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Pharm I ( Melicia) > Drug Induced Kidney Dz - EG > Flashcards

Drug Induced Kidney Dz - EG Flashcards

1
Q

What is the MC manifestation of drug induced kidney disease (DIKD)

A

decline in GFR

rise in serum creatine and BUN

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2
Q

Nephrotoxicity is often reversible if…

A

offending agent is discontinued

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3
Q

How does the kidney maintain glomerular ultrafiltration when renal blood flow is diminished?

A

vasodilating afferent arterioles & vasoconstricting efferent arterioles

(afferent > glomerulus > efferent)

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4
Q

postrenal impairment

A

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

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5
Q

acute glomerulonephritis

A

inflammation and damage to the glomerular membrane

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6
Q

acute interstitial nephritis

A

an allergic reaction, may be caused by a variety of drugs

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7
Q

acute tubular necrosis causes:

A

nephrotoxic agents

prolonged hypoperfusion

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8
Q

What is the MC presentation of DIKD in hospitalized patients? examples of primary agents that can cause this?

A

Acute tubular necrosis (ATN)

- aminoglycosides, contrast, amphotericin B, cyclosporin

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9
Q

Name 2 drugs that cause hemodynamically mediated kidney injury

A

ACEI’s and NSAID’s

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10
Q

Clinical manifestations of Acute allergic interstitial nephritis (AIN)

A

fever, maculopapular rash, eosinophilia, arthralgia, pyuria, hematuria, proteinuria, oliguria

approx. 14 days after initiation of therapy

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11
Q

List 3 medications affected by pharmacokinetic alterations

A

Vancomycin
Aminoglycosides
Low-molecular-weight heparins

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12
Q

How does edema affect the distribution of many drugs?

A

can significantly increase the volume of distribution

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13
Q

What is the MC electrolyte disorder and why is it important to monitor frequently?

A

HYPERkalemia bc it can lead to life-threatening cardiac arrhythmias

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14
Q

What 2 electrolytes are eliminated by the kidneys and not removed efficiently by dialysis?

A

Phosphorus

Magnesium

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15
Q

What electrolyte disorder leads to protein catabolism and negative nitrogen balance?

A

protein metabolism

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16
Q

What 2 conditions cause tubular epithelial cell damage

A

ATN

osmotic nephrosis

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17
Q

Describe the pathogenesis of Aminoglycoside (AG) nephrotoxicity

A
  • accumulation of high concentrations w/in tubular epithelial cells –> kidney necrosis
  • toxicity related to # of cationic groups on molecule (i.e. Neomycin > gentamycin > tobramycin > amikacin)
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18
Q

Describe the clinical presentation AG nephrotoxicity?

A
  • Nonoliguria (>500ml urine production/day)
  • evidence of injury w/in 5-10 days of therapy
  • gradual rise in serum Cr and BUN & decrease in CrCl
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19
Q

Can a patient make a full recovery of renal function after AG nephrotoxicity if the drug is immediately discontinued?

A

YES

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20
Q

Risk factors of AG nephrotoxicity

A
  • aggressiveness of AG dosing
  • synergistic toxicity w/other nephrotoxins
  • preexisting clinical conditions
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21
Q

Best prevention for AG nephrotoxicity

A

Avoid volume depletion

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22
Q

Pathogenesis of Contrast-induced nephrotoxicity (CIN)

A

renal ischemia from systemic hypotension and acute vasoconstriction

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23
Q

Clinical presentation for Contrast-induced nephrotoxicity (CIN)

A

nonoligura (>500ml urine production/day)
injury w/in first 24/48hrs of administration
serum Cr peaks between 3-5 days
recovery after 7-10 days

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24
Q

Risk factors for CIN

A
  • preexisting kidney disease, GFR <60
  • decreased renal blood flow
  • concurrent use of nephrotoxins (NSAIDS, ACEI’s)
25
Q

Prevention for CIN

A

use alternative imaging procedures*

hydration

26
Q

Pathogenesis of Amphotericin B Nephrotoxicity

A
  • increasing permeability and necrosis

- reduction in renal blood flow exacerbates ischemia

27
Q

Clinical presentation of Amphotericin B Nephrotoxicity

A
  • Nonoligura (>500ml urine production/day)
  • K, Na, & Mg wasting
  • dysfunction apparent in 1-2 weeks
  • decr. in GFR, rise in serum Cr and BUN
  • damage may be irreversible
28
Q

Prevention of Amphotericin B Nephrotoxicity

A

switching to liposomal form in high risk pt’s
increase infusion time
alternative antifungal agents (azoles, caspofungin)

29
Q

Pt’s taking cyclosporine to prevent kidney allograft rejection often need ____, to distinguish transplant rejection from cyclosporine toxicity

A

A kidney biopsy

30
Q

Pathogenesis of ACEI and ARB nephrotoxicity

A
  • becomes nephrotoxic particularly when renal blood flow is reduced*
  • synthesis of Angiotensin II is decreased
  • efferent arteriole remains dilated
  • reduced outflow resistance from glomerulus
  • decreases hydrostatic pressure in glomerular capillaries
31
Q

