Management of AKI

1. Acute Renal Failure (ARF)

2. Acute kidney injury (AKI) is an abrupt and usually reversible decline
in the glomerular filtration rate (GFR). This results in an elevation of
serum blood urea nitrogen (BUN), creatinine, and other metabolic
waste products that are normally excreted by the kidney.
AKI replaced the older term acute renal failure (ARF)

3. History of ARF
• First description was by William Heberden in 1802 termed
“ischuria renalis”.
• At the beginning of the twentieth century- named “Acute
Bright’s disease” described in William Osler’s Textbook for
Medicine (1909)
• During the First WorldWar the syndrome was named ‘‘war
nephritis’’
• During the Second World War, Bywaters and Beall published
their classical paper on “crush syndrome”
• Homer W. Smith first introduction of the term ‘‘acute renal
failure’’, in his textbook “The kidney-structure and function in
health and disease” (1951)

4. Why AKI not ARF
• A precise biochemical definition of ARF was never proposed
• Arbitrarily considered the advanced stage of this spectrum
• Subtle rise in serum creatinine is associated with significantly
increased morbidity and mortality.
• In 2004 The Acute Dialysis Quality Initiative (ADQI) group
developed a system for diagnosis and classification of a broad range
of acute impairment of kidney function the RIFLE criteria
• RIFLE first introduced the term AKI (acute kidney
injury/impairment)

6. AKI definition
• AKI is defined as any of the following (Not Graded):
– Increase in SCr by X0.3 mg/dl (X26.5 lmol/l) within 48
hours; or
– Increase in SCr to X1.5 times baseline, which is known
or presumed to have occurred within the prior 7 days; or
Urine volume o0.5 ml/kg/h for 6 hours.

8. ARF is an abrupt decline in glomerular and
tubular function, resulting in the failure of the
kidneys to excrete nitrogenous waste
products and to maintain fluid and electrolyte
homeostasis.
Definition

9. Normal Kidney Function
• Fluid Balance
• Electrolytes Balance
• Acid-base balance
• Excretion of Metabolic Waste product
• Endocrine Functions
• Clinical feature

10. Classification
• Prerenal (hypoperfusion)
• Renal (intrinsic)
• Postrenal (obstructive)

12. Prerenal
• Decreased perfusion without cellular injury
• Renal tubular and glomerular functions are intact
• Reversible if underlying cause is corrected

13. Prerenal
• Common etiologies:
– dehydration
– hypovolemia
– hemodynamic factors that can compromise
renal perfusion (CHF, shock)
Sustained prerenal azotemia is the main factor
that predisposes patients to ischemia- induced
acute tubular necrosis (ATN)

14. Prerenal azotemia and ischemic tubular necrosis represent
a continuum. Azotemia progresses to necrosis when blood
flow is sufficiently compromised to result in the death of
tubular cells.
Most cases of ischemic ARF are reversible if the
underlying cause is corrected.

15. Renal
• Classified according primary site of
injury:
– tubular
– interstitium
– vessels
– glomerulus

16. Postrenal
• Obstruction of urinary tract
• Important to rule out quickly:
– potential for recovery of renal function is often
inversely related to the duration of the obstruction

19. Clinical feature
• Features of Primary Disease
• azotemia
• hypervolemia
• electrolytes abnormalities:
– K+ phosphate
– Na+ calcium
• metabolic acidosis
• hypertension
• oliguria - anuria

20. Investigation
Urea , Creatinine :
Electrolyte
Calcium , Phosphate
Albumin
CBC
CRP
Urinalysis

21. Urine Microscopy
Renal USG
Culture
Chest X-Ray
Serology
ECG
Complement ,ANCA
Renal Biopsy
•
II

22. Diagnosis
• History and Physical examination
• Blood tests : CBC, BUN/creatinine, electrolytes, uric acid,
PT/PTT, CK
• Urine analysis
• Renal Indices
• Renal ultrasound (useful for obstructive forms)
• Doppler (to assess renal blood flow)
• Nuclear Medicine Scans
DMSA: anatomy
DTPA and MAG3: renal function, urinary
excretion and upper tract outflow

