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Acute Kidney Injury (AKI) KDIGO Clinical Practice Guidelines Ali AlSahow.

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Presentation on theme: "Acute Kidney Injury (AKI) KDIGO Clinical Practice Guidelines Ali AlSahow."— Presentation transcript:

1 Acute Kidney Injury (AKI) KDIGO Clinical Practice Guidelines Ali AlSahow

2 Introduction  Common & serious medical emergency characterized by: 1) Rapid decline in GFR that evolves over hrs-days-wks 2) Retention of waste products & dysregulation of ECV & electrolyte 3) Oliguria with U/O 0.5 ml/min/d complicates 50% of cases 4) High mortality rate with high rate of development or progression of CKD

3  1802 – W. Heberden:  Gives the 1 st description of AKI as Ischria Renalis – Renal Retention  1909 – W. Osler:  Describes AKI as acute Bright illness in Principles & Practices of Medicine  1917 – F. Davies:  Describes AKI as war nephritis in WW1 in the Lancet  1941 – Waters & Beall:  AKI D/T crush injuries during 1941 London bombing in WW2 explained  1945 – W. Kolff:  1 st successful hemodialysis for AKI in Holland at the end of WW2  1951 – H. Smith:  Coins term ARF in The Kidney: Structure & Function in Health & Disease  2004 – ADQI:  Coins the term AKI as the official scientific term Historical Background of AKI

4 Definition & Staging of AKI Stage Cr criteriaUO criteria 1 Increase in Cr by ≥26.5 µmol/l within 48hrs OR 50 – 99% increase in Cr from baseline Baseline is known or presumed to have occurred within prior 7 days < 0.5 ml/kg/h for 6-12h 2100 – 199% rise in Cr< 0.5 ml/kg/h for ≥ 12h 3 ≥ 200% rise in Cr OR Cr rising ≥ 354 OR Initiation of RRT In pts younger than 18 decrease in eGFR to < 35 ml/min/ 1.73 m 2 < 0.3 ml/kg/h for ≥ 24h OR Anuria for ≥ 12h

5  Lack of standardized definition made incidence / outcome unclear  Incidence is rising & will continue to rise  Population is ageing with multiple comorbidities & polypharmacy A. Developed countries:  AKI affects 20% of adults & 35% of children hospitalized for acute illness  AKI affects 65% of ICU pts & 5-10% of all ICU pts will require RRT  Subacute kidney injury affects 1% of hospitalized pts & raises mortality  Rise in Cr over more than 7 days B. Developing Countries:  Information come from small studies with low methodological quality  Incidence is high & rising with high morbidity / mortality rates & cost  Socioeconomic & environmental factors influence rate / etiology / outcome  Infectious diseases, obstetric complications, envenoming (snake/spider bites) Epidemiology of AKI

6 Pattern of AKI & Country Income  High & Most Middle Income Countries:  Well developed health care systems & optimal renal services 1) Occurs mainly in ICU 2) Associated with MOF 3) D/T sepsis, trauma or surgery 4) Affects mainly the elderly 5) Difficult to prevent 6) Expensive to treat  Low & Some Middle Income Countries:  Poorly developed health care system & poor renal services 1) Seen in Various hospitals (1 o, 2 o, 3 o ) & various hospital units 2) MOF less common 3) D/T infections or diarrhea 4) Affects Mainly young otherwise healthier subjects 5) Preventable 6) Inexpensive to treat if detected early but too costly for pt if detected late

7  Mortality for hospitalized AKI pts is 3-5 X higher than non-AKI pts  Estimated AKI associated mortality: 24% for adults & 14% for children  In hospital mortality is 25% W/O RRT & 60% with RRT  90 day AKI mortality is 35% W/O RRT & 45% with RRT  90% of cases with MODS  AKI – associated mortality is decreasing in rich countries  Despite ageing population, more comorbidities & more illness severity  Avoidable deaths in poor communities are still unacceptably high  Up to 50% of AKI survivors are left with CKD or ESKD  15-30% of RRT requiring AKI pts remain RRT dependent at discharge  Number drops at 6 & at 12 months  Risk factors for lack of recovery  Old age, Severity of CKD at baseline, Severity of AKI & Fluid overload Outcome of AKI

