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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
Contrast Induced Nephrotoxicity: presentation
nonoliguria presents w/in 24-48hrs ser Cr peaks bt 3 -5d after exposure recovery after 7-10d
26
Contrast Induced Nephrotoxicity: risk factors
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
27
Contrast Induced Nephrotoxicity: prevention
use alternative imaging procedures hydration antioxidants (ascorbic acid, N acetylcysteine) hemofiltration
28
Contrast Induced Nephrotoxicity: management
supportive care monitoring (renal function, electrolytes, volume status) renal replacement therapy
29
Amphotericin B Nephrotoxicity: pathogenesis
interaction w/ tubular cell membrane (inc permeability and necrosis) reduction in renal blood flow exacerbates ischemia
30
Amphotericin B Nephrotoxicity: presentation
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
Amphotericin B Nephrotoxicity: risk factors
``` CKD large ind doses large cum doses short infusion times vol depletion hypokalemia inc age concomitant diuretics concomitant nephrotoxins ```
32
Amphotericin B Nephrotoxicity: prevention
switch from liposomal form limit cum dose inc (slow) infusion time hydration concomitant nephrotoxins alternative antifungal agents - azole - caspofungin
33
Amphotericin B Nephrotoxicity: management
discontinue and substitute monitor renal function correct electrolytes
34
Cyclosporine Toxicity
dose dependent toxicity causes - distal tubular dysfunction - sev vasoconstriction renal function improves w/: - discontinuation - reducing dose
35
What diagnostic test is used to distinguish transplant rejection from cyclosporine toxicity?
kidney biopsy
36
Hemodynamically Mediated Kidney Alterations: offending agents
``` ACE-I ARB NSAIDs cyclosporine, tacrolimus OKT3 immunosuppresant (muromonab) ```
37
ACE-I and ARB Nephrotoxicity: pathogenesis
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
ACE-I and ARB Nephrotoxicity: presentation
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
What changes occur following initiation of ACE-I therapy?
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
ACE-I and ARB Nephrotoxicity: risk factors
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
ACE-I and ARB Nephrotoxicity: prevention
shorter acting agents (captopril, enalapril >lisinopril, benazepril) low dose w/ gradual titrations
42
ACE-I and ARB Nephrotoxicity: management
discontinue if ser Cr >30% above baseline over 1-2 wks can reinitiate after correcting volume depletion
43
NSAIDs and COX 2 Selective Nephrotoxicity: pathogenesis
inhibition of vasodilatory prostaglandins --> unopposed vasoconstriction of afferent arteriole --> renal ischemia, dec GFR
44
NSAIDs and COX 2 Selective Nephrotoxicity: clinical presentation
dec urine output occurs w/in days of event weight gain, edema inc ser Cr, BUN, K, BP
45
NSAIDs and COX 2 Selective Nephrotoxicity: risk factors
``` age >60 CKD CHF volume depletion concurrent diuretic therapy hepatic dz w/ ascites concurrent nephrotoxic drugs ```
46
NSAIDs and COX 2 Selective Nephrotoxicity: prevention
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
NSAIDs and COX 2 Selective Nephrotoxicity: management
severe injury is rare rapid recovery
48
Tubulointerstitial Diseases
acute allergic interstitial nephritis chronic interstitial nephritis papillary necrosis
49
Acute Allergic Interstitial Nephritis: offending agents
``` penicillins ciprofloxacin NSAIDs, COX2 inhibitors proton pump inhibitors loop diuretics ```
50
Chronic Interstitial Nephritis: offending agents
cyclosporine | lithium
51
Papillary Necrosis: offending agents
NSAIDs
52
Methicillin Induced Allergic Interstitial Nephritis: pathogenesis
hypersensitivity response diffuse infiltrate of lymphocytes, eosinophils, neutrophils tubular necrosis
53
Methicillin Induced Allergic Interstitial Nephritis: clinical presentation
associated w/ all beta lactams 14 days after initiation of therapy -- delayed presentation ``` fever maculopapular rash eosinophilia arthralgia oliguria ```
54
Methicillin Induced Allergic Interstitial Nephritis: risk factors
none
55
Methicillin Induced Allergic Interstitial Nephritis: prevention
none
56
Methicillin Induced Allergic Interstitial Nephritis: management
corticosteroids -- immediately discontinue --> full recovery
57
Obstructive Neuropathies
crystal neuropathy nephrolithiasis nephrocalcinosis
58
Crystal Nephropathy: offending agents
``` acyclovir sulfonamides indinavir foscarnet methotrexate ```
59
Nephrolithiasis: offending agents
sulfonammides triamterene indinavir ciprofloxacin amoxicillin nitrofurantoin
60
Nephrocalcinosis: offending agents
oral sodium phosphate solution
61
Crystal Nephropathy: pathogenesis
precipitation of drug crystals in tubular lumen
62
Nephrolithiasis: pathogenesis
formation of renal calculi or kidney stones **GFR NOT dec
63
Nephrolithiasis: presentation
pain hematuria infection urinary tract obstruction **high urine vol and alkalinization may be protective
64
Vasculitis and Thrombosis: offending agents
``` hydralazine propylthiouracil allopurinol penicillamine gemcitabine mitomycin C methamphetamines cyclosporine, tacrolimus adalimumab bevacizumab ```
65
Vasculitis and Thrombosis: clinical presentation
hematuria proteinuria red cell casts fever malaise myalgias arthralgias
66
Vasculitis and Thrombosis: treatment
withdraw offending drug administer corticosteroids/immunosuppressive therapy resolution in wks-mos
67
Cholesterol Emboli: offending agents
warfarin | thrombolytic agents
68
Cholesterol Emboli: clinical presentation
purple discoloration of toes mottled skin over legs
69
Cholesterol Emboli: treatment
supportive kidney injury is generally IRREVERSIBLE
70
Glomerular Disease: clinical presentation
nephrotic range proteinuria w/ or w/out decline in GFR

PHA 550 (26 decks)

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