This presentation is about acute kidney injury

1. Definition
Acute kidney injury (AKI) is abrupt reduction in
kidney functions as evidence by changed in
laboratory values; serum creatinine, blood urea
nitrogen(BUN)and urine output.

2. Definition
Acute kidney injury (AKI) is diagnosed if one of the following criteria is
met :
• Increase in serum creatinine (SCr) of at least 0.3 mg/dL within 48
hours or
• 50% increase in baseline SCr within 7 days or
• Urine output of less than 0.5 mL/kg/hour for at least 6hours

3. EPIDEMIOLOGY
• Between 5% and 7% of all hospitalized patients develop AKI.
• A greater prevalence of AKI is found in critically ill patients ( ICU-
Acquired AKI).
• Despite improvements in the medical care of individuals with AKI,
mortality generally exceeds 50%.

5. CLASSIFICATION OF AKI
Criteria used for AKI classification
• RIFLE: Risk, Injury, Failure, Loss of Kidney Function and End Stage
Renal Disease)
• AKIN: Acute Kidney Injury Network
• KDIGO: Kidney Disease Improving Global outcome

7. PATHOPHYSIOLOGY
There are typically three categories of AKI:
• Prerenal AKI
•Intrinsic AKI
•Postrenal AKI

9. PRERENAL AKI
Prerenal AKI is characterized by reduced blood delivery to
the kidney :common causes are:
• Volume depletion
• Hemorrhage
• Dehydration
• GI fluid losses
• Decrease effective circulatory blood volume

10. PRERENAL AKI
• Decrease cardiac output (CHF, MI, hypotension
• Pulmonary hypertension
• Liver failure
• Sepsis
• Functional :ACEIs, NSAIDs, ARBs, Cyclosporine and tacrolimus
Prompt correction of volume depletion can restore kidney
function to normal because no structural damage to the
kidney has occurred.

11. INTRINSIC AKI
Damage is within the kidney (structure of the nephron)
• Vascular damage (renal thrombosis)
• Glomerular damage (nephrotic/nephritic glomerulonephritis
• Acute tubular necrosis(ATN)(it accounts for 50% of all cases of AKI)
Ischemia (hypotension, sepsis
• Endogenous toxins(uric acid ,hemoglobin, Myoglobin)

12. INTRINSIC AKI
Exogenous toxin
• Aminoglycosides
• contrast induced nephropathy (CIN)
• amphotericin B
Acute interstitial nephritis
NSAIDs
Infections
Prerenal AKI can progress to intrinsic AKI if the underlying condition is
not promptly corrected

13. • Postrenal AKI is due to obstruction of urinary outflow 
• Bladder outlet obstruction
• Benign prostatic hypertrophy,Prostate cancer,Anticholinergic drug,
Ureteral obstruction
• Malignancy
• Renal obstruction
• Postrenal AKI accounts for less than 10% of cases of AKI
Rapid resolution of Postrenal AKI without structural damage restore
kidney function

15. • By monitoring renal function test on a routine basis, it can be
estimated whether kidney function is improving or worsening
• Kidney function can also be evaluated based on urine output. Oliguria
and anuria
• Oliguria is defined as urine outputs of less than 400 ml over 24 hours
• anuria is defined as urine output of less than 50 mL over 24 hours

16. CLINICAL PRESENTATION AND DIAGNOSIS OF
AKI
• Peripheral edema
• Weight gain
• Nausea/vomiting/diarrhea/anorexia
• Mental status changes
• Fatigue
• Shortness of breath
• Pruritus

17. LABORATORY TESTS
• CP
• RFT, Electrolytes, BUN: creatinine ratio
• (greater than 20:1 in Prerenal AKI Less than 20:1 in renal)
• Ultrasound
• ABGS
• Calcuim,Phosphate
• Special test

19. PREVENTION APPROACHES
• Non-pharmacology for prevention
• Hydration to prevent contrast induced nephrotoxicity
• KDIGO guideline recommend using normal saline or sodium
bicarbonate infusion Normal saline regimen: 1ml/kg/h for 12hours
before and after procedure. Sodium bicarbonate regimen:
3ml/kg/hours for one hour before procedure and 1ml/kg/hours for 6
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