2155 (IC16) AKI

Question 1

Definition of Acute Kidney Injury

Answer 1

Abrupt decline in renal function (GFR) occurring over hours or days

Question 2

2 most common causes of AKI

Answer 2

1. Intravascular volume depletion
2. Drugs eg. NSAIDs, ACE, ARB

Question 3

What is the normal urine output? And terms for decreased urine output and volume

Answer 3

Normal urine output >1200ml/day
Non-oliguria (normal): >500ml
Oliguria: <500ml
Anuria: <50ml

Question 4

Classification of AKI (3pts)

Answer 4

Prerenal: Sudden drop in BP or decreased perfusion to kidneys
Intrinsic: Structural damage within kidney
Postrenal: Obstruction to urine flow

Question 5

Risk factors for AKI

Answer 5

Old age
Female
Acute infection
Pre-existing chronic respiratory or cardio disease
Dehydration / Volume depletion
Pre-existing CKD → Acute on Chronic Kidney Disease (AOCKD)
Patients with CKD suddenly experience worsening of kidney function

Question 6

Clinical presentation of AKI

Answer 6

Decreased urine output (Oliguria, Anuria)
Peripheral oedema
Flank pain
Lab abnormalities
Elevated SCr, BUN (Blood urea nitrogen), K
Metabolic acidosis

Urinalysis:
Presence of casts, cells, crystals, WBC, RBC, protein
Abnormal specific gravity (SG), fractional excretion of Na, urine osmolality

Question 7

Causes of Prerenal AKI

Answer 7

Volume depletion
Reduced cardiac output
Renal hypoperfusion

Question 8

How does Prerenal AKI develop?

Answer 8

Kidneys sense volume depletion/dehydration → cause vasoconstriction to preserve effective circulating blood volume

Because of drop in BP, compensatory mechanisms (eg. RAAS, release ADH)
Maintain BP via vasoconstriction
Stimulate thirst receptor
Promote Na and water retention to preserve circulatory volume, prevent further drop in BP

The decrease in renal blood flow results in
Decreased solute excretion
Increased tubular reabsorption of glomerular filtrate eg. urea, water, Na

Result: Reduction in urine volume, Urine highly concentrated

decrease in renal perfusion is severe or precipitating factor eg. bleeding, overdiuresis not removed → can progress to AKI and renal cell damage can occur

Question 9

How to diagnose prerenal AKI

Answer 9

History
Physical exam

Question 10

How do NSAIDs and ACE/ARB cause AKI?

Answer 10

NSAIDs inhibit Prostaglandin (PG) synthesis, PG is needed for vasodilation of afferent arteriole
Afferent arteriole constricted, reduces blood flow to glomerulus → causing intraglomerular filtration pressure / hydrostatic pressure to decrease

ACE/ARB inhibit Angiotensin 2 (AT2) synthesis, AT2 is needed for vasoconstriction of efferent arteriole
Efferent arteriole dilated, lose intraglomerular pressure/hydrostatic pressure

Question 11

Causes of Intrinsic AKI

Answer 11

Acute Tubular Necrosis (ATN)
Nephrotoxins eg. contrast dye

Acute Interstitial Nephritis (AIN)
Drugs eg. penicillin, ciprofloxacin, sulfonamides

Glomerular damage

Vascular damage

Question 12

How does Acute Tubular Necrosis occur?

Answer 12

Injury to tubular cells -> inflammation, tubular cells found in urine

Kidney lose ability to concentrate urine, defective sodium reabsorption and reduction in GFR

Question 13

What are the 4 phases of ATN?

Answer 13

Initiating
Oliguric
Diuretic
Recovery

Question 14

What happens in Initiating phase?

Answer 14

Ischaemia or exposure to nephrotoxic agent
Protective role of prostaglandins
PG Inhibitors eg. NSAIDs can subject kidney to severe ischemia and precipitate ATN

Question 15

What happens in Oliguric phase?

Answer 15

Oliguria (<500ml urine per day) occurs
Duration: 1-2 weeks, longer the duration → greater risk of complications, worser the outcome and prognosis
May present w oedema

Treatment:
Diuretics
CCB (reverse renovascular constriction, increase renal blood flow and GFR)
Water, Na, K, P acid base balance
Nutrition. Drug dosage adjustment, short term dialysis

Question 16

What diuretics should be used in ATN?

