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PHA 550 > Drug Induced Kidney Disease > Flashcards

Drug Induced Kidney Disease Flashcards

1
Q

What are the MC manifestations of drug induced kidney disease?

A

decline in GFR

rise in serum CR and BUN

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2
Q

BUN

A

blood urea nitrogen

marker of renal health

if GFR and blood volume dec –> BUN inc

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3
Q

With drug induced kidney disease, is the nephrotoxicity reversible or irreversible?

A

reversible

discontinue offending agent

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4
Q

Drug Induced Kidney Disease: what to look for

A 
acid base abnormalities
electrolyte imbalance
urine sediment abnormalities
proteinuria
pyuria 
hematuria
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5
Q

What causes a prerenal reduction in renal function?

A

dec in blood flow and renal perfusion

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6
Q

What causes an intrinsic AKI?

A

damage to the glomerular or tubular regions

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7
Q

What causes postrenal impairment?

A

obstruction of urine flow in the collecting tubule , ureter, bladder or urethra

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8
Q

Parameters for possible drug induced AKI

A

inc serum Cr 0.3+ within 48 hrs

inc serum Cr 50%+ (1.5 times baseline) within 7d

red urine output (<0.5/hr for 6hrs)

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9
Q

What is the MC presentation of DIKD in hospitalized patients?

A

acute tubular necrosis

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10
Q

What are the primary agents implicated in ATN with DIKD?

A 
aminoglycosides
radiocontrast media
cisplatin
amphotericin B
osmotically active agents
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11
Q

What is the pathogenesis of hemodynamically mediated kidney injury?
What are the primary implicated agents?

A

dec in glomerular capillary hydrostatic pressure

ACE-I, NSAIDs

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12
Q

Acute Allergic Interstitial Nephritis: clinical presentation

A

present ~14d after initiation of therapy

fever
maculopapular rash
eosinophilia
arthralgia

pyuria
hematuria
proteinuria
oliguria

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13
Q

Pharmokinetic Alterations

A

edema (inc volume of distribution)

multisystem organ failure (red cardiac output and liver function)

ex: vancomycin, aminoglycosides, low MW heparin

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14
Q

Hyperkalemia

A

MC electrolyte disorder

life threatening cardiac arrhythmias (ser K >6)

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15
Q

Phosphorus and Magnesium Elimination

A

eliminated by kidneys

not removed efficiently by dialysis

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16
Q

Drugs causing tubular epithelial cell damage: ATN

A 
AMINOGLYCOSIDES
RADIOGRAPHIC CONTRAST MEDIA
cisplatin, carboplatin
AMPHOTERICIN B
CYCLOSPORINE, tacrolimus
adefovir, cidofovir, tenofovir
pentamidine
foscarnet
zoledronate
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17
Q

Drugs causing tubular epithelial cell damage: osmotic nephrosis

A

mannitol
dextran
IV immunoglobulin

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18
Q

Aminoglycoside Nephrotoxicity: pathogenesis

A

high concentration of drug in proximal tubular epithelial cells –> mitochondrial injury –> kidney necrosis

reversible!

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19
Q

Aminoglycoside Nephrotoxicity: ranked most to least nephrotoxic

A

neomycin>gentamicin>tobramycin>amikacin

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20
Q

Aminoglycoside Nephrotoxicity: clinical presentation

A

nonoliguria

evidence of injury w/in 5-10d of therapy

gradual rise in ser Cr and BUN
dec in CrCl

AG discontinued –> full recovery of renal function

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21
Q

Aminoglycoside Nephrotoxicity: risk factors

A

aggressiveness of AG dosing

synergistic toxicity w/ other nephrotoxins

preexisting clinical conditions

  • CKD
  • diabetes
  • inc age
  • dehydration
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22
Q

