1. Update in the management of AKI
Professor Harun-Ur-Rashid
PhD, FCPS, FRCP
Chief Consultant,Nephrology
and
Founder President
Kidney Foundation, Bangladsh

2. Introduction
AKI is a global problem and occurs in the community and in the hospital
It is a predictor of immediate and long term adverse outcomes.
World wide incidence of AKI is poorly known

3. Incidence of AKI around the world
USA cases /1000 discharge
Kuwait per 100,000 cases / year
Nigeria per year in children
North India cases / 1000 discharge
Bangladesh cases /1000 discharge
in a tertiary care hospital

4. Definition of ARF
AKI is defined by an abrupt decrease in kidney function that includes but not limited to ARF.
It is a broad clinical syndrome with various aetiologies
KDIGO,2012

5. History of ARF Ischaemia Renalis -by William Heberden in 1802.
Acute Bright’s disease-William oslears 1909.
ARF- Homer W. Smith, 1951

6. A 27 year male ,with severe diarrhoea for 2 days
BP 90/60,develop oliguria
Serum Cr 272 micromol,K-2.6,Na-123
In next 2 days, S.Cr jumped to 450
What is the diagnosis ?

7. Rifle criteria for diagnosis and classification of AKI
Serum creatinine of GFR
Urine output
Risk
Increase in serum creatinine x 1.5 or GFR decrease >25%
Less than 0.5ml/kg/h for more than 6 hours
Injury
Serum creatinine x 2 or GFR decreased >50%
Less than 0.5 ml/kg per hour for more than 12 hours
Failure
Serum creatinine x 3, or serum creatinine >4mg/dl (>354 μmol/l) with an acute rise >0.5 mg/dl (>44 μmol/l) or GFR decreased >75%
Less than 0.3 ml/kg/h for 24 hours or anuria for 12 hours
Loss
Persistent acute renal failure-complete loss of kidney function >4 weeks
End-stage kidney disease
ESRD>3 months

8. Criteria for diagnosis of AKI
Increase in Scr. by ≥ 0.3 mg/dl (≥26.5 μmol/L) within 48 hours. or
Increase in Scr. to >1.5 times baseline which is known or presumed to have occurred within the prior 7 days
Urine volume <0.5ml/kg/h for 6 hours.
AKIN,2007

9. Staging of AKI Stages Sr Cr Urine Output 1 1.5-1.9 times baseline or
≥0.3mg/dl (26.5 (μmol/L)
<0.5ml/kg/h for 6-12 hours 2
times baseline
<0.5ml/kg/h for >12 hours 3.
3.0 times baseline Or
Increasing in Sr Cr to
≥ 4.0 mg/dl (≥353.6 μmol/L
Initiation of RRT
<0.3ml/kg/h for ≥ 24 hours
Anuria for ≥12 hours
AKIN criteria,2007

10. Diagnosis of AKI, CKD and AKD
Functional criteria Structural criteria
AKI Increase in SCr by 50% within 7 days, OR No criteria
Increase in SCr by 0.3 mg/dl (26.5µmol/l)
within 2 days, OR Oliguria
CKD GFR <60 ml/min per 1.73m2 >3 months Kidney damage for
>3 months
AKD AKI, OR Kidney damage for
GFR <60ml/min per 1.73m2 for <3 months, OR <3 months
Decrease in GFR by ≥35% or increase in
SCr by >50% for <3 months
NKD GFR ≥60ml/min per 1.73 m2 Stable SCr No damage

11. Classification of AKI
Pre-renal
Renal
Post-renal

12. Classification of AKI Pre-renal Cause:
Hypovolemic state i.e Gastroenteritis
Low cardiac out-put state ie CCF
Systemic vasodilatation ie sepsis
D.I.C
Renal vasoconstriction ie cyclosporine
Impaired renal auto reguletory response ie ACE. ARB, COX
Plants and toxin

13. Classification of AKI Renal Cause: AGN/RPGN Interstitial nephropathy
Post renal :
Renal Stone disease
Other obstructive disease

14. Risk assessment of AKI

15. Factors that cause AKI:
Sepsis
Critical illness
Circulatory shock
Burns
Trauma
Cardiac and Non-cardiac Surgery
Nephrotoxic drug
Radio contrast agent
Poisonous plants and animal

16. Factors that determine susceptibility of AKI
De hydration or Volume Depletion
Advanced age
Presence of CKD
Chronic Disease i.e. heart, lung, liver DM
Cancer
Anaemia

17. Biomarkers for early diagnosis of AKI
Biomarkers Associated Injury
Cystatin –C Proximal tubular Injury
KIM-1 Ischaemic and Nephrotoxin
NGAL Ischaemic and Nephrotoxin
Cytokine- Toxic and
IL6,8,18 Delayed graft function
a-GST Proximal and distal T injury
&
n-GST

18. Evaluation and general management of patients with AKI
Patients should evaluate promptly to determine the cause.
Monitor the patients with Scr & urine output .
Manage according to cause & stage of AKI
Evaluate patients at 3 months for resolution or worsening of preexisting CKD.

