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SG - Pharm 4 > DIKD 2 > Flashcards

DIKD 2 Flashcards

1
Q

Pathogenesis of what?

  • Interaction w/ tubular cell membrane
    • increasing permeability & necrosis*
  • Reduction in renal blood flow exacerbates ischemia*
A

Amphotericin B Nephrotoxicity

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2
Q

Presentation of what?

  • Nonoliguria (>500ml urine production/day)
  • K, Na, Mg wasting*
  • Impaired urinary concentration
  • Dysfunction apparent in 1-2 weeks*
  • Decrease in GFR / Rise in Scr and BUN*
  • Damage may be irreversible*
A

Amphotericin B Nephrotoxicity

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3
Q

What leads to wasting of Na, K, and Mg?

A

Direct damage of distal tubular membranes–>

Tubular glomerular feedback: further constriction of arterioles–>

Constriction of afferent arterioles leading to decreased glomerular filtration

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4
Q

What “retains” calcium?

A

Hydrochlorithiazide

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5
Q

Potassium needs to be around what # to be effective?***

A

4

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6
Q

Risk Factors of what?

  • CKD
  • Large individual doses
  • Large cumulative doses
  • Short infusion times
  • Volume depletion
  • Hypokalemia
  • Increased age
  • Concomitant diuretics
  • Concomitant nephrotoxins
A

Amphotericin B Nephrotoxicity

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7
Q

How to prevent Amphotericin B Nephrotoxicity

(3 main things)

A
  • Switching from liposomal form in high risk patients**
  • Increase infusion time**
  • Alternative antifungal agents**
    • Azoles
    • Caspofungin
  • Low threshold for stopping
  • Limit cumulative dose
  • Concomitant nephrotoxins
  • Hydration
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8
Q

Management of Amphotericin B Nephrotoxicity

(3 things)

A
  • Discontinuation & Substitution
  • Monitoring of renal function
  • Correct electrolytes as needed
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9
Q

Which drug?

  • Toxicity is usually dose dependent
  • It causes distal tubular dysfunction (a type 4 renal tubular acidosis) & severe vasoconstriction
  • Regular blood level monitoring is important to prevent both acute & chronic nephrotoxicity
  • Renal function usually improves after reducing the dose or stopping the drug
A

Cyclosporine

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10
Q

With patients who are taking ______ to prevent kidney allograft rejection, kidney biopsy is often necessary to distinguish transplant rejection from _______ toxicity.

A

Cyclosporine / Cyclosporine

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11
Q

Drug Induced Kidney Structural - Functional Alterations:

Hemodynamically Mediated Kidney Injury

What is the treatment?

A
  • ACE-I**
  • ARB**
  • NSAIDs**
  • Cyclosporine, tacrolimus
  • OKT3-immunosuppresant (muromonab) (Anti-rejection drugs)
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12
Q

Pathogenesis of what?

  • Synthesis of angiotensin II is decreased
  • Efferent arteriole remains dilated (mismatch)
  • Reduces outflow resistance from the glomerulus
  • Decreases hydrostatic pressure in the glomerular capillaries
  • Becomes nephrotoxic particularly when renal blood flow is reduced!***
A

ACE-I and ARB nephrotoxicity

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13
Q

Presentation of what?**

  • Decrease in urine output
  • Acutely reduces GFR, rise in Scr should be expected
  • Scr rise up to 30% within 3-5 days
    • desired pharmacologic effect
    • Rise associated w/ preservation of renal function
  • Stablilizes in 1-2 weeks
  • Reversible upon stopping
A

ACE-I & ARB Nephrotoxicity

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14
Q

What drug blocks prostaglandins?

A

NSAIDs

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15
Q
  • Are located in the stomach lining and kidney
  • Involved in afferent blood flow
  • NOT involved in efferent blood flow
A

Good prostaglandins

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16
Q

What drug therapy?

  • Synthesis of angiotensin II is decreased
  • Preferential dilation of the efferent arteriole
  • Reduces outflow resistance from the glomerulus & decreases hydrostatic pressure in the glomerular capillaries
  • Alters Starling Forces across the glomerular capillaries to decrease intraglomerular pressure & GFR**
  • Leads to nephrotoxicity**
  • Particularly in the setting of reduced renal blood flow or effective arterial blood volume in pre-renal settings (CHF)
A

ACE-I

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17
Q

What drug therapy?