Aminoglycoside Nephrotoxicity: prevention

A

careful selection of patients

use alternative abx when possible

avoid volume depletion

limit total dose administered

avoid concomitant nephrotoxic drugs

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23
Q

Aminoglycoside Nephrotoxicity: management

A

discontinue drug/revise dosing

stop other nephrotoxic drugs

adequate hydration

renal replacement therapy

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24
Q

Contrast Induced Nephrotoxicity: pathogenesis

A

renal ischemia from systemic hypotension and acute vasoconstriction

may last for several hours

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25
Q

Contrast Induced Nephrotoxicity: presentation

A

nonoliguria

presents w/in 24-48hrs

ser Cr peaks bt 3 -5d after exposure

recovery after 7-10d

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26
Q

Contrast Induced Nephrotoxicity: risk factors

A

inc RF –> inc mortality

preexisting kidney disease (GFR<60)

dec renal blood flow

  • CHF
  • dehydration/volume depletion
  • hypotension
  • diabetes

concurrent use of nephrotoxins

  • NSAIDs
  • ACE-Is
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27
Q

Contrast Induced Nephrotoxicity: prevention

A

use alternative imaging procedures

hydration

antioxidants (ascorbic acid, N acetylcysteine)

hemofiltration

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28
Q

Contrast Induced Nephrotoxicity: management

A

supportive care

monitoring (renal function, electrolytes, volume status)

renal replacement therapy

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29
Q

Amphotericin B Nephrotoxicity: pathogenesis

A

interaction w/ tubular cell membrane (inc permeability and necrosis)

reduction in renal blood flow exacerbates ischemia

30
Q

Amphotericin B Nephrotoxicity: presentation

A

nonoliguria

K, Na, Mg wasting

impaired urinary concentration

dysfunction apparent in 1-2 wks

dec in GFR
rise in serCr and BUN

irreversible damage

31
Q

Amphotericin B Nephrotoxicity: risk factors

A 
CKD
large ind doses
large cum doses
short infusion times
vol depletion
hypokalemia
inc age
concomitant diuretics
concomitant nephrotoxins
32
Q

Amphotericin B Nephrotoxicity: prevention

A

switch from liposomal form

limit cum dose

inc (slow) infusion time

hydration

concomitant nephrotoxins

alternative antifungal agents

  • azole
  • caspofungin
33
Q

Amphotericin B Nephrotoxicity: management

A

discontinue and substitute

monitor renal function

correct electrolytes

34
Q

Cyclosporine Toxicity

A

dose dependent toxicity

causes

  • distal tubular dysfunction
  • sev vasoconstriction

renal function improves w/:

  • discontinuation
  • reducing dose
35
Q

What diagnostic test is used to distinguish transplant rejection from cyclosporine toxicity?

A

kidney biopsy

36
Q

Hemodynamically Mediated Kidney Alterations: offending agents

A 
ACE-I
ARB
NSAIDs
cyclosporine, tacrolimus
OKT3 immunosuppresant (muromonab)
37
Q

ACE-I and ARB Nephrotoxicity: pathogenesis

A

dec synthesis of angiotensin II

dilated efferent arteriole

reduced outflow resistance from glomerulus

dec hydrostatic pressure in glomerular capillaries

becomes nephrotoxic particularly when renal blood flow is reduced

38
Q

ACE-I and ARB Nephrotoxicity: presentation

A

dec urine output

acute reduction in GFR

30% rise in ser Cr w/in 3-5d (associated w/ preservation of renal function)

stabilizes in 1-2wks

reversible

39
Q

What changes occur following initiation of ACE-I therapy?

A

dec synthesis of angiotensin II

dilation of efferent arteriole

red outflow resistance from the glomerulus
dec hydrostatic pressure in the glomerular capillaries

dec intraglomerular pressure and GFR

NEPHROTOXICITY

40
Q

ACE-I and ARB Nephrotoxicity: risk factors

A

dependent on renal vasoconstiction to maintain BP and GFR (renal artery stenosis)

dec arterial blood volume

  • CHF
  • volume depletion
  • hepatic cirrhosis w/ ascites

CKD

Concurrent nephrotoxic drugs

41
Q

ACE-I and ARB Nephrotoxicity: prevention

A

shorter acting agents (captopril, enalapril >lisinopril, benazepril)

low dose w/ gradual titrations

42
Q

ACE-I and ARB Nephrotoxicity: management

A

discontinue if ser Cr >30% above baseline over 1-2 wks

can reinitiate after correcting volume depletion

43
Q

NSAIDs and COX 2 Selective Nephrotoxicity: pathogenesis

A

inhibition of vasodilatory prostaglandins –> unopposed vasoconstriction of afferent arteriole –> renal ischemia, dec GFR

