DIKD

Question 1

What does DIKD stand for?

Answer 1

Drug-induced kidney disease

Question 2

What are the changes in lab values in DIKD?

Answer 2

Lower GFR
Decreased UO
Increased SCr
Increased BUN

Question 3

What is normal BUN?

Answer 3

5-20

Question 4

What is normal SCr?

Answer 4

0.8-1.2

Question 5

What is normal BUN:SCr ratio?

Answer 5

10-15:1

Question 6

What is normal UO?

Answer 6

> 500 mL/day

Question 7

What medications can cause DIKD?

Answer 7

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

Question 8

What are the risk factors for DIKD?

Answer 8

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

Question 9

What should always be monitored in DIKD?

Answer 9

SCr

Question 10

What drugs are the cause of pre-renal DIKD?

Answer 10

ACE/ARBs
NSAIDs
TAC
CsA

Question 11

What drugs are the cause of intrinsic ATN DIKD?

Answer 11

AGs
Ampho B
Radiocontrast dye

Question 12

What drugs are the cause of intrinsic AIN DIKD?

Answer 12

PCN

Cipro/Levo

Question 13

What drugs are the cause of intrinsic CIN DIKD?

Answer 13

TAC

CsA

Question 14

What drugs are the cause of postrenal DIKD?

Answer 14

Acyclovir
MTX
Calcium

Question 15

What happens to GFR when the AA is constricted?

Answer 15

Decreased

Question 16

What happens to GFR when the AA is dilated?

Answer 16

Increased

Question 17

What happens to GFR when the EA is constricted?

Answer 17

Increased

Question 18

What happens to GFR when the EA is dilated?

Answer 18

Decreased

Question 19

How do ACE/ARB affect the kidney?

Answer 19

Dilate the EA and inhibit constriction of the EA

Decreases perfusion pressure

Question 20

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

Answer 20

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

Question 21

A rise greater than ___% in SCr may indicate AKI

Answer 21

30%

Question 22

How do NSAIDs affect kidney function?

Answer 22

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

Question 23

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

Answer 23

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

Question 24

What is NSAIDs cause if not managed properly?

Answer 24

ATN

Question 25

How do TAC/CsA affect kidney function?

Answer 25

``` 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 ```

Question 26

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

Answer 26

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

Question 27

What is supportive care for AKI?

Answer 27

Maintain adequate hemodynamic status Maintain glucose control Manage complications

Question 28

What drugs should not be combined?

Answer 28

TAC/CsA/NSIADs with ACE/ARBs

Question 29

What does ATN stand for?

Answer 29

Acute tubular necrosis

Question 30

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

Answer 30

ATN

Question 31

What are the lab values in ATN?

Answer 31

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

Question 32

How do AGs cause ATN?

Answer 32

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

Question 33

How do we manage the affects of AG in ATN?

Answer 33

D/c or adjust dose/frequency: - if SCr increases > 0.5 mg/dL - maintain adequate hydration

Question 34

How do we prevent the affects of AG in ATN?

Answer 34

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

Question 35

How does ampho B affect kidney function?

Answer 35

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

Question 36

What is the management of ampho B in ATN?

Answer 36

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

Question 37

What are preventative measures for ATN when taking ampho B?

Answer 37

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

Question 38

What is the mechanism for ATN when using radiocontrast dye?

Answer 38

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

Question 39

What is the prevention for ATN when using radiocontrast dye?

Answer 39

Use lowest dose possible | Sodium bicarbonate or fluid hydration pre- and post-administration - controversial

Question 40

What is the management of ATN when using radiocontrast dye?

Answer 40

Supportive care

Question 41

What is the cause of AIN?

Answer 41

Interstitial tissue and tubules inflame d/t hypersensitivity

Question 42

What are the drugs that cause AIN?

Answer 42

PCN | Levo/Cipro

Question 43

What will present in the labs in patients with AIN?

Answer 43

Blood smear will show eosinophils | UA will have eosinophils, WBCs and casts

Question 44

What is the management of AIN?

Answer 44

Methylprednisolone or prednisone

Question 45

What drugs cause CIN?

Answer 45

Calcineurin Inhibitors and Lithium

Question 46

What is the pathophysiology of CIN?

Answer 46

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

Question 47

What intrinsic DIKD is dose dependent?

Answer 47

AIN

Question 48

What are the etiologies of post-renal AKI?

Answer 48

``` 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 ```

Question 49

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

Answer 49

Acyclovir

Question 50

What drugs can cause nephrolithiasis?

Answer 50

Acyclovir MTX Calcium

Question 51

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

Answer 51

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

Question 52

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

Answer 52

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