Presentation of ACEI and ARB nephrotoxicity

A
  • decrease in urine output
  • acutely reduces GFR
  • serum Cr rise 30% w/in 3-5 days
  • stabilizes in 1-2 weeks
  • reversible upon stopping
32
Q

Risk factors for ACEI and ARB nephrotoxicity

A
  • patients dependent on renal vasoconstriction to maintain BP and GFR (renal a. stenosis)
  • decreased arterial blood volume
33
Q

Prevention of ACEI and ARB nephrotoxicity

A

choose shorter acting agent in at risk pt’s…

Captopril, enalapril > lisinopril, benazepril

34
Q

Management of ACEI and ARB nephrotoxicity

A
  • discontinue if serum Cr increases >30% above baseline over 1-2 wks
  • serum Cr and hyperkalemia will resolve over several days
  • re-initiation can be attempted after correcting volume depletion
35
Q

Pathogenesis NSAIDs and COX2 selective nephrotoxicity

A
  • inhibit synthesis of vasodilatory prostaglandins
  • unopposed renal vasoconstriction in afferent arteriole
  • promotes renal ischemia and GFR reduction
36
Q

Presentation of NSAIDs and COX2 selective nephrotoxicity

A
  • occurs w/in days of event
  • diminished urine output
  • weight gain or edema
  • elevated serum Cr, BUN, K, and BP
37
Q

Biggest risk factor for NSAIDs and COX2 selective nephrotoxicity

A

Age >60

38
Q

Management of NSAIDs and COX2 selective nephrotoxicity

A

injury is rarely severe

recovery is usu. rapid

39
Q

Prevention of NSAIDs and COX2 selective nephrotoxicity

A
  • avoid potent compounds in high risk groups (indomethacin)
  • use analgesics w/less PGE inhibition (APAP)
  • consider drugs w/short half lives (Sulindac)
  • COX-2 agents have similar renal effect (Meloxicam, Celecoxib)
40
Q

drugs that account for 70% of cases of acute allergic interstitial nephritis

A 
penicillins
ciprofloxacin
nsaids, cox2 inhibitors
PPI's
Loop diuretics
41
Q

What medication causes papillary necrosis?

A

NSAID’s

42
Q

What drugs cause chronic interstitial nephritis

A

Cyclosporine

lithium

43
Q

Methicillin-induced allergic interstitial nephritis (AIN) pathogenesis

A
  • diffuse infiltrate of lymphocytes, eosinophils, neutrophils
  • tubular necrosis is relatively common
44
Q

Methicillin-induced allergic interstitial nephritis (AIN) clinical presentation

A
  • assoc. w/ beta-lactam abx
  • presents 14 days after initiation of therapy
  • fever, macropupular rash, eosinophilia, arthralgia, oliguria
45
Q

Methicillin-induced allergic interstitial nephritis (AIN) management

A

corticosteroids should be initiated immediately

46
Q

Intratubular obstruction is caused by which meds?

A

acyclovir
sulfonamides
methotrexate

47
Q

nephrolithiasis is caused by which meds?

A

Sulfonamides
Ciprofloxacin
Amoxicillin
Nitrofurantoin

48
Q

Examples of intratubular obstruction from crystal nephropathy

A

precipitation of drug crystals in tubular lumen
hyperuricemia
rhabdomyolysis

49
Q

Which drugs are highly associated with rhabdomyolysis? and when is risk increased?

A

HMG-CoA reductase inhibitors (simvastatin, lovastatin)

risk increased w/concurrent CYP34A drugs (Gemfibrozil, Niacin, Erythromycin)

50
Q

Clinical presentation of nephrolithiasis

A

pain, hematuria, infection, urinary tract obstruction

GFR not usu. decreased

51
Q

What drugs are associated with renal vasculitis, thrombosis and cholesterol emboli?

A

vasculitis and thrombosis –> Hydralazine, methamphetamines

Cholesterol emboli –> Warfarin, thrombolytic agents

52
Q

How do pt’s with renal vasculitis and thrombosis present?

A

hematuria, proteinuria, oliguria, red cell casts, and frequently along w/ fever, malaise, myalgias, arthralgias

53
Q

What are important clues that a pt may have a renal cholesterol emboli?

A

purple discoloration of the toes

mottled skin over the legs

54
Q

What is a hallmark sign of glomerular injury?

A

nephrotic range proteinuria (>3.5g/day) w/ or without a decline in GFR

55
Q

which meds can lead to glomerular disease?

A

NSAID’s & COX-2 inhibitors*
gold
lithium
pamidronate

56
Q

At what level in the nephron does ATN occur?

A

proximal tubules

57
Q

What are signs of distal tubular injury?

A

polyuria from failure to maximally concentrate urine
metabolic acidosis d/t urinary acidification
hyperkalemia from impaired K+ excretion

58
Q

What are signs of proximal tubular injury?

A

metabolic acidosis w/ bicarbonaturia

glycosuria in absence of hyperglycemia

59
Q

What lab test/results indicate a drug-induced AKI?

A
  • increase in serum Cr of greater or equal to 0.3mg/dL or 50% w/in 7 days
  • reduction in urine output (oliguria <0.5ml/kg/h for more than 6hrs)

Pharm I ( Melicia) (18 decks)

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