44
Q

NSAIDs and COX 2 Selective Nephrotoxicity: clinical presentation

A

dec urine output

occurs w/in days of event

weight gain, edema

inc ser Cr, BUN, K, BP

45
Q

NSAIDs and COX 2 Selective Nephrotoxicity: risk factors

A 
age >60
CKD
CHF
volume depletion
concurrent diuretic therapy
hepatic dz w/ ascites
concurrent nephrotoxic drugs
46
Q

NSAIDs and COX 2 Selective Nephrotoxicity: prevention

A

avoid potent compounds w/ high risk pts (indomethacin)

use alternative drugs

  • less PGE inhibition: acetaminophen
  • shorter half life: sulindac

COX2 agents have similar renal effect (meloxicam, celecoxib)

47
Q

NSAIDs and COX 2 Selective Nephrotoxicity: management

A

severe injury is rare

rapid recovery

48
Q

Tubulointerstitial Diseases

A

acute allergic interstitial nephritis
chronic interstitial nephritis
papillary necrosis

49
Q

Acute Allergic Interstitial Nephritis: offending agents

A 
penicillins
ciprofloxacin
NSAIDs, COX2 inhibitors
proton pump inhibitors
loop diuretics
50
Q

Chronic Interstitial Nephritis: offending agents

A

cyclosporine

lithium

51
Q

Papillary Necrosis: offending agents

A

NSAIDs

52
Q

Methicillin Induced Allergic Interstitial Nephritis: pathogenesis

A

hypersensitivity response

diffuse infiltrate of lymphocytes, eosinophils, neutrophils

tubular necrosis

53
Q

Methicillin Induced Allergic Interstitial Nephritis: clinical presentation

A

associated w/ all beta lactams

14 days after initiation of therapy – delayed presentation

fever
maculopapular rash
eosinophilia
arthralgia
oliguria
54
Q

Methicillin Induced Allergic Interstitial Nephritis: risk factors

A

none

55
Q

Methicillin Induced Allergic Interstitial Nephritis: prevention

A

none

56
Q

Methicillin Induced Allergic Interstitial Nephritis: management

A

corticosteroids – immediately

discontinue –> full recovery

57
Q

Obstructive Neuropathies

A

crystal neuropathy
nephrolithiasis
nephrocalcinosis

58
Q

Crystal Nephropathy: offending agents

A 
acyclovir
sulfonamides
indinavir
foscarnet
methotrexate
59
Q

Nephrolithiasis: offending agents

A

sulfonammides
triamterene
indinavir

ciprofloxacin
amoxicillin
nitrofurantoin

60
Q

Nephrocalcinosis: offending agents

A

oral sodium phosphate solution

61
Q

Crystal Nephropathy: pathogenesis

A

precipitation of drug crystals in tubular lumen

62
Q

Nephrolithiasis: pathogenesis

A

formation of renal calculi or kidney stones

**GFR NOT dec

63
Q

Nephrolithiasis: presentation

A

pain
hematuria
infection
urinary tract obstruction

**high urine vol and alkalinization may be protective

64
Q

Vasculitis and Thrombosis: offending agents

A 
hydralazine
propylthiouracil
allopurinol
penicillamine
gemcitabine
mitomycin C
methamphetamines
cyclosporine, tacrolimus
adalimumab
bevacizumab
65
Q

Vasculitis and Thrombosis: clinical presentation

A

hematuria
proteinuria
red cell casts

fever
malaise
myalgias
arthralgias

66
Q

Vasculitis and Thrombosis: treatment

A

withdraw offending drug

administer corticosteroids/immunosuppressive therapy

resolution in wks-mos

67
Q

Cholesterol Emboli: offending agents

A

warfarin

thrombolytic agents

68
Q

Cholesterol Emboli: clinical presentation

A

purple discoloration of toes

mottled skin over legs

69
Q

Cholesterol Emboli: treatment

A

supportive

kidney injury is generally IRREVERSIBLE

70
Q

Glomerular Disease: clinical presentation

A

nephrotic range proteinuria

w/ or w/out decline in GFR

PHA 550 (26 decks)

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