19. Treatment and prevention of AKI
Management of Specific cause
Management of Hypotension and shock
Treatment of infection
Glycaemic control and nutrition support
Use of diuretic
Vasodilator therapy
Growth factor intervention
Role of Erythropoietin
RRT

20. Management of Hypotenison and shock in AKI
Careful titration of fluid:
ORS for children and infant
IV isotonic Saline for adults
4% albumin Vs saline for ICU
Hydroxyethyl Starch Vs Albumin for ICU
Bouchard J,MehtaRL,2010;Finfer et al, N Engl J Med,2004

21. Management of Hypotension and shock in AKI
Vasoachive medication:
Non epinephrine, dopamine or vasopressin only after dehydration is corrected to maintain BP
-Useful in septic shock, burns, liver failure
-Not suitable for Cardiogenic shock
Marik,Intensive Care Med,2002;KellumJA,Decker J,2001

22. Glycaemic control and nutritional support in AKI
Tight glycaemic control :
Pl. glucose mg/dl
Total calorie intake kcal/kg
Protein intake g/ kg/day-
noncatabolic state g/kg/day Catabolic state
Van den Berghe et al,N Engl J Med,2001

23. Role of Diuretics in AKI
No evidence to reduce incidence or severity of AKI
Indicate only if patients are volume over loaded
Diuretic only Convert oliguric to non oliguric
It promote earlier diuresis but no effect on survival
Ho and Power;Anaesthesia,2010;Cantarovich et al,Am J Kid Dis,2004

24. Role of Vasodilator therapy in AKI
Low dose dopamine – no benifit
Fenoldopen – not useful
Atrial natruretic peptide - not useful
Friedrich et al, Ann. Intern med,2005

25. Growth factor intervention in AKI
Recombinant human IGF-1- Not useful
Hirscberg et al,Kid Int,1999

26. Role of EPO in the prevention of AKI
Use of Erythropoetin in the Prevention of
AKI in ICU –Not Useful
Endre et al,Kid Int,2010

27. Role of RRT in AKI
Indicated only if Acute and severe renal failure, volume over load, hyperkalema, acidosis & symptoms of uraemia
Intermittent HD and CRRT- found equally effective
SLED – combines both IHD and CRRT
Rabindranath et al,Syst. Review,2007;
Bagshaw et al,Crit Care Med,2008.

28. Role of PD Vs HD in AKI Optimum Treatment of AKI remain uncertain
Studies looking at various therapeutic approach give different results
Optimum dose of PD is uncertain
Considered reasonable Treatment in Developing Countries
Karen Yeates,PDI,2012

29. Comparing PD and EBP for RRT
Variable
Phu et al., 2002 (2)
Reference
Gabriel et al., 2009 (4)
George et al., (12)
Country
Vietnam
Brazil
India
Setting
ICU
Mostly ICU (77%)
Patietns
Study group (n) 70
120 50
Mean age (years)
35.5
63.4
46.9
Sepsis (%)
31.4
44.5 38
PD technique
Exchanges
Manual
Cycler
EBP technique
Type
CVVH
Daily intermittent HD
CVVHDF
Mortality on PD [n/N(%)]
17/36 (47)
35/60 (58)
18/25 (72)
Mortality on EBP [n/N(%)]
5/34 (15)
32/60 (53)
21/25 (84)

30. AKI in ICU in a Tartiary Care Hospital

31. AKI in a ICU in a tartiary care hospital in Dhaka
Study period = Jan Dec 2010
Total No patients studied = 121
No of AKI detected (RIFLE criteria) = 46(38%)
Mean age: 50±12 yrs.(Range yrs;
M 72,F 49)
Alam B et al ,2011

32. Causes of AKI in ICU patients
Trauma
4.3
Surgical
28.3
Metabolic/poisoning
0.0
4.3
Hepatic
Gastrointestinal
4.3
Respiratory
10.9
Neurological
26.1
Cardiac
28.3
Sepsis/Septic Shock
45.7
Par cent

33. Severity of AKI as RIFLE criteria
no %
Risk
Injury
Failure

34. AKI following Coronary Angiography

35. Study period = January 2010- December 2010 Total No CAG = 111
AKI following Contrast during elective CAG and percutanious intervention
Study period = January December 2010
Total No CAG = 111
Mean age =51.9± 9.6 yrs
Non-ionic radio contrast agent used
AKI detected in 13 (11.7%)
Alam M,et al,2011

36. Risk factors for contrast induced AKI:
Diabetes mellitus
Pre-existing renal insufficiency
HTN
ACE/ARB/NSAIDs
LVEF-40%
Dose of Contrast:

37. What are the precaution needed before doing CAG:
Evaluate the risk : Baseline Sr Cr ≥115μmol in men and ≥88.4μmol in female
Risk out weigh potential benefits – use contrast
Use low –osmolar or iso-osmolor contrast and volume as low as possible
Volume status be optimized before administration of contrast

38. Summary and Conclusion
AKI is a global problem and is common, harmful and a treatable condition
Etiological factors are rapidly changing all over the world
Early diagnosis and appropriate management can improve the overall prognosis of AKI

39. THANK YOU