Update in the management of AKI

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 - 24 cases /1000 discharge • Kuwait - 4 per 100,000 cases / year • Nigeria - 12 per year in children • North India - 20 cases / 1000 discharge • Bangladesh -24 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

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 or • Urine volume <0.5ml/kg/h for 6 hours. AKIN,2007

9. Staging of AKI

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 BiomarkersAssociated 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 -80-110 mg/dl • Total calorie intake -20-30 kcal/kg • Protein intake -0.8-1.0 g/ kg/day- noncatabolic state -1.0-1.5 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

30. AKI in ICU in a Tartiary Care Hospital

31. AKI in a ICU in a tartiary care hospital in Dhaka • Study period = Jan 2010- Dec 2010 • Total No patients studied = 121 • No of AKI detected (RIFLE criteria) = 46(38%) Mean age: 50±12 yrs.(Range 18-80 yrs; M 72,F 49) Alam B et al ,2011

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

33. Severity of AKI as RIFLE criteria no. % • Risk - 23 19.0 • Injury -15 12.4 • Failure - 8 6.6

34. AKI following Coronary Angiography

35. AKI following Contrast during elective CAG and percutanious intervention • Study period = January 2010- 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