This document summarizes the pathophysiology of acute kidney injury (AKI). It describes AKI as an abrupt reduction in kidney function that can be diagnosed through changes in creatinine, BUN, and urine output levels. The pathophysiology of AKI is categorized into pre-renal, intrinsic, and post-renal forms. Pre-renal AKI is due to reduced blood flow to the kidneys, intrinsic AKI involves direct kidney damage, and post-renal AKI is caused by urinary outflow obstruction. The goals of treatment are to minimize injury, reduce complications, and restore kidney function through supportive care, fluid management, and renal replacement therapies like hemodialysis in severe cases

1. PATHOPHYSIOLOGY OF
ACUTE KIDNEY INJURY
BY: DARWIN INJETE SITETI
MSC.CLINICAL MEDICINE-ACCIDENTS & EMERGENCY MEDICINE
MOUNT KENYA UNIVERSITY

2. INTRODUCTION
• Acute kidney injury is abrupt reduction in kidney functions as
evidence by changed in laboratory values; serum creatinine, blood
urea nitrogen and urine output
• Diagnosis criteria;
 increase in serum creatinine of atleast 0.3 mg/Dl within 48 hours.
 a 50% increase in baseline serum creatinine within 7 days
 a urine output of less than 0.5mL/Kg/hr for at least 6 hours

3. CRITERIA USED FOR CLASSIFICATION OF ACUTE
KIDNEY INJURY
• RIFLE: Risk, Injury, Failure, Loss of kidney function and End stage renal
disease.
• AKIN: Acute Kidney Injury Network.
• KDIGO: Kidney disease Improving Global Outcome

4. PATHOPHYSIOLOGY
• There a typically 3 categories of AKI:
• 1. Pre-renal AKI
• 2. Intrinsic AKI
• 3. Post renal AKI

5. Pre renal AKI
• Pre-renal AKI: characterized by reduced blood delivery to the kidney.
• Common causes are:
1. volume depletion
hemorrhage
Dehydration
G.I fluid loses
2. Decrease effective circulatory blood volume
Decreased cardiac output (CCF, MI Hypotension)
Liver failure, Sepsis, pulmonary, pulmonary hypertension

6. • 3. Functional
ACEIs, NSAIDS, ARBs, tacrolimus,cyclosporine.
Prompt correction of volume depletion can restore kidney function to
normal because no structural damage to kidney has occurred.

7. INTRINSIC AKI
• Damage is within the kidney (structure of the nephrone)
1. Vascular damage (renal thrombosis)
2. Glomerular damage (nephrotic/nephritic glomerulonephritis)
3. Acute tubular necrosis (accounts for 50% of AKI):
 Ischemia (hypotension and sepsis)
 Endogenous toxins (uric acid)
 Exogenous toxins (aminoglycosides, contrast induced nephropathy,
amphoterism B)
4. Acute interstitial nephritis: NSAIDS & infections
Pre-renal AKI can progress to intrinsic AKI if underlying condition is not promptly
corrected

8. POST RENAL AKI
• Post renal AKI is due to obstruction of urinary outflow.
1. Bladder outlet obstruction:
Benign prostatic hyperplasia
Prostate Cancer
Anticholinergic drugs
2. Ureteral obstruction
Malignancy
3. Pelvic/Renal obstruction
Post renal AKI accounts to less than 10% of cases of AKI.
Rapid resolution of post renal AKI without structural damage restore kidney function.

9. CLINICAL PRESENTATION
• Peripheral edema
• Weight gain
• Nausea, vomiting
• Mental status change
• Fatigue
• Pruritis
• Shortness of breath

10. PREVENTION APPROACHES OF AKI
NON-PHARMACOLOGICAL
Hydration to prevent contrast induced nephrotoxicity-use of normal
saline 1ml/kg/h for 12 hours before and after procedure or sodium
bicarbonate infusion 3ml/kg/hr for one hour before procedure and 1
ml/kg/hr for 6 hours post contrast.
PHARMACOLOGICAL THERAPY
Ascorbic acid 3g orally pre and 2mg orally for 2 doses post procedure
and N-acetylcysteine 600-1200mg orally every 12 hours for 2-3 days.
Moderate control of blood glucosewith insulin to prevent ICU acquired
AKI

11. GOALS OF TREATMENT
• Minimize degree of injury
• Reduce extra renal complications
• Restoration of renal function

12. SUPPORTIVE CARE IN AKI
• Adequate nutrition
• Correction of electrolyte and acid base abnormalities
• Fluid management
• Correction of hematological abnormalities
• Medical managent of infections, cardiovascular, GI conditons and
respiratory failure
• All drugs to be reviewed dosage adjustment be made based on an
estimate of Patients GFR

13. NON-PHARMACOLOGICAL THERAPY
• Mantainance of adequate cardiac output and and blood pressure to
optimize tissue perfusion.
• Discontinues medication associated with diminished renal blood flow.
• Initiate appropriate fluid and electrolytw
• Renal replacement therapy in severe AKI: Hemodialysis, peritoneal dialysis.
Absolute indications For Dialysis
BUN greater than 100mg/dl (35.7 mmol/L)
Potassium greater than 6mEq/L (6mmol/L)
Diuretic resistant fluid overload
Metabolic acidosis with PH less than 7.15
Magnesium > 9.7mh/DL (4 MMOL/L)

14. INDICATIONS FOR RRT
• Acid base abnormalities
• Electrolite imbalance
• Intoxication-phenobab,ethanol,methanol
• Overload of fluid
• Uremia

15. PHARMACOLOGICAL THERAPY
• LOOP DIURETICS- 40-60 mg loading IV dose then continuos 10-
20mg/hr
• THIAZIDE DIURETICS-when used as single agent are not effective
• MANNITOL- recommended for Rx of volume overload associated with
AKI
• Potassium sparing diuretics- are not recommended

16. • THANK YOU
• injetedarwin@gmail.com