2155 (IC16) AKI Flashcards
Definition of Acute Kidney Injury
Abrupt decline in renal function (GFR) occurring over hours or days
2 most common causes of AKI
- Intravascular volume depletion
- Drugs eg. NSAIDs, ACE, ARB
What is the normal urine output? And terms for decreased urine output and volume
Normal urine output >1200ml/day
Non-oliguria (normal): >500ml
Oliguria: <500ml
Anuria: <50ml
Classification of AKI (3pts)
Prerenal: Sudden drop in BP or decreased perfusion to kidneys
Intrinsic: Structural damage within kidney
Postrenal: Obstruction to urine flow
Risk factors for AKI
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
Clinical presentation of AKI
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
Causes of Prerenal AKI
Volume depletion
Reduced cardiac output
Renal hypoperfusion
How does Prerenal AKI develop?
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
How to diagnose prerenal AKI
History
Physical exam
How do NSAIDs and ACE/ARB cause AKI?
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
Causes of Intrinsic AKI
Acute Tubular Necrosis (ATN)
Nephrotoxins eg. contrast dye
Acute Interstitial Nephritis (AIN)
Drugs eg. penicillin, ciprofloxacin, sulfonamides
Glomerular damage
Vascular damage
How does Acute Tubular Necrosis occur?
Injury to tubular cells -> inflammation, tubular cells found in urine
Kidney lose ability to concentrate urine, defective sodium reabsorption and reduction in GFR
What are the 4 phases of ATN?
Initiating
Oliguric
Diuretic
Recovery
What happens in Initiating phase?
Ischaemia or exposure to nephrotoxic agent
Protective role of prostaglandins
PG Inhibitors eg. NSAIDs can subject kidney to severe ischemia and precipitate ATN
What happens in Oliguric phase?
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
What diuretics should be used in ATN?
Loop diuretics eg. Furosemide, Bumetanide Torsemide, Ethacrynic acid (for pts with sulfa allergy)
What should you do if diuretic resistance occurs? (3 pts)
Aggressive Na restriction
Combination diuretic therapy eg. Furosemide + Metolazone
Give IV dosing or continuous infusion instead of oral diuretics
What happens during diuretic phase?
having an improvement in urine output
Renal blood flow and glomerular filtration increase
Concentrating ability to reabsorb Na+ and concentrate urine improves
What happens in recover phase?
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
risk factors for radiocontrast media-induced ATN
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)
Prevention for radiocontrast media induced ATN
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
Examples of aminoglycosides
Amikacin, Gentamicin, Tobramycin
Prevention of AG induced ATN
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
Strategies to limit AKI for amphotericin B induced toxicity
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
Symptoms of Post renal AKI
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
Supportive management for AKI (4 pts)
Hemodynamic support, volume replacement
Remove agent that causes AKI eg. medications
Treat underlying disease eg. bleeding, enlarged prostate
Remove obstruction causing AKI
How to maintain water and sodium balance in AKI? (3 pts)
Maintain cardiac output, renal perfusion
Prevent fluid accumulation eg. oedema, SOB
Use diuretics for fluid management, Na (<2-3g per day), fluid restriction
Why is nutritional support important for pts w AKI?
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
When do we need to do emergent dialysis?
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