23. Reabsorption of water and sodium:
- intact in pre-renal failure
- impaired in tubulo-interstitial disease and ATN
Since urinary indices depend on urine sodium
concentration, they should be interpreted cautiously if the
patient has received diuretic therapy
renal indices

24. Renal Failure Index (RFI)
RFI: urine [Na]
urine creatinine / serum creatinine
renal indices

25. Fractional Excretion of Na (FENa)
FENa: [ urine Na/serum Na] x 100 %
[urine creatinine/serum creatinine]
renal indices

26. Prerenal :
– Urine sediment: hyaline and fine granular casts
– Urinary to plasma creatinine ratio: high
– Urinary Na: low
– FENa: low
Increased urine output in response to hydration

27. • Renal :
– Urine sediment: brown granular casts and tubular
epithelial cells
– Urinary to plasma creatinine ratio: low
– Urinary Na: high
– FENa: high

28. urine and serum laboratory values
Prenal Renal
BUN/Cr >20 <20
FeNa <1% >1%
RFI <1% >1%
UNa (mEq/L) <20 > 40
Specific gravity high low
Urine sodium < 20 > 40
Urine
osmolality
> 500 < 350

29. Therapy of ARF
• The goal of any focused evaluation of ARF is
immediate correction of its reversible causes.
• Recognition and relief of urinary outlet obstruction
should be given the highest priority,especially for
patient with anuria.

30. Management
• treat the underlying disease
• strictly monitor intake and output (weight, urine
output, insensible losses, IVF)
• monitor serum electrolytes
• Protein restriction
• Fluid restriction
• Sodium potassium and phosphate restriction
• Use of diuretics to correct volume overload
• Use of bicarbonate to correct acidosis
• Adjustment of doses of medication
• Dialysis

31. fluid therapy
If patient is fluid overloaded
• fluid restriction (insensible losses)
• ?attempt furosemide 1-2 mg/kg
• Renal replacement therapy (see later)
If patient is dehydrated:
• restore intravascular volume first
• then treat as euvolemic (below)
If patient is euvolemic:
• restrict to insensible losses (30-35
ml/100kcal/24 hours) + other losses (urine,
chest tubes, etc)

32. Sodium
• most patients have dilutional hyponatremia which
should be treated with fluid restriction
• severe hyponatremia or hypernatremia : dialysis
or hemofiltration

33. Potassium
Oliguric renal failure is often complicated by hyperkalemia,
increasing the risk in cardiac arrhythmias
Treatment of hyperkalemia:
•sodium bicarbonate
• insulin + hypertonic dextrose:
• sodium polystyrene (Kayexalate):
• dialysis

34. nutrition
• provide adequate caloric intake
• limit protein intake to control increases in BUN
• minimize potassium and phosphorus intake
• limit fluid intake
If adequate caloric intake can not be achieved due
to fluid limitations, some form of dialysis should be
considered

35. protein
• We suggest administering 0.8–1.0 g/kg/d of protein in
noncatabolic AKI patients without need for dialysis (2D),
• 1.0–1.5 g/kg/d in patients with AKI on RRT (2D),
• 1.7 g/kg/d in patients on continuous renal replacement
therapy (CRRT) and in hypercatabolic patients. (2D)

36. Indications Of Renal Replacement
Therapy

37. Myths
• Frusemide
– Theoretically may reduce tubular injury
– Due to shutting down Na/K/Cl ATPase
– Reduces oxygen demand
– May help with fluid balance
• But
– No clinical evidence
– Accumulates in Oliguria
– Nephrotoxic and Ototoxic
– May actually increase mortality and or need for RRT

38. Myths
• Dopamine
– Low dose Dopamine (2-3mcg/kg/min), known as “renal
dose”
– No effect on mortality or need for Renal replacement
therapy

39. Myths
• Vasopressors and AKI
– Although Noradrenaline causes vasoconstriction with renal
vasculature
– No evidence of worsening AKI
– But should be used after adequate volume resuscitation

