Acute kidney injury (AKI) is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days.It's most common in those who are critically ill and already hospitalized.

1. ACUTE KIDNEY INJURY
BY
RAJEE RAVINDRAN

2. INTRODUCTION
Acute kidney injury is rapid and usually reversible decline in renal function as
evident by rapid decline in GFR over a period of hours to days.
It may occur in patient with previously normal renal function or patient with CKD.

3. EPIDEMIOLOGY
5-7% of acute care hospital admissions.
30% of ICU admissions with mortality rates 50%.
Hoste, E.A.J., Kellum, J.A., Selby, N.M. et al. Global epidemiology and outcomes of acute kidney
injury. Nat Rev Nephrol 14, 607–625 (2018)

4. DEFINITION
In 2002, ADQI (Acute Dialysis Quality Initiative) developed RIFLE criteria:
For increase in serum creatinine should be both abrupt within 1-7 days and
sustained > 24 hours.
GFR CRITERIA URINE OUTPUT CRITERIA
RISK SCr >1.5 x baseline or
GFR > 25% reduction
<0.5 ml/kg/hr x 6 hours
INJURY SCr >2 x baseline or
GFR > 50% reduction
<0.5 ml/kg/hr x 12 hours
FAILURE SCr >3 x baseline or
GFR > 75% reduction or
SCr> 4mg/dl
<0.3 ml/kg/hr x 24 hours
Or anuria x 12 hours
LOSS Persistent renal failure=complete loss of function for >4 weeks
ESRD End stage renal disease >3 months

5. DEFINITION
In 2007, AKIN (Acute Kidney Injury Network) criteria :
(the increase in serum creatinine must occur in less than 48 hours)
Abrupt (within 48 h) reduction in kidney function currently defined as an
absolute increase in serum creatinine of 0.3 mg/dL or more (≥26.4 μmol/L) or
A percentage increase in serum creatinine of 50% or more (1.5-fold from
baseline) or
A reduction in urine output (documented oliguria of < 0.5 mL/kg/h for >6 h)
Mehta RL, Kellum JA, Shah SV, MolitorisBA, Ronco C; Warnock DG et al. Acute Kidney Injury
Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;
11(2):R31

6. DEFINITION
In 2012, KDIGO (Kidney Disease Improving Global Outcomes) criteria:
Increase in serum creatinine by>0.3mg/dl (>26.5 umol/L) within 48
hours.
Or
Increase in Serum Cr >1.5 times baseline, which is known or
presumed to have occurred withi the prior 7 days;
Or
Urine volume<0.5 ml/kg/h for 6 hours.

7.  High sensitivity for early diagnosis of AKI
 Allow detection of patient at risk to develop
AKI
 Allow detection of patient with established AKIManual of Nephrology : Daignosis and Therapy 7th Edition: By Robert W Schrier MD by
Lippincott Williams & Wilkins Publishers
The term Acute kidney injury now replaces the term ARF.
The term ARF should now be restricted to the patient
who have AKI and needs renal replacement therapy

8. Calculation of GFR
COCKCROFT – GAULT FORMULA
GFR (ml/min) = [(140-Age) x Lean body weight (kg)] x (0.85 if
female)
72 x S. creatinine
MDRD EQUATION (Modification of diet for renal disease)
GFR (ml/min/1.73m2 = 1.86 x (Pcr) -1.154 x (age) -0.203
 Multiplied by 0.742 for women
 Multiplied by 1.21 for African Americans
Harison’s Principles of Internal Medicine 18th ed.

9. CLASSIFICATION
PRERENAL
AKI (55%)
INTRINSIC
AKI (40%)
POSTRENAL
AKI (5%)
Manual of Nephrology : Daignosis and Therapy 7th Edition: By Robert W Schrier MD by Lippincott
Williams & Wilkins Publishers

10. 2. Effective volume depletion from
arterial underfilling
 Reduced cardiac output
Congestive heart failure
Cardiogenic shock (eg: acute
MI)
Pericardial effusion with
tapenade
Massive pulmonary embolism
 Peripheral vasodilation
• Gram negative sepsis
• Antihypertensive medications
• Anaphylaxis
• Anesthesia
• Cirrhosis and other liver
diseases
CAUSES
CAUSES OF
PRERENAL
AKI
3. Intrarenal hemodynamic
changes
Glomerular afferent arteriolar
vasoconstriction
 NSAIDS
 COX-2
 Cyclosporine
 Tacrolimus
 Radiocontrast dye
 Hypercalcemia
Glomerular efferent arteriolar
vasoconstriction
 ACE inhibitors
 ARBs
1. Intravascular
volume depletion
 Hemorrhage
 Renal fluid losses
 Gastrointestinal fluid
loss
 Third space losses
 Burns
 Traumatized
tissue
 Peritonitis
 Pancreatitis

