1. AKI (acute kidney injury) is defined as an acute decrease in kidney function over hours to days, previously known as acute renal failure. Biomarkers can help detect AKI earlier than creatinine. 2. Causes of AKI include decreased blood flow to the kidneys (pre-renal), direct injury to the kidneys (intrinsic renal), and urinary tract obstruction (post-renal). The most common causes are decreased blood flow due to shock, sepsis, or surgery. 3. Early nephrology consultation and avoiding nephrotoxins may help reduce mortality in AKI. Biomarkers, fluid management, and considering renal replacement therapy are important

1. Dr. Osama El-Shahat
Consultant Nephrologist
Head of Nephrology Department
New Mansoura General Hospital (international)
ISN EducationalAmbassador

2. Objectives
Definatinon
ARF AKI
Diagnosis
Incidence
Mortality
Biomarkers
Treatment
Non- dialytic support
Dialytic support

3. ARF AKI
Ischuria Renalis (William Heberden)
Acute Bright’s Disease (William Osler)
War Nephritis
Acute Kidney Insufficiency (Bywaters &
1802:
1909:
W.W.I:
W.W.II:
Beall)
1951:
2006 :
Acute Renal Failure (Homer W. Smith)
Acute Kidney Injury (AKI Network)

4.  By AKI we actually mean “loss of smallsolute
clearance” (urea/creatinine increase in
blood)
 This implies loss of GFR
 So…clinically we actually mean
“acute decrease in GFR”
What do we mean byAKI?

5. Lameire N, Van BW, Vanholder R. Nat Clin Pract Nephrol 2006; 2: 364–377.
Can we do staging for AKI?

6. AKIN Classification

7. What is the advantages of RIFLE Criteria?
 Applying the RIFLE criteria revealed new insights.
 Firstly, the RIFLE classification is feasible and
fairly straightforward.
 Secondly, the patients categorized as RIFLE-F had a
far higher mortality than RIFLE-I and -R patients.
Max Bell et al; Nephrol Dial Transplant 2005 20:354–360

8. Number ofARF Hospitalizations: 1979 to 2002
Rates per 1,000 persons
0.0
1.0
0.5
2.0
1.5
2.5
1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002
Source: National Center for Health Statistics, National Hospital DischargeSurvey

9. Kidney International advance online publication , 1
May 2013
Mortality inAKI

10. Causes of AKI
Pre renal Intrinsic renal Post renal
Decrease in
effective
blood volume.
Arterial
occlusion
Or
stenosis.
Homodynamic
Form.
Vascular
Vasculitis.
Malignant
hypertension
Acute
Glomerulo
nephritis
Acute
Interstitial
nephritis
Acute
Tubular
necrosis
Ischemic. Nephrotoxic.
Obstruction
Of
Collecting
System
Or
Extra renal
drainage
Exogenous
Antibiotic
Radio contrast
cisplatin
Endogenous
Intra tubular pigment
Intra tubular protein.
Intra tubular crystal.

11. Causes of AKI
Obstructive
uropathy 15%
Glomerulonephritis 5%
Nephrotoxic agents 10%
Post-OP, sepsis,
shock,multi-organ
failure 70%
reduced blood flow
ischemia
acute tubular necrosis

12. Timing nephrology consultation
(Mehta, Am JMed2002)
In-hospital mortality
Early
consult
Delayed
consult
P
40% 67% <0,001
Early nephrologist involvement in patients with
AKI may reduce the risk of a further decrease in
kidney function.
Am J Kidney Dis. 2011;57(2):228-234

13. Kidney International (2013) 83, 901–908
Early Referral

14. Biomarkers are foot prints ofactual
organ damage
 Creatinine Not ABiomarker
 The creatinine level is influenced by multiple non-
renal factors, such as age, gender, muscle mass, muscle
metabolism, diet, medications, and hydration status
 In AKI, the serum creatinine level can take several
hours or days to reach a new steady state and thus does
not reflect the actual decrease in GFR in the acute
setting
 Because of renal reserve, the serum creatininelevel
may not rise until more than half of the kidney
function has been lost

15. Creatinine is late, or is it too late?

16. New urinary biomarkers for the early detectionof
acute kidney disease
Han, Bonventre,Current Opin Crit Care 2004, 10:476–482
Neutrophil gelatinase associated lipocalin

