

A
  • Acute Allergic Interstitial Nephritis
  • Inflammed tubules and interstitium
  • Patho: immune-mediated, idiosyncratic, not dose related
  • Presentation: onset ~2 weeks or as short as 3-5 days with re-exposure, causes fever or rash commonly, also eosinophilia/eosinophiluria/pyuria (while cell casts)
  • Outcome: usually reversible when drug is stopped, costicosteroids may increase rate/extent of renal recovery
18
Q

AIN Examples

A
  • Antibiotics: B-lactams

- PPIs

19
Q

Chronic Interstitial Nephritis

A
  • Tubular atrophy and interstitial fibrosis
  • Patho: not immune mediated usually, and potentially dose related
  • Presentation: slow, indolent progression to CKD
  • EX: lithium, cyclosporine, tacrolimus
  • Outcome: depends on underlying cause and severity of damage; usually permanent, leads to overt kidney failue
20
Q

Obstructive Nephropathy

A

-Any structure after glomerular filter can be affected
Patho: obstruction due to crystallization of drugs in tubules, leads to degradation products
-Clinical presentation: dependent on cause

21
Q

Precipitate of Drug/Metabolite

A
  • Example of obstructive nephropathy
  • Presentation: lower back/flank pain, hematuria
  • Example: acyclovir, sulfonamides
  • Outcome: usually reversible
22
Q

Tissue Degradation Products

A
  • Example of obstructive nephropathy
  • Presentation: oliguria/anuria
  • EX: acute tubular necrosis or Tumor-lysis syndrome
  • Outcome: dependent on underlying cause
23
Q

Acute Tubular Necrosis

A
  • Precipitation of myoglobin released
  • Drug induced rhabdomyolysis
  • Prevention: hydration, alter pH. Alkalinization with sulfonamides, uric acid nephropathy, and rhabdomyolysis
24
Q

Tumer-Lysis Syndrome

A
  • Chemo causes massive tumor cell destruction
  • Leads to intracellular contents being released
  • Causes metabolic abnormalities which increases uric acid levels
  • Prevention: hydration, allopurinol, rasburicase
25
Q

Acute Phosphate Nephropathy

A
  • Tubules and interstitium affected
  • Patho: calcium phosphate crystals in tubules/interstitium, related to transient hyperphosphatemia and volume depletion
  • Presentation: increased SCr in asymptomatic patients for days to months following oral sodium phosphate administration
  • EX: oral sodium phosphate
  • Outcome: develop long term CKD
26
Q

Acute Phosphate Nephropathy Prevention

A
  • Avoid in higher risk patients
  • Higher risk patients: CKD, ACEIs, ARBs, old, drugs, female, comorbidities
  • Limit the number of oral doses
27
Q

Managing Drug-Induced Nephrotoxicity

A
  1. Know which drugs are nephrotoxins
  2. Identify at risk patients
  3. Precautions to prevent: know baseline function, adjust doses, avoid exposure to multiple nephrotoxins, correct risk factors first OR use strategies to prevent DIN (like hydration)
  4. Monitor for lab and clinical signs of renal dysfunction (increase SCr/BUN, changes in urine, pain in back/flank)
  5. Resolve DIN if it occurs: stop nephrotoxic drugs, AKI will take time to heal

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