not all drugs are good drugs: Kidney Flashcards

1
Q

Drug induced kidney disease risk factors

A
  • 65+
  • CKD
  • Conmitant nephrotoxins
  • Renin-dependent state
    • Low effective circulating volume
      • HF
      • Cirrhosis
  • Known drug allergy
  • Duration of therapy
  • DM
  • HTN
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2
Q

Drug induced kidney disease general prevention

A
  • Directly prevent the drugs MOA of kidney injury
  • Avoid the drugs in high risk pts
  • Maintain adequate kidney perfusiion
    • Hydration
    • IV isotonic crystalloids in pts at risk of AKI
      • Lacated ringers
      • Plasma-lyte A
      • 0.9% NaCl
  • TDM if relevant
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3
Q

Kidney function monitorinng

A
  • SCr, BUN, eGFR, urinary output
  • Novel biomarkers: are markers of damage;
  • Traditional biomarkers: SCr and BUN are markers of function
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4
Q

Drugs that cause hemodynamic mediated renal injury via reduction in glomerular pressure dt alterations in arteriole tone

A
  • ACE/ARB
  • NSAID
  • SGLT2
  • CNI (cyclosporine, tacrolimus)
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5
Q

ACE/ARB mechanism of kidney injury

A

decrease angiotensin II → efferent arteriole dilation

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6
Q

NSAID mechanism of kidney injury

A

decrease PGE2 production → afferent arteriole constriction

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7
Q

Calcineurin inhibitor mechanism of kidney injury

A

afferent arteriole constriction

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8
Q

hemodynamic mediated renal injury via reduction in glomerular pressure dt alterations in arteriole tone risk factors

A
  • dehydration/low volume state + the culprit drugs → highest risk for AKI
  • NSAID + ACE/ARB = loss of autoregulation → increased risk of decreased intraglomerular hydrostatic pressure → decreased GFR
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9
Q

hemodynamic mediated renal injury via reduction in glomerular pressure dt alterations in arteriole tone prevention methods

A
  • Adequate fluid intake
  • Risk factor management
  • Start with lowest dose in pts with highest risk
    - monitor SCR, BUN, K, wt Q2W until stable
    - hold diuretics during intiating/titrating
  • Avoid NSAID + ACE/ARB combo in pts with CKD, HF, liver disease
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10
Q

hemodynamic mediated renal injury via reduction in glomerular pressure dt alterations in arteriole tone treatment

A
  • DC offending agent
  • Provide sufficient fluids
    - typically 0.9% NaCl
  • Monitor kidney function and electrolytes
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11
Q

Drugs that cause pre-renal kidney injury via reduced blood flow in the kidney

A

diuretics; decreases effective circulatory volume if over-diuresis occurs

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12
Q

Drugs that cause glomerulonephritis

A
  • Gold
  • Allopurinol
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13
Q

Drugs that cause acute tubular necrosis (ATN)

A
  • aminoglycosides
  • amphotericin B (conventional has higher risk than liposomal)
  • IV contrast media (iohexol, iodixanol)
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14
Q

IV contrast media induced kidney injury risk factors

A

Agent specific
- Large volume
- High osmolal contrast
- Ionic contrast
- Short interval between contrast admin
Pt specific
- DM
- Age
- GFR < 60
- low ECV
- LVEF < 40%

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15
Q

Aminoglycoside risk factor for kidney injury

A
  • related to trough [ ] → TDM and PK individualization much important
  • no difference in extennded and regluar interval dosing → but most places use extended
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16
Q

Prevention method fo IV contrast media induced kidney injury

A

For contrast media: 0.9% NaCl give 1-1.5 ml/kg/hr 12 hours before and after
- can also add PO NAC 1200mg PO BID x 4 doses (limited evidence on efficacy but is well tolerated)

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17
Q

Drug induced acute tubular nerosis treatment

A
  • SUPPORTIVE CARE
  • DC offending agent
  • Hydration
  • Electrolyte management
  • Dialysis if severe (anuria, uremia, edema, K>7)

THIS IS ATN TREATMENT

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18
Q

Drugs that cause acute interisitial nephritis

A
  • Allopurinol
  • Anti-epileptics
  • Beta-lactams
  • Diuretics
  • *NSAIDs
    Penicillins
    PPIs
    Sulfa drugs**
  • Vanco
19
Q

Mechanism of injury for acute interstitial nephritis (AIN)

A

Immune activation / hypersensitivity → leukocyte infiltration → inflammation → AIN