Answer 16

Loop diuretics eg. Furosemide, Bumetanide Torsemide, Ethacrynic acid (for pts with sulfa allergy)

Question 17

What should you do if diuretic resistance occurs? (3 pts)

Answer 17

Aggressive Na restriction
Combination diuretic therapy eg. Furosemide + Metolazone
Give IV dosing or continuous infusion instead of oral diuretics

Question 18

What happens during diuretic phase?

Answer 18

having an improvement in urine output
Renal blood flow and glomerular filtration increase
Concentrating ability to reabsorb Na+ and concentrate urine improves

Question 19

What happens in recover phase?

Answer 19

New tubular cells regenerated
Azotemia (build up of nitrogenous waste) resolves after a few weeks
GFR may return to normal
Permanent loss in renal function may occur due to fibrosis, atrophy → lead to CKD, require dialysis

Question 20

risk factors for radiocontrast media-induced ATN

Answer 20

Risk factors
Renal disease, CKD
Advanced age
DM, HTN, CHF, metabolic syndrome
Volume depletion / hypotension / hemodynamic instability
Taking other nephrotoxins eg. NSAIDs, antibiotics, high dose diuretics, metformin, ACE/ARB
Using high osmolar contrast media
(Use low, iso-osmolar contrast media instead)

Question 21

Prevention for radiocontrast media induced ATN

Answer 21

Use lowest dose of contrast medium
Use low or iso osmolar
IV Hydration is key eg. Normal saline, Hypotonic saline, Sodium bicarbonate
Start 1hr before and continue 3-6hrs after
N-acetylcysteine
Antioxidant effect (Give 2 doses before and after procedure)
Statins may have some benefit

Question 22

Examples of aminoglycosides

Answer 22

Amikacin, Gentamicin, Tobramycin

Question 23

Prevention of AG induced ATN

Answer 23

Only use AG if have no other antibiotics, less nephrotoxic drugs available
Normal renal function: Extended interval dosing (once daily) instead of multiple dose daily
AG have concentrated-dependent killing
Post-antibiotic effect (antibiotic effect after drug has been cleared)
CKD patients: Prolong dosing interval eg. take every 2 days

Question 24

Strategies to limit AKI for amphotericin B induced toxicity

Answer 24

Continuous infusion rather than 2 - 4hr infusion
Alternate day dosing instead of daily
Using lipid formulation instead of conventional formulation
Use azole antifungals if equal efficacy

Question 25

Symptoms of Post renal AKI

Answer 25

Symptoms
Anuria (<50ml/day) → complete obstruction
Polyuria (more urine produced) → partial occlusion
Body try to produce more urine to counter the obstruction
Stagnant urine → cause reabsorption of urea by urinary tract mucosa → elevated BUN/SCr ratio

Question 26

Supportive management for AKI (4 pts)

Answer 26

Hemodynamic support, volume replacement
Remove agent that causes AKI eg. medications
Treat underlying disease eg. bleeding, enlarged prostate
Remove obstruction causing AKI

Question 27

How to maintain water and sodium balance in AKI? (3 pts)

Answer 27

Maintain cardiac output, renal perfusion
Prevent fluid accumulation eg. oedema, SOB
Use diuretics for fluid management, Na (<2-3g per day), fluid restriction

Question 28

Why is nutritional support important for pts w AKI?

Answer 28

Patients are in catabolic state (breaking down body stores)
Hence, important to maintain caloric intake to minimise hypercatabolic state
Target: 20-30kcal/kg/day
Use enteral (preferred) or parenteral nutrition

Question 29

When do we need to do emergent dialysis?

Answer 29

AEIOU

Acid Base Imbalance
Metabolic acidosis that cannot be treated w Sodium Bicarbonate

Electrolyte abnormalities
High K+, can cause heart to stop, High phosphate

Intoxication
Overdose of medications, can use dialysis to clear

Overload
Fluid overload, oedema

Uremia
High urea concentration, clear uremic toxins