This document discusses acute kidney injury (AKI), including its definition, diagnosis criteria, epidemiology, classification, pathogenesis, etiology, treatment, and management. AKI is defined as an abrupt reduction in kidney function, diagnosed by changes in serum creatinine, BUN, and urine output. Between 5-7% of hospitalized patients and a greater percentage of ICU patients develop AKI. Mortality from AKI exceeds 50% despite improvements in care. AKI is classified using criteria like RIFLE, AKIN, and KDIGO which consider risk, injury, failure, and loss of kidney function. Causes include prerenal issues like dehydration, intrinsic renal damage, and postrenal obstruction

1. Acute kidney injury (AKI)

2. ACUTE KIDNEY INJURY
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.
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,
 A 50% increase in baseline SCr within 7 days, or
 A urine output of less than 0.5 mL/kg/hour for at least 6 hours.

3. EPIDEMIOLOGY AND ETIOLOGY
 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%.

4. 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

5. PATHOGENESIS OF SEPSIS-INDUCED AKI

6. CLASSIFICATION OF AKI BASED ON ETIOLOGY

7. PRERENAL AKI
 Prerenal AKI: is characterized by reduced blood delivery to the
kidney.
 A common causes are:
 Volume depletion
 Haemorrhage
 Dehydration
 GI fluid losses
 Decrease effective circulatory blood volume
 Decrease cardiac output (CHF, MI, hypotension)
 Pulmonary hypertension
 Liver failure
 Sepsis

8. INTRINSIC AKI
 Damage is within the kidney (structure of the nephron,)
 Vascular damage (renal thrombosis)
 Glomerular damage (Nephrotic/Nephritic;Glomerulonephritis)
 Acute tubular necrosis(ATN)
 Ischemia (hypotension, sepsis)
 Endogenous toxins
 Exogenous toxin
 Acute interstitial nephritis
NSAIDs
Infections

9. POSTRENAL AKI
 Postrenal AKI is due to obstruction of urinary outflow
 Bladder outlet obstruction
 Benign prostatic hypertrophy
 Prostate cancer
 Anticholinergic drug
 Ureteral obstruction
 Malignancy
 Pelvic / renal obstruction

11. TREATMENT OF ACUTE
KIDNEY INJURY

12. SUPPORTIVE CARE IN AKI
 Adequate Nutrition
 Correction of electrolyte and acid-base abnormalities
 Fluid management
 Correction of any hematologic abnormalities
 Medical management of infections, cardiovascular and GI conditions,
and respiratory failure
 Drug dosage adjustments made based on an estimate of the
patient’s GFR

13. NON-PHARMACOLOGICAL THERAPY
Maintenance of adequate cardiac output and blood pressure to optimize
tissue perfusion
Discontinue medication associated with diminished renal blood flow
Initiate appropriate fluid and electrolyte
Renal replacement therapy RRT in sever AKI
 Hemodialysis
 Peritoneal dialysis

14. RENAL REPLACEMENT THERAPY

15. ANTIMICROBIAL DOSE IN RENAL REPLACEMENT
THERAPY

16. PHARMACOLOGIC THERAPY
Loop diuretics: are effective to reduce fluid overload
Thiazide diuretics
Mannitol is also not recommended for treating volume overload
associated with AK
Potassium sparing diuretics are not recommended
Low dose dopamine LDD is not indicated in treating the AKI.

17. ELECTROLYTE MANAGEMENT
Loop diuretics: are effective to reduce fluid overload
Thiazide diuretics
Mannitol is also not recommended for treating volume overload
associated with AK
Potassium sparing diuretics are not recommended
Low dose dopamine LDD is not indicated in treating the AKI.