  • Afferent & Efferent are affected
  • Prostaglandin is NOT affected
  • Increase in Scr of 30%
A

ACE-I

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18
Q

Risk Factors of what toxicity?

  • Patient’s dependent on renal vasoconstriction to maintain BP and GFR*
    • Renal Artery Stenosis*
  • Decreased arterial blood volume*
    • CHF
    • Volume depletion from excess diuresis
    • Hepatic cirrhosis w/ ascites
  • CKD
  • Concurrent use of nephrotoxic drugs
A

ACE-I and ARB Nephrotoxicity

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19
Q

How to prevent ACE-I and ARB Nephrotoxicity?

(2 things)

A
  • Choose shorter acting agent in patients at risk
    • Captopril, enalapril > lisinopril, benazepril
  • Use low doses w/ gradual titrations
    • 2-4 weeks
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20
Q

ACE-I and ARBs can cause what?

A

Hyperkalemia

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21
Q

Management of ACE-I and ARB Nephrotoxicity

A
  • Discontinue if Scr increases >30% above baseline over 1-2 weeks
    • Scr and hyperkalemia will resolve over several days
    • Reinitiation can be attempted after correcting volume depletion

(be careful giving older pts NSAIDs bc/ their kidney function is dependent on prostaglandin…)

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22
Q

Pathogenesis of what?

  • Inhibit synthesis of vasodilatory prostaglandins**
  • Alters normal response in reduced renal bood flow
    • Unopposed renal vasoconstriction in afferent arteriole**
  • Promotes renal ischemia & GFR reduction**
A

NSAIDs and COX-2 Selective Nephrotoxicity

23
Q

Presentation of what?**

  • Occurs within days of volume loss or initiating therapy
  • Diminished urine output
  • Weight gain or edema
  • Scr , BUN, potassium, and BP are elevated
A

NSAIDs and COX-2 Selective Nephrotoxicity

24
Q

Risk factors of NSAIDs and COX-2 Selective Nephrotoxicity

(a bunch and 1 main one*)

A
  • **Age >60**
  • CKD
  • CHF
  • Volume Depletion
  • Concurrent diuretic therapy
  • Hepatic disease w/ ascites
  • Concurrent nephrotoxic drugs
25
Q

Management of what?**

  • Injury is rarely severe
  • Recovery is usually rapid
A

NSAIDs & COX-2 Selective Nephrotoxicity

26
Q

Prevention of what toxicity?**

  • Avoid potent compounds in high risk groups
    • Indomethacin (used for gout)
  • Use analgesics w/ less PGE inhibition
    • APAP (acetaminophen)
  • Consider drugs w/ short half-lives
    • Sulindac
  • 2 agents w/ similar effect
    • Meloxicam
    • Celecoxib
A

NSAIDs and COX-2 Selective Nephrotoxicity

27
Q

Drug-Induced Kidney Structural-Functional Alterations:

Tubulointerstitial Disease

  • What is the condition we learned about in this category?
A

Acute Allergic Interstitial Nephritis

28
Q

What do these drugs cause?

  • Penicllins
  • Ciprofloxacin
  • NSAIDs
  • Cyclooxygenase-2 inhibitors
  • Proton pump inhibitors (omeprazole)
  • Loop diuretics (furosemide)
A

Acute Allergic Interstitial Nephritis

(Tubulointerstitial Disease)

29
Q

2 drugs which cause Chronic Interstitial Nephritis

(Tubulointerstitial Disease)

A
  • Cyclosporine**
  • Lithium
30
Q

What drug causes Papillary Necrosis

(Tubulointerstitial Disease)

A

NSAIDs

31
Q

3 types of Tubulointerstitial Diseases

A
  • Acute allergic Interstitial Nephritis
  • Chronic Interstitial Nephritis
  • Papillary Necrosis
32
Q

Pathogenesis of what?

  • Allergic hypersensitivity response
  • Diffuse infiltrate of lymphocytes, eosinophils, and neutrophils
  • Tubular necrosis is relatively common
A

Methicillin - Induced Allergic Interstitial Nephritis (AIN)

33
Q

Presentation of what?***

  • Associated w/ all Beta-Lactam abx
  • Presents 14 days after initiation of therapy (delayed presentation**)
  • Clinical signs:
    • fever
    • macropapular rash
    • eosinophilia
    • arthralgia
    • oliguria
A

Methicillin-Induced Allergic Interstitial Nephritis (AIN)

34
Q

What are the risk factors and prevention of Methicillin-Induced Allergic Interstitial Nephritis (AIN)?