40. Myths
• Mannitol
– Currently no evidence of protective effect
– Causes an osmotic diuresis with may benefit fluid balance

41. Prognosis of ARF
• Outcome is usually determined by the severity of the
underlying disorder and other complications, rather
than by renal failure itself.
• In uncomplicated ARF, such as that due to simple
haemorrhage or drugs, mortality is low even when
renal replacement therapy is required.
• In ARF associated with serious infection and multiple
organ failure, mortality is 50-70%.
• Overall mortality is 40% with patients required
dialysis

43. AKI – definition
KDIGO clinical practice guidelines
Acute kidney injury is defined when one of
the following criteria is met
– Serum creatinine rises by ≥ 26µmol/L within 48
hours or
– Serum creatinine rises ≥ 1.5 fold from the
reference value, which is known or
– presumed to have occurred within one week or
– urine output is < 0.5ml/kg/hr for >6 consecutive
hours

44. The reference serum creatinine should be the
lowest creatinine value recorded within 3
months of the event
If a reference serum creatinine value is not
available within 3 months and AKI is
suspected repeat serum creatinine within 24
hours
A reference serum creatinine value can be
estimated from the nadir serum creatinine
value if patient recovers from AKI

45. staging classification
Stage Serum creatinine (SCr) criteria Urine output criteria
1
increase ≥0.3 mg/dl{≥ 26 μmol/L
}within 48hrs or
increase ≥1.5 to 1.9 X reference SCr
<0.5 mL/kg/hr for > 6
consecutive hrs
2 increase ≥ 2 to 2.9 X reference SCr
<0.5 mL/kg/ hr for > 12
hrs
3
increase ≥3 X reference SCr or
increase≥4.0 mg/dl { ≥354 μmol/L}
or
commenced on renal replacement
therapy (RRT) irrespective of stage
<0.3 mL/kg/ hr for > 24
hrs or anuria for 12 hrs

46. RIFLE CRITERIA — The RIFLE criteria consists of three
graded levels of injury (Risk, Injury, and Failure) based
upon either the magnitude of elevation in serum
creatinine or urine output, and two outcome measures
(Loss and End-stage renal disease). The RIFLE strata are
as follows [4]:
Risk — 1.5-fold increase in the serum creatinine or GFR
decrease by 25 percent or urine output <0.5 mL/kg per
hour for six hours
Injury — Twofold increase in the serum creatinine or GFR
decrease by 50 percent or urine output <0.5 mL/kg per
hour for 12 hours
Failure — Threefold increase in the serum creatinine or
GFR decrease by 75 percent or urine output of <0.3
mL/kg per hour for 24 hours, or anuria for 12 hours
Loss — Complete loss of kidney function (eg, need for
renal replacement therapy) for more than four weeks
ESRD — Complete loss of kidney function (eg, need for

47. Serum creatinine criteria Urine output criteria
RIFLE
Definition
Increase in SCr by ≥1.5 times
baseline within seven days
Staging
R (Risk): Increase in SCr by 1.5 -
<2.0 times baseline
UO <0.5 mL/kg/h x 6 hr
I (Injury): Increase in SCr by 2.0 -
<3.0 times baseline
UO <0.5 mL/kg/h x 12 hr
F (Failure): Increase in SCr by ≥3.0
times baseline
UO <0.3 mL/kg/h x 24 hr or
anuria x 12 hrs
AKIN
Definition
Increase in SCr by 0.3 mg/dL or ≥1.5
times baseline within 48 hours
Staging
1: Increase in SCr by ≥0.3 mg/dL or
≥1.5 - <2.0 times baseline
Less than 0.5 mL/kg per hour
for more than 6 hours
2: Increase in SCr by ≥2.0 - <3.0
times baseline
Less than 0.5 mL/kg per hour
for more than 12 hours
3: Increase in SCr by ≥3.0 times
baseline
Less than 0.3 mL/kg per hour
for 24 hours or anuria for 12
hours