20
Q

Vanco AKI risk factors

A
  • high trough >20 mg/L
  • AUC >600
  • TDD >4g
  • LOT >7D
  • wt >101.4kg
21
Q

Prevention methods for vanco induced kidney injury

A

avoid concomitant use with aminoglycosides, amphotericin, and contrast

22
Q

drug indcued acute interstitial nephritis treatment

A
  • Stop offending drug
  • Avoid cross-reacting drugs
  • Supportive care
  • Steroids: early aggressive steroid may improve long-term renal outcome
    > give large bolus, then taper
    MePn 250-500mg IV QD x 3-5 days
    Then Pred 1 mg/kg/d tapered x 8-12 weeks
23
Q

Drugs that cause vasculitis

A
  • PTU
  • Allopurinol
  • Phenytoin
  • Cocaine
24
Q

Drugs that cause nephrolithiasis

A
  • Acyclovir
  • Allopurinol
  • Furosemide
  • Sulfonamides
  • Topiramate
25
Q

Prevention methods for drug indcued nephrolithaisis

A
  • Adequate hydration
    - goal urine output >2.5 L/day
  • TZD diuretic if high urinary Ca → decrease the amount of Ca that can precipitate into stones
26
Q

Drug indudced nephrolithiasis treatment

A
  • Hydration
  • Pain management
  • Lithotripsy: shockwave disintegration of stone
27
Q

Drugs that cause rhabdomyolysis intra-tubular obstruction

A
  • statins/statin-fibrate combos
28
Q

Statin induced kidney injury MOA

A

Statins → rhabdomyolysis → muscle breakdown → precipitation of myoglobin in kidneys

29
Q

drug induced rhabdomyolysis intra-tubular obstruction treatment

A
  • DC offending agent
  • Aggressive IV fluid -> treats the intra-tubular
    myoglobin obstruction)
  • may require urinary alkanization if urine pH < 6.5
    • alternate between IV NaCl and sodium bicarb to fix
  • Target UOP ~ 3ml/hr
30
Q

Lithium indcued CKD risk factors

A

cumulative lithium dose and other common sense things

31
Q

lithium induced CKD prevention methods

A
  • Lithium TDM
  • Stay hydrated
  • Renal monitoring
  • Avoid DDI (e.g. HCTZ)
32
Q

lithium induced CKD treatment

A
  • damage is IRREVERSIBLE
  • DC lithium
  • Hydrate
  • Amiloride 5-20mg QD if polydipsia/polyuria and especially if nephrogenic diabetes insipidus)
  • Avoid other nephrotoxic drugs
  • Monitor renal function
33
Q

1 cause of CKD

A

diabetes

34
Q

number 2 cause of CKD

A

HTN

35
Q

A patient is considered high risk for drug induced kidney disease if:

A

Renin dependent disease states
- late stage CKD
- HF
- liver disease
- pronounced albuminuria @ baseline
On many nephrotoxic drugs

36
Q

24 hour trough goal for EIAD

A

undetectable
EIAD = extended interval aminoglycoside dosing

37
Q

CIN agent: Iohexol [Omnipaque 450]

A

nonionic
lower osmolality

38
Q

CIN agent: Iodixanol [Visipaque 320]

A
  • nonionic
  • iso-osmolar
  • preferred contrast media
39
Q

Monitoring for CIN (contrast media)

A

Renal fx
- SCr, BUN Q12H x 2 days, then Q24H x 5-7 days inpatient

UOP
- strict in/out x 4 days

Med review
Electrolytes - only if renal injury develops

40
Q

When monitoring for CIN, we regularly monitor for electrolytes: True/False?

A

False
Electrolytes only checked if kidney injury develops - does not tell you about RISK or the presence of injury

41
Q

IBW

A

F: 45.5 + 2.3 (inches over 60)
M: 50 + 2.3 (inches over 60)

41
Q

Cockcroft gault

A

[(140 - age ) x IBW] / (72xSCr)
- if female x 0.85

42
Q

ATN presentation

A
  • Acute progression - rapid recovery
  • ↑SCr, BUN
  • ↓GFR, UO (non-oligu/olig )
  • Proteinuria
  • Muddy brown casts, granular
  • +/- acidosis, hyperkalemia
  • FeNa >1% (pre-renal AKI would have FeNa<1%)
43
Q

AIN presentation

A
  • Type 4 hypersensitivity
  • Fever, rash, eosinophilia
  • WBC casts