11. CAUSES OF
INTRINSIC
AKI

12. 1. Acute tubular necrosis

13. 2. Vascular –large vessels
3. Diseases of Glomeruli &
renal microvasculature
4. Acute interstitial nephritis
Renal artery stenosis
Thrombosis
Embolism
 Operative arterial cross
clamping
 Bilateral renal vein
thrombosis
 Glomerulonephritis and vasculitis
 Hemolytic uremic syndrome
 Thrombotic thrombocytopenic
purpura
 DIC
 Toxemia of pregnancy
 Drug hypersensitivity
a. Antibiotics (beta lactam, rifampicin,
sulfonamides, erythromycin,
ciprofloxacin
b. Diuretics (furosemide, thiazides,
chlorthalidone)
c. NSAIDs
d. Anticonvulsant drugs (phenytoin,
carbamazepine)
e. Allopurinol
 Infection associated AIN
a. Bacterial ( staphylococcus,
streptococcus)
b. Viral (CMV, EBV)
c. Tuberculosis
d. Fungal (candidiasis)

14. CAUSES OF
POSTRENAL
AKI

15. PATHOPHYSIOLOGY
Decrease in effective circulatory volume
Activation of central baroreceptor
Angioten
sin II
Norepinephri
ne
ADH
Vasoconstriction of non essential
vascular beds
Maintain renal blood flow & GFR
If hypotension sufficient to overwhelm
renal autoregulatory defense
Ischemic injury to renal parenchyma
1. Preferential
constriction of
efferent arterioles
2. Prostaglandin
synthesis
3. Autoregulation

16. PATHOPHYSIOLOGY
Endothel
ial
dysfuncti
on
Medullar
y
congesti
on
Tubule
epithelial
cell
injury
Persisitent
medullary
ischemia
Back leak of
filtration and
tubular
obstruction
Recovery
of renal
perfusio
n
Regenerati
on of
tubular
epithelium
Reduction in GFR
Recovery of GFR

17. CLINICAL MANIFESTATIONS
PRERENAL AKI
HISTORY OF:
1. Excessive fluid losses from vomiting or
diarrhea; third space losses in burn and
pancreatitis.
2. Compromised cardiac function in patients
with CHF; recent MI
3. Liver cirrhosis and failure (hepatorenal
syndrome)
4. Drugs (cyclosporine, NSAID or ACE
inhibitor use)
SYMPTOMS
(related to hypovolemia)
 Increased thirst
 Decrease urine output
 Postural hypotension
 Dizziness
 Fatigue
 Muscle cramp

18. PRERENAL AKI
PHYSICAL FINDINGS
1. Reduction in ECF volume
 Tachycardia
 Orthostatic hypotension
 Dry mucus membrane
 Absence of axillary sweat
 A recent reduction in body weight
 Tenting of upper thorax skin when pinched between fingers
 Jugular venous pulse not visible
1. Arterial underfilling with expanded ECF
 Elevated jugular venous pressure
 Ascites
 Peripheral edema
 CHF (pulmonary crackles & S3 gallop)
 Liver failure may be identified by jaundice, palmer erythema, spider angiomas,
decrease liver size

19. INTRINSIC/
INTRARENAL AKI
HISTORY OF:
1. Use of nephrotoxic agents, current
medications, Contrast agent.
2. Glomerular disease
• Nephrotic syndrome with hematuria,
edema and hypertension
3. Tubular disease (ATN should be suspected
in any patient presenting after aperiod of
hypotension secondary to cardiac arrest,
hemorrhage or sepsis)
PHYSICAL FINDINGS
 Peripheral edema
 Raised JVP
 Pulmonary rales
 Signs of uremia
 Asterixis
 Myoclonus
 pericardial rub

20. POST RENAL AKI
HISTORY OF:
 Urinary frequency
 Urgency
 Hesitancy
PHYSICAL FINDINGS
 Costovertebral Angle Tenderness
 Pelvic and Rectal Masses
 Prostatic Hypertrophy
 Distended Bladder
Usually occur in elderly male with prostatic
obstruction

21. DIAGNOSIS

22. INVESTIGATIONS
 Complete blood count
 Blood urea
 S. Creatinine
 Serum sodium, potassium, calcium,
phosphate, uric acid
 CPK-MM
-Rhabdomyolsis
 LDH
-Tumor lysis syndrome
-Acute urate nephropathy
 C-ANCA,P-ANCA, Complement level
 Anti GBM antibody
 Urine analysis
IMAGING
 USG Abdomen
 CT Abdomen
 Doppler USG
 Plain X ray Abdomen
 MR angiography

