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

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Presentation on theme: "Update in the management of AKI Professor Harun-Ur-Rashid PhD, FCPS, FRCP Chief Consultant,Nephrology and Founder President Kidney Foundation, Bangladsh."— Presentation transcript:

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 Acute Bright’s disease-William oslears 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 ClassSerum creatinine of GFRUrine output RiskIncrease in serum creatinine x 1.5 or GFR decrease >25% Less than 0.5ml/kg/h for more than 6 hours InjurySerum creatinine x 2 or GFR decreased >50% Less than 0.5 ml/kg per hour for more than 12 hours FailureSerum 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 LossPersistent 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 or Urine volume <0.5ml/kg/h for 6 hours. AKIN,2007

9 Staging of AKI StagesSr CrUrine Output times baseline or ≥0.3mg/dl (26.5 (μmol/L) <0.5ml/kg/h for 6-12 hours times baseline 12 hours times baseline Or Increasing in Sr Cr to ≥ 4.0 mg/dl (≥353.6 μmol/L Or 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 CKDGFR 3 months Kidney damage for >3 months AKDAKI, OR Kidney damage for GFR <60ml/min per 1.73m 2 for <3 months, OR <3 months Decrease in GFR by ≥35% or increase in SCr by >50% for <3 months NKDGFR ≥60ml/min per 1.73 m 2 Stable SCrNo 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 –CProximal tubular Injury KIM-1Ischaemic and Nephrotoxin NGALIschaemic and Nephrotoxin Cytokine-Toxic and IL6,8,18Delayed graft function a-GSTProximal 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 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 Management of Hypotension and shock in AKI

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., 2011 (12) CountryVietnamBrazilIndia SettingICUMostly ICU (77%)ICU Patietns Study group (n) Mean age (years) Sepsis (%) PD technique ExchangesManualCyclerManual EBP technique TypeCVVHDaily intermittent HDCVVHDF 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 Surgical Metabolic/poisoning Hepatic Gastrointestinal Respiratory Neurological Cardiac Sepsis/Septic Shock Par cent

33 Severity of AKI as RIFLE criteria no. % Risk Injury Failure- 86.6

34 AKI following Coronary Angiography

35 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

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