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9  Functional Pre-Renal injury or stress D/T hypoperfusion:  The most common cause of AKI responsible for 50-60% of cases  70% of community-acquired & 40% of hospital-acquired  Severe hypoperfusion is the commonest cause of ischemic ATN  Structural Renal injury:  Intrinsic AKI accounts for 40% of all cases  Ischemic/Toxic tubular injury (ATN) causes 90% of such cases  Interstitial injury causes 10% of cases  Glomerular/Microvascular disease causes 5% of cases  Macrovascular injury is uncommon  Obstructive Post-Renal injury:  Acute obstruction causes <5% of cases of AKI  It has to be bilateral or unilateral with solitary kidney Etiology of AKI

10 Complications of AKI 1) Hyperkalemia with risk of malignant arrhythmias 2) Metabolic Acidosis decreasing CO & gut barrier function 3) Hyperphosphatemia & Hypocalcemia 4) Volume overload causing Pulmonary edema & Hypertension 5) Delayed wound healing 6) Anemia 7) Bleeding tendency D/T plt dysfunction 8) Increased risk of infections D/T WBC dysfunction 9) Encephalopathy / Pericarditis / Tamponade 10) Stress GI ulcers 11) Compromised investigations by contraindicated contrast 12) Compromised management by contraindicated drugs

11 ISN 5 R’s Approach to AKI Management 1. Risk Assessment:  Assess risk factors for development, & progression of AKI  Prevent exposure to insults in high risk pts  Use Scoring Systems / Screening / Electronic Surveillance Systems  Electronic surveillance for drug dose modification / Avoidance

12 Risk Factors for AKI A. Non-modifiable: 1) Old age 2) Male sex 3) Black race 4) Comorbidities: a) Pre-Existing CKD b) DM c) HTN d) CLD / IBD e) CHF / CAD / Recent MI f) PAD g) COPD h) Malignancy B. Potentially modifiable: 1) Anemia / Hypoxemia 2) Sepsis 3) Trauma 4) Contrast / Nephrotoxic drugs 5) Volume status a) Volume Depletion b) Volume Overload c) Using colloids / Cl rich fluids 6) Surgery: a) Cardiac surgery b) Major non-cardiac surgery c) Emergency procedures C. Environmental Factors: 1) Poor Sanitation & No clean water 2) Poor control of parasites & vectors D. Infrastructural Factors: 1) Poor HC budget & Services 2) Poor Transportation

13  High & Most Middle Income Countries: 1) Sepsis 2) Circulatory shock 3) Trauma & Burns 4) Cardiac Surgery & Major non – cardiac Surgeries 5) Nephrotoxic Drugs & Agents  Low & Some Midle Income Countries: 1) Diarrhea 2) Obstetric Complications Including septic abortion 3) Infections: Malaria, Leptospirosis, Dengue Fever, Cholera 4) Animal Venoms: Snakes, Wasps, Spiders 5) Natural medicines & Natural dyes 6) Prolonged Heavy Physical Work in Unhealthy Environment Exposure to be avoided in high risk pts

14 ISN 5 R’s Approach to AKI Management 2. Recognition of Injury:  Diagnose & Stage AKI early according to Cr & U/O criteria  Electronic alert system to alert about rise in Cr or drop in U/O  Telemedicine & point of care testing  Novel biomarkers?  They must produce real outcome improvement & cost effectiveness

15 ISN 5 R’s Approach to AKI Management 3. Response to Injury:  The ABC’s Of Non-Dialytic Management of AKI  Correct reversible factors  Avoid further exposure to insults - Nephrotoxins  Manage complications – Volume overload, Acidosis, Hyperkalemia