17. Early detection of AKI by Cystatin C
Definition of AF
Area under the ROC
Day - 2 Day - 1 Day 0
≥ 50 % increase 0.82 0.97 0.99
≥ 100 % increase 0.92 0.98 0.98
≥ 200 % increase 0.97 0.99 0.99
•Changes in cystatin C were able to detect the onset ofAKI
one to two days earlier than comparable changes in serum creatinine
1. RIFLE- R ( ≥ 50 % increase ): 1.5 ± 0.6 days earlier
2. RIFLE- I ( ≥ 100 % increase): 1.2 ± 0.9 days earlier
3. RIFLE- F ( ≥ 200 % increase): 1.0 ± 0.6 daysearlier
Herget-Rosenthal et al, Kidney Int 2004, 66: 1115- 1122

18. Indications of Renal
Biopsy
1
Urine
No cast
FENa<1%
Muddy
brown cast
FENa>1%
Red cell
cast
White cell
cast
eosinophil
Pre-renal
ATN Glomerular Interstitial
Biopsy
2. Unknown cause
3. ProlongedATN

19. Loop diuretics inAKI
Diuretics, particularly high doses of loop diuretics, are frequently
administered to patients with acute renal failure. This is done in part
in an attempt to convert oliguric to nonoliguric acute renalfailure.
However, a retrospective observational report found that the use of
diuretics in this setting may increase the risk of death and no
recovery of renal function.
3.4.1: We recommend not using diuretics to prevent AKI. (1B )
3.4.2: We suggest not using diuretics to treat AKI, except in the
management of volume overload. (2C )

20. There is insufficient evidence that the low-dose dopamine
improves survival or obviates the need for dialysis in persons with
acute renal failure. The routine use of low-dose dopamine should be
discouraged until a prospective, randomized, placebo-controlled trial
establishes its safety and efficacy.
Is the administration of dopamine associated with adverse or
favorable outcomes in acute renal failure? AuriculinAnaritide
Acute Renal Failure Study Group.
Low Dose Dopamine in AKI
3.5.1: We recommend not using low-dose dopamine to prevent or
treat AKI. (1A)

21. IV Fluids in AKI
3.1.1:In the absence of hemorrhagic shock, we
suggest using isotonic crystalloids rather than
colloids (albumin or starches) as initial
management for expansion of intravascular
volume in patients at risk for AKI or with AKI.
(2B)

22. Contrast InducedAKI
4.4.1:We recommend i.v
.volume expansion with either isotonic sodium
chloride or sodium bicarbonate solutions,rather than no i.v
.volume expansion,
in patients at increased risk for CI-AKI. (1A)
4.5.1:We suggest not using prophylactic intermittent hemodialysis (IHD) or
hemofiltration (HF) for contrast-media removal in patients at increased risk for
CI-AKI. (2C)
4.4.3:We suggest using oral NAC, together with i.v
.isotonic crystalloids, in
patients at increased risk of CI-AKI. (2D)
4.3.2:We recommend using either iso-osmolar or low-osmolar iodinated
contrast media, rather than high-osmolar iodinated contrast media inpatients
at increased risk of CI-AKI. (1B)

23. Bicarbonate or Saline
Among the large
randomized trials there
was no evidence ofbenefit
for hydration with sodium
bicarbonate compared
with sodium chloride for
the prevention of CI-AKI.
Contrast InducedAKI

24. Stage-based management
General Principles
Stage 1 (Risk)
Risk for more severeAKI
Monitor (prevent
progression)
Stage 2 (Injury)
Risk ofAKI-related
mortality/morbidity high
Conservative therapy)
Stage 3 (Failure)
Highest risk of death
Consider RRT
Avoid subclavian catheters if possible
Discontinue all nephrotoxic agents when possible
Consider invasive diagnostic workup
Consider Renal Replacement Therapy
1 2 3
Non-invasive diagnostic workup
Ensure volume status and perfusion pressure
Check for changes in drug dosing
AKI Stage
Consider functional hemodynamic monitoring
Monitoring Serum creatinine and urine output
Consider ICU admission
Avoid hyperglycemia
Consider alternatives to radiocontrast procedures

25. Indications for RRT in critically ill AKI patients
Renal Indications
Life-threatening indications
Hyperkalemia
MetabolicAcidosis
Pulmonary edema
Uremic omplications

26. Dialysis Interventions for Treatment of AKI
5.1.1: Initiate RRT emergently when life-threatening
changes in fluid, electrolyte, and acid-base balance
exist.(Not Graded)
5.1.2: Consider the broader clinical context, the presence
of conditions that can be modified with RRT, and trends
of laboratory tests—rather than single BUN and
creatinine thresholds alone—when making the decision
to start RRT. (Not Graded)

27. Conclusions
Early detection and treatment of AKI may improve
outcomes.
Even a minor acute reduction in kidney function has
an adverse prognosis.
Hunting AKI in ICU….use a RIFLE .
Early referral will improve outcome inAKI