23. Urine Sediment in the differential diagnosis of AKI
 Normal or few Red Blood cells or White Blood Cells
 Prerenal AKI
• Arterial thrombosis or embolism
• Preglomerular vasculitis
• Scleroderma crisis
• Postrenal AKI
 Granular Casts
• Acute tubule necrosis (muddy brown)
• Glomerulonephritis
• Interstitial nephritis
 Red Blood Cell Casts
• Glomerulonephritis
• Malignant hypertension
• Rarely interstitial nephritis
 White blood cell casts
• Acute interstitial nephritis
• Severe pyelonephritis
• Marked leukemic or lymphomatous
infiltration
 Eosinophiluria
• Allergic interstitial nephritis
• Atheroembolic disease
 Crystalluria
• Acute urate nephropathy
• Calcium oxalate
• Acyclovir
• Indinavir
• Sulphonamides
• Radiocontrast agents

24. Indications of Renal Biopsy
1. ARF of unknown etiology
1. Suspicion of glomerulonephritis, systematic disease (eg: vasculitis) or ATN as the cause of ARF.
A renal biopsy in such circumsatnces may provide the basis and justification for aggressive and
lifesaving therapy (eg., high dose steroids, cytotoxic agents, plasmapheresis)
3. ATN not recovering after 4-6 weeks of dialysis with no more recurrent insults.
A renal biopsy may be determine that a less favourable condition, such as diffuse cortical necrosis
has developed and that chronic hemodynamically may need to be instituted.

25. MANAGEMENT
MEDICAL
MANAGEMENT
DIALYSIS
TREATMENT OF
COMPLICATIONS
1. Conservative medical management of ARF requires
2. Complete fluid intake and output record
3. Daily weight record
4. Intravascular volume should be assessed clinically daily
5. Frequent (3 times/week ) measurement of serum sodium
/potassium, blood urea, creatinine, calcium & phosphate

26. PRE RENAL AKI
1. Correction of underlying disorder
a. Pure volume depletion
 When pre renal AKI is due to deficits in ECF volume, therapy is directed to restoring
that are similar to those lost.
 In severe acute hemorrhage, packed RBC is indicated.
 In less severe acute blood loss or plasma loss i.e. burn and pancreatitis isotonic
normal saline indicated.
 Gastrointestinal fluid losses vary widely in electrolyte content and tonicity and
laboratory analysis for sodium, potassium and chloride concentrations is the most
precise way to determine the type of replacement fluid.

27. PRE RENAL AKI
 Crystalloid solution are less expensive and equally effective as colloid.
 In severe hypovolemia, 0.9% saline should be used.
 In less severe hypovolemia 0.45% saline should be used
FLUID CHALLENGE
 In young stable patient 500ml-100ml bolus should be given in one hour
 In elderly patient in whom cardiac status is unknown, bolus of 250ml over one hour should be
given.
 after that patient should be monitored for hypo or hypervolemia.
 Once euvolemia is achieved serum electrolytes should be monitored and replaced.
 Total fluid requirement = total output of kidney & GI tract in previous 24 hr with additional 500
ml-100ml for inaccessible loss.

28. PRE RENAL AKI
b. Ineffective arterial blood volume with edema
 Prerenal AKI occurring in this setting usually represents a secondary problem
overshadowed by aprimary cardiac & hepatic disease.
1. In case of cardiac failure
 Diuretic agents + Digitalis thearpy may increase the cardiac output and improve renal
perfusion, thus lessen the azotemia.
 ACE inhibitors, nitrates, hydralazine may also improve cardiac function

29. 2. In case of Cirrhosis & Hepatorenal Syndrome
 Ascertain intravascular status.
 Administer IVF. Excessive volume administration may result in worsening of ascites and
pulmonary compromise.
 Albumin may prevent AKI in those treated with antibiotics for spontaneous bacterial peritonitis.
 The definitive treatment of the hepatorenal syndrome is Liver transplantation
 Drugs
 Terlipressin (a vasopressin analog)
 Combination therapy with octreotide (a somatostatin analog)
 Milirodrine (alpha adrenergic agonist)
 norepinephrine
Along with Albumin
(1gm/kg body wt,
maximum 100g/day)