A

None

35
Q

Management of Methicillin-Induced Allergic Interstitial Nephritis (AIN)?

A
  • Corticosteroids should be initiated immediately*** + stop the drug!!
  • Discontinue offending agent
  • Full recovery if prompt discontinuation
36
Q

Drug-Induced Kidney Structural-Functional Alterations:

Obstructive Nephropathy (post-renal)

  • What are the 3 types?
A
  • Crystal Nephropathy**
  • Nephrolithiasis**
  • Nephrocalcinosis
37
Q

5 drugs which cause Crystal Nephropathy

(Obstructive Nephropathy) post renal

A
  • Acyclovir**
  • Sulfonamides**
  • Methotrexate
  • Indinavir
  • Foscarnet
38
Q

3 drugs which cause Nephrolithiasis

(Obstructive Nephropathy)

A
  • Sulfonamides** (Bactrim DS, take w/ large volume of water)
  • Triamterene
  • Indinavir
39
Q

Obstructive Nephropathy:

  • Precipitation of drug crystals in tubular lumen**
  • Hyperuricemia**
    • adequate hydration
    • allopurinol
  • Rhabdomyolysis
    • precipitation of myoglobin
A

Crystal Nephropathy

40
Q

What 2 types of drugs cause Rhabdomyolysis associated w/ Crystal Nephropathy?

A
  • HMG-CoA reductase inhibitors**
    • Simvastatin
    • Lovastatin
  • Risk is increased w/ concurrent CYP3A4 drugs**
    • Gemfibrozil
    • Niacin
    • Erythromycin
41
Q

Obstructive Nephropathy

  • Formation of renal calculi or kidney stones**
    • GFR not usually decreased
  • Presentation:
    • pain, hematuria
    • infection, urinary tract obstruction
A

Nephrolithiasis

42
Q

3 drugs are implicated for Nephrolithiasis

A
  • Ciprofloxacin**
  • Amoxicillin**
  • Nitrofurantoin**
43
Q

What 2 drugs cause Renal Vasculitis* and thrombosis*?

A
  • Hydralazine
  • Methamphetamines
44
Q

Most drug induced cases of vasculitis result in the development of what?

A

Anti-neutrophil cytoplasmic antibody (ANCA) positive vasculitis

45
Q

Presentation of what?

  • hematuria
  • proteinuria
  • oliguria
  • red cell casts
  • fever
  • malaise
  • myalgias
  • arthralgias
A

Drug Induced Renal Vasculitis and thrombosis

46
Q

Tx of drug induced renal vasculitis and thrombosis?

A
  • Withdraw offending drug
  • Administer corticosteroids or other immunosuppressive therapy

(leads to resolution of sxs within weeks to months) = takes a long time to resolve

47
Q

What 2 drugs cause Cholesterol Emboli?

A
  • Warfarin –> purple toes
  • Thrombolytic agents
48
Q

Warfarin and other thrombolytic agents act to remove / prevent thrombus formation over ulcerative plaques or may induce hemorrhage within clots, thereby causing showers of _______ that lodge in small diameter arteries of the kidney (renal arterioles and glomerular capillaries)

A

Cholesterol crystals

49
Q

______ induce an endothelial inflammatory response which leads to complete obstruction, ischemia, and necrosis of affected vessels within weeks to months after initiation of therapy

A

Cholesterol crystal emboli

50
Q

Purple discoloration of the toes and ____ over the legs are important clinical clues of what?

A

mottled skin

(Warfarin causing cholesterol emboli)

51
Q

Tx of cholesterol emboli?

A

Supportive in nature, since the kidney injury is generally irreversible

52
Q

DIKD: Glomerular Disease

What is the hallmark sign of glomerular injury?

A

Proteinuria (nephrotic range >3.5g/day) with or without a decline in GFR

53
Q

3 types of Glomerular Disease

A
  • Minimal Change Disease
  • Membranous Disease
  • Focal Segmental Glomerulosclerosis
54
Q

What medications are implicated for glomerular disease?

(2 main ones)

A
  • NSAIDs**
  • Cyclooxygenase inhibitors**
  • Lithium
  • Pamidronate
  • Interferon alpha and beta
  • anabolic steroids

SG - Pharm 4 (16 decks)

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