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Renal > DIKD > Flashcards

DIKD Flashcards

1
Q

What does DIKD stand for?

A

Drug-induced kidney disease

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2
Q

What are the changes in lab values in DIKD?

A

Lower GFR
Decreased UO
Increased SCr
Increased BUN

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3
Q

What is normal BUN?

A

5-20

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4
Q

What is normal SCr?

A

0.8-1.2

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5
Q

What is normal BUN:SCr ratio?

A

10-15:1

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6
Q

What is normal UO?

A

> 500 mL/day

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7
Q

What medications can cause DIKD?

A

Abx: AG, sulfonamides, PCN, cipro, Levo
Antifungal: Ampho B
Antivirals: Acyclovir, foscarnet, indinivir
OTC: NSAIDs, PPIs, Calcium
Other: ACE/ARB, diuretics, TAC, CsA, Allopurinol, MTX, Celecoxib

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8
Q

What are the risk factors for DIKD?

A
  1. Medications that can cause DIKD
  2. Age > 60
  3. Critically ill (ICU)
  4. Dehydration
  5. High dose of medications
  6. Multiple medications
  7. Increase in SCr >/= 0.3 w/in 48 hours; SCr increase >/= 1.5 x baseline w/in 7 days
  8. UO < 0.5 mL/kg/h for 6 hours - Patient produces < 400-500 mL of urine in a day; check Is & Os in the chart or ask a nurse to begin checking
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9
Q

What should always be monitored in DIKD?

A

SCr

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10
Q

What drugs are the cause of pre-renal DIKD?

A

ACE/ARBs
NSAIDs
TAC
CsA

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11
Q

What drugs are the cause of intrinsic ATN DIKD?

A

AGs
Ampho B
Radiocontrast dye

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12
Q

What drugs are the cause of intrinsic AIN DIKD?

A

PCN

Cipro/Levo

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13
Q

What drugs are the cause of intrinsic CIN DIKD?

A

TAC

CsA

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14
Q

What drugs are the cause of postrenal DIKD?

A

Acyclovir
MTX
Calcium

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15
Q

What happens to GFR when the AA is constricted?

A

Decreased

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16
Q

What happens to GFR when the AA is dilated?

A

Increased

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17
Q

What happens to GFR when the EA is constricted?

A

Increased

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18
Q

What happens to GFR when the EA is dilated?

A

Decreased

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19
Q

How do ACE/ARB affect the kidney?

A

Dilate the EA and inhibit constriction of the EA

Decreases perfusion pressure

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20
Q

How do we manage the affects of ACE/ARB on the kidney?

A

Remove/decrease offending agent
Start or reinitiate at a low dose and titrate up
Supportive care for AKI

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21
Q

A rise greater than ___% in SCr may indicate AKI

A

30%

22
Q

How do NSAIDs affect kidney function?

A

Constrict AA and inhibit prostaglandin-mediated dilation of AA
Decreased perfusion pressure

23
Q

What is the management of the affect of NSAIDs on the kidney?

A

Remove offending agent or decrease dose
Patients with a high dose of IBU and AKI should be switched to APAP
Supportive care for AKI

24
Q

What is NSAIDs cause if not managed properly?

A

ATN

25
Q

How do TAC/CsA affect kidney function?

A 
Increase potent vasoconstrictors (TXA2, endothelin, renin)
Decrease vasodilators (NO, prostacyclin, prostaglandin E2)
Presents w/in days w/HTN and oliguria
**Net imbalance of afferent and efferent tone, but more vasoconstriction of AA
26
Q

What is the management of the affect of TAC/CsA on the kidney?

A

Dose reduction and/or D/c interacting drugs
Monitor trough levels if SCr and/or BUN increase
Supportive care for AKI

27
Q

What is supportive care for AKI?

A

Maintain adequate hemodynamic status
Maintain glucose control
Manage complications

28
Q

What drugs should not be combined?

A

TAC/CsA/NSIADs with ACE/ARBs

29
Q

What does ATN stand for?

A

Acute tubular necrosis

30
Q

What is the most common cause of acute injury and failure?

A

ATN

31
Q

What are the lab values in ATN?

A 
BUN:SCr = 20:1
Brown urine
Granular casts (b/c of dead cells)
32
Q

How do AGs cause ATN?

A

Absorbed in proximal tubule, stored in lysosomes
Lysosomes burst and release large amount into rest of nephron -> saturation -> epithelial damage
Presents gradually 5-10 days after initiation

33
Q

How do we manage the affects of AG in ATN?

A

D/c or adjust dose/frequency:

  • if SCr increases > 0.5 mg/dL
  • maintain adequate hydration
34
Q

How do we prevent the affects of AG in ATN?

A

Monitor levels

Once daily dosing: except in seriously ill, immunocompromised, and elderly

35
Q

How does ampho B affect kidney function?

A

Direct tubular toxicity from interaction with cholesterol
-Ion channels form -> increase permeability -> lipid peroxidation -> necrosis
Renal ischemia - Decreased perfusion intrarenally
Presents with K, Na, and Mg wasting; also non-oliguria -> usually in 1-2 weeks

36
Q

What is the management of ampho B in ATN?

A

Consider using other formulations: liposomal, lipid complex, colloidal, dispersion
D/c therapy and use another antifungal

37
Q

What are preventative measures for ATN when taking ampho B?

A

Monitor electrolytes daily (order chem 7 and Mg)
Administer 1 L IV NaCl daily during treatment
AND
10-15 mL/kg before each dose

38
Q

What is the mechanism for ATN when using radiocontrast dye?

A

Renal ischemia - hypotension and/or vasoconstriction decreases intrarenal perfusion
Direct proximal tubule toxicity

39
Q

What is the prevention for ATN when using radiocontrast dye?

A

Use lowest dose possible

Sodium bicarbonate or fluid hydration pre- and post-administration - controversial

40
Q

What is the management of ATN when using radiocontrast dye?

A

Supportive care

41
Q

What is the cause of AIN?

A

Interstitial tissue and tubules inflame d/t hypersensitivity

42
Q

What are the drugs that cause AIN?

A

PCN

Levo/Cipro

43
Q

What will present in the labs in patients with AIN?

A

Blood smear will show eosinophils

UA will have eosinophils, WBCs and casts

44
Q

What is the management of AIN?

A

Methylprednisolone or prednisone

45
Q

What drugs cause CIN?

A

Calcineurin Inhibitors and Lithium

46
Q

What is the pathophysiology of CIN?

A 
May affect all 3 tubule compartments
Results from chronic ischemia from: 
-Increased endothelin-1
-Decreased Nitric acid
-Upregulation of TGF-beta
47
Q

What intrinsic DIKD is dose dependent?

A

AIN

48
Q

What are the etiologies of post-renal AKI?

A 
BPH
Nephrolithiasis
Pelvic or cervical cancer
Bladder cancer
Urethral obstruction
Neurogenic bladder
Precipitation of drugs in a low urine volume with relative insolubility in either alkaline or acidic urine
49
Q

What drug causes precipitation at phsyiologic urine pH in dehydrated oliguric patients?

A

Acyclovir

50
Q

What drugs can cause nephrolithiasis?

A

Acyclovir
MTX
Calcium

51
Q

What will we see in a lab analysis of patients with post-renal AKI?

A

Little proteinuria
Resembles pre-renal but progresses to intrinsic
BUN:SCr >/= 20:1

52
Q

What is the management of patients with post-renal AKI?

A

Hydrate patient before administration
Increase fluids if nephrolithiasis
Catheterization or stenting to relieve pain
Pain management

Renal (8 decks)

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