30. MONITORING OF THERAPY
 Patient’s response to replacement therapy is frequently monitored by jugular venous pulsation,
orthostatic changes in blood pressure and pulse
 In a normovolemic patient, jugular venous pulsations are visible when the patient is supine but
disappear when the patient assumes the sitting position. Jugular venous pulsations are not visible in
the volume depleted patient.
 Thus, their reappearance following fluid administration suggests that CVP has returned to normal
 The presence of basilar crackles or a third heart sound imples too vigorous fluid replacement with
resultant pulmonary congestion

31. MONITORING OF THERAPY
The patients in whom vigorous resuscitation efforts are required and cardiovascular tolerance to sudden
fluid challenges in doubt , monitoring should be done by central venous catheter.
CVP (normal range- 8-12 cm H20)
 In volume depleted states, CVP may be zero or below. Before vigorous volume repletion is begun, a
fluid challenge of 200 to 300ml of normal saline should be attempted over a10- 20 minute period
 In uncomplicated volume depleted patient, this amount of saline has little effect on the CVP reading.
 A CVP rise of 5cm H2O suggests cardiac failure and the infusion should be immediately discontinued.

32. INTRA RENAL AKI

33. INTRA RENAL AKI

34. INTRA RENAL AKI

35. INTRA RENAL AKI

36. Supportive Management of Intrinsic AKI
1. Intravascular volume overload
Restriction of salt (1-1.5g/day) and water
(<1L/day)
Diuretics – Furosemide may be given as a bolus
(200mg) followed by an intravenous drip (10-40
mg/hour) with or without a thiazide diuretic
Diuretic therapy should be stopped if there is no
response & ultrafiltration should be considered.
2. Hyperkalemia
Restriction of dietary potassium
Discontinue potassium supplements or potassium
sparing diuretics
Calcium gluconate (10mL of 10% solution over 3
min.
Glucose (50ml of 50% dextrose)+ insulin (10 unit)
Intravenously.
Inhaled beta 2 agonist therapy (10-20 mg of
nebulized albuterol in 4 ml of normal saline over 10
minute)
K binding resin
Loop diuretics
Sodium bicarbonate (150 mEq in 1L of D5W) IV
infusion if concomitant metabolic acidosis present.
Dialysis/ hemofiltration

37. 3. Metabolic acidosis
Restriction of dietary protein sodium bicarbonate ( if
HCO3 < 15 mEq /L)
Dialysis/ Hemofiltration
4. Hyperphosphatemia
Restriction of dietary phosphate intake
Phosphate binding agents (calcium carbonate,
calcium acetate, sevelmer)
5. Hypocalcemia
Restriction of dietary protein sodium bicarbonate ( if
HCO3 < 15 mEq /L)
Dialysis/ HemofiltrationCalcium carbonate (if
symptomatic or sodium bicarbonate is to be
administered)
6. Hypermagnesemia
Discontinue magnesium containing antacids
7. Hyponatremia
Restriction of oral and intravenous free water
8. Nutrition
Restriction of dietary protein (< 0.8g/kg/day upto
1.5g/kg/day on continuous venovenous
hemodialysis) 25-30 Kcal/day. Enteral route of
nutrition preferred.

38. PRE RENAL AKI
 The site of obstruction defines the treatment approach. Transurethral or suprapubic bladder
catherization is needed initially for urethral strictures, bladder neck obstruction or functional
bladder impairment.
 Ureteric obstruction may be treated by percutaneous nephrostomy tube placement or
ureteral stent placement.
 Relief of obstruction is usually followed by an appropriate diuresis for several days.
 In rare cases, severe polyuria persisits due to tubular dysfunction and may require continued
administration of intravenous fluids and electrolytes for aperiod of time.

39. DIALYSIS THERAPY
The indications to start dialysis
CLINICAL
 Anuria (<50ml/day) more than 3
days
 Uremic encephalopathy
 Uremic pericarditis
 Uremic bleeding
 Volume overload
 Pulmonary edema
BIOCHEMICAL
 S.Cr more than 6.7 mg/dl
 BUN more than 100mg/dl
 Metabolic acidosis
 hyperkalemia

40. Modes of Dialysis
Intermittent
hemodialysis
Intermittent
peritoneal
hemodialysis
Continuous renal
replacement
therapy
Standard If hemodialysis
not available
Hemodynamic
instability
Active bleeding

41. SUMMARY ACUTE
KIDNEY
INJURY
PRERENAL
RENAL
POSTRENAL
Intrinsic
Surgical treatment
Hypovolemi
a
Euvolemia
Correct Fluid challenge
Improve
d Not improved Acute
tubular
necrosis
Hypovolemia
Euvolemia
Hypervolemia
Correct
Fluid challenge
Improved
Not improved
Diuretic
challenge Dialysis

42. THANK YOU