Acute Kidney Injury Drugs

Question 1

Prerenal
- Drugs

Answer 1

ACEi/ARBs
NSAIDS
Celcinerurin Inhibitors

Question 2

Intrarenal (Acute Tubular Necrosis)
- Drugs

Answer 2

Amphotericin B
Aminoglycosides
Radiographic Contrast Dye

Question 3

Intrarenal (Acute Interstitial Nephritis)
- Drugs

Answer 3

Penicillins
Lithium

Question 4

Intrarenal (Chronic Interstitial Nephritis)
- Drugs

Answer 4

Calcineurin Inhibitors
Lithium
NSAIDs

Question 5

Postrenal
- Drugs

Answer 5

Acyclovir
Indinavir
Sulfonamide Antibiotics

Question 6

AKI and ACE/ARB
- Presentation

Answer 6

Therapy causes Serum Creatinine to rise by 25-30% within 2-7 days of initiation of therapy
- Stabilizes within 1 week

Question 7

AKI and ACE/ARB
- Mechanism

Answer 7

ACEi dilute efferent arteriole –> Reduces glomerular hydrostatic pressure
- Lower GFR

Summary: Prevents vasoconstriction of efferent arteriole

Question 8

AKI and ACE/ARB
- Lab Values

Answer 8

Urine
- Low urine
- Low sodium

Very concentrated urine
- High urea, High creatinine

No cells in urine

Question 9

AKI and ACE/ARB
- Prevention

Answer 9

Maintain hydration

Do not use with NSAIDS

Low dose and titrate slowly

Monitor SCr and Potassium

Question 10

AKI and NSAIDS
- Considerations

Answer 10

Do not combine ACE and NSAID, both alter renal blood flow

Low dose ASA does not impair renal function

Question 11

AKI and NSAIDS
- Presentation

Answer 11

Low urine volume
Edema/Weight gain
Elevated SCr, K+ and Urea

Question 12

AKI and NSAIDS
- Mechanism

Answer 12

NSAIDS inhibit COX-2, which normally forms prostaglandins which compensate altered renal perfusion

Without COX-2, PGE2 response is inhibited
- afferent arterial dilation and reduce GFR

Question 13

AKI and NSAIDS
- Lab Values

Answer 13

Low urine volume
Low urine sodium

Concentrated urine
- High Urea, High Creatinine

No cells in urine

Question 14

AKI and NSAIDS
- Prevention

Answer 14

Avoid prolonged NSAID use in elderly patients, Heart failure patients, or CKD patients

Do not use with ACE/ARB

Start with low dose and titrate slowly

Monitor BP and SCr

Question 15

AKI
- NSAIDS vs ACE/ARB

Answer 15

NSAIDS affect PGE2 and afferent arteriole
- Inhibit afferent arteriole dilation = Less Blood = Low GFR

ACE/ARB affect Angiotensin II and efferent arteriole
- Causes dilation of efferent arterioles = Less pressure = Low GFR

Question 16

Most common intrarenal AKI

Answer 16

Acute Tubular Necrosis

Question 17

ATN
- Different phases

Answer 17

Oliguric Phase
- Within 24 hours, lasts 1-3 weeks

Diuretic Phase
- Indicates renal recovery

Question 18

ATN
- Different kinds

Answer 18

Nephrotoxic ATN
- Endogenous or Exogenous
–> Myoglobin
–> Aminoglycosides (Tobramycin, Gentamicin)
–> CT Contrast Dye

Ischemic ATN
- Ischemia and Toxin related

Question 19

AKI and Aminoglycosides
- Mechanism

Answer 19

ATN

Epithelial cell damage at proximal tubular cells
- Caused by cationic charge

Question 20

AKI and Aminoglycosides
- Lab Values

Answer 20

ATN

Brown Cast Cells and Epithelial Cells in Urine
High Sodium in urine

Question 21

AKI and NSAIDS
- Management

Answer 21

Discontinue
Supportive Therapy

Question 22

AKI and ACE/ARB
- Management

Answer 22

Discontinue
Supportive Therapy

Question 23

AKI and Aminoglycosides
- Management

Answer 23

Discontinue
Supportive Therapy
- Correct volume derangements
- Correct metabolic acidosis
- Hemodialysis/Renal Replacement Therapy

Question 24

AKI and Aminoglycosides
- Prevention

Answer 24

Avoid hypovolemia
Avoid nephrotoxic drugs
Avoid high risk populations
- Elderly
- Pre-existing renal failure

Question 25

AKI and Amphotericin B - Mechanism

Answer 25

ATN Direct toxicity to cells in distal nephron - Cell death and necrosis Kidneys lose ability to filter and concentrate urine

Question 26

AKI and Amphotericin B - Management

Answer 26

Hydration Use of liposomal formulations Limit dose Monitor renal function Avoid Nephrotoxic drugs

Question 27

AIN - Presentation

Answer 27

Acute Interstitial Nephritis - Fever, - Rash - Pyuria/Hematuria - Oliguria - Metabolic acidosis - Hyperkalemia - Salt wasting Occurs 14 days after drug

Question 28

AIN - Mechanism

Answer 28

Hypersensitivity reaction - Lymphocytes infiltrate the interstitium

Question 29

AIN - Lab Values

Answer 29

Urine - High Sodium - WBC - Protein - Eosinophils

Question 30

AIN - Management

Answer 30

Discontinue offending drug - Penicillins, Lithium Supportive Therapy - Correct volume derangements - Prednisone therapy for up to 4 weeks - Intermittent hemodialysis

Question 31

Obstructive Neuropathy - Different Kinds

Answer 31

All are Postrenal AKI - Renal Tubular Obstruction - Extrarenal Urinary Tract Obstruction - Nephrolithiasis (Kidney Stones)

Question 32

Obstructive Neuropathy - Renal Tubular Obstruction

Answer 32

Precipitation of drug crystals or other tissue degradation products in the tubule - Acyclovir, Rhabdomyolysis with statins

Question 33

Obstructive Neuropathy - Extrarenal Urinary Tract Obstruction

Answer 33

Males with BPH given Anticholinergic drugs

Question 34

Obstructive Neuropathy - Nephrolithiasis

Answer 34

Precipitation of stone forming components into ureters - Indinavir

Question 35

Obstructive Neuropathy - Lab Values

Answer 35

RBC and WBC in Urine Crystals - Acyclovir = Needle Shaped - Indinavir = Rectangular plates or rosettes

Question 36

Obstructive Neuropathy - Management

Answer 36

Discontinue drug Hydration Loop diuretic Supportive Therapy

Question 37

Obstructive Neuropathy - Prevention

Answer 37

Aggressive hydration Avoid rapid infusions and large bolus doses of drugs that crystalize (Ex. Acyclovir) Urine alkalinzation

Question 38

Drug Induced Stones - Crystalize in urine

Answer 38

Antibacterials - Sulphonamides Protease Inhibitors - Indinavir, Acyclovir Antihypertensives - Triamterene Others - Methotrexate

Question 39

Drug Induced Stones - Metabolically induced

Answer 39

Change in fluid balance Change pH Hypercalcemia Hypophosphatemia Hyperoxaluria