16 1) Identify the cause of AKI & start specific therapy 2) Judge volume status: BP, HR, JVP, Postural  BP, Skin turgor, U:Cr  Fluids &/or inotropes to optimize CO, BP & renal perfusion if dry & ↓BP  Diuretics to optimize urine output for volume overloaded pt 3) Correction of K / HCO 3 / Ca / PO 4 / Uric acid disorders  Use NaHCO 3 cautiously to avoid volume overload & hypernatremia 4) Adequate BS control to keep BS lowers mortality 5) Search for & aggressively treat infections with antibiotics 6) ESA for anemia 7) Early enteral nutritional support better than parenteral nutrition  AKI is a pro-inflammatory state with protein hypercatabolism  Protein intake is 1g/kg/d for non-catabolic non-dialyzed pts  Protein intake is 1.5g/kg/d for IHD & 1.7/kg/d for CRRT & catabolic pts  Total energy intake of Kca/kg/d is advised for any stage of AKI 8) Adjust doses of drugs that are renally excreted or protein-bound 9) Avoid nephrotoxins: Dye, aminoglycosides, ampho B, NSAIDs 10) Assess the need for urgent RRT

17 Hemodynamic Support - Fluids  In absence of hemorrhagic shock use crystalloids rather than colloids as initial management for volume expansion in pts with AKI or at risk of AKI  No conclusive evidence that colloids are safer or more effective  Colloids may be better for SBP in CLD or when large volume needed  Cost of colloids is higher  Hypertonic starch may be nephrotoxic – Osmotic Nephrosis  Not yet proved that LMW colloids (iso-oncotic) less nephrotoxic  Balanced crystalloids (RL & Hartmann) less Cl & less osmolality than NS  Less Acidosis, Less ↑ K, Less Coagulopathy, Better pt & renal outcome  Maintenance fluid requirement per day:  ml/kg/ d H 2 O + 1 mmol/kg/d Na/K/Cl g/d glucose  This does not take into account ongoing losses / oliguria / hyperkalemia  Aggressive fluid repletion in the early setting is probably beneficial  Restrictive fluid approach better once AKI occur & hemodynamics stable  Positive fluid balance increases AKI mortality

18 Hemodynamic Support - Vasopressors  Use vasopressors plus fluids in pts with vasomotor shock  High CO – Low SVR in septic shock, pancreatitis, burns & CLD  Persistent hypotension despite optimization of IV volume status  Vasopressors needed to preserve or improve renal perfusion  Not known which vasopressor most effective for prevention or treatment of AKI & septic shock  NA is useful for MOF or sepsis  Vasopressin may be used for shock refractory to NA  Improves BP & enhances diuresis  May reduce progression of AKI & lowers mortality in septic shock  Dopamine may be more arrhythmogenic compared to NA

19 Protocolized Hemodynamic Management  Protocol – based management of hemodynamic & oxygenation  Prevent development or worsening of AKI in septic shock or high risk postoperative pts  Early Goal – Directed Therapy (EGDT)  Early detection & management of hypotension  Fluids, blood products, O 2 delivery optimization, vasopressors use  Reestablish tissue perfusion within 6hrs aiming for: 1) Return of MAP to ≥ 65 mmHg 2) CVP between 8-12 mmHg 3) Improvement in blood lactate level 4) Central Vein Oxygenation Saturation > 70% 5) UO ≥ 0.5 ml/kg/hr  EGD septic shock resuscitation had no impact on outcome - NEJM

20 Diuretics in AKI  Loop diuretics inhibit Na-K-2Cl cotransporter in TAL of LoH  No evidence they reduce incidence or severity of AKI or mortality  Minimal human data to support the following benefits: 1) Reduced ATPase activity & renal tubular O 2 consumption may decrease ischemic damage of vulnerable outer medullary tubules 2) Increased UO may wash out necrotic debris blocking tubules 3) Inhibition of PG dehydrogenase reduces renovascular resistance & may increase renal blood flow  May cause interstitial nephritis & thrombocytopenia  High dose may cause ototoxicity  Do not use diuretics to prevent or treat AKI  They do not influence recovery from AKI or mortality  Use diuretics to manage volume overload & hyperkalemia  Adjust dose according to renal function

21 Dopamine – Receptor Agonists 1) Dopamine:  Low-dose dopamine IVI in healthy ppl causes renal vasodilation  This increases GFR & induces natriuresis  Dopamine increases renal vascular resistance in AKI pts  Dopamine has no value in prevention or treatment of AKI  May cause tachyarrhythmias & Cardiac & GI ischemia 2) Fenoldopam  Dopamine receptor 1 agonist W/O systemic α or β stimulation  24h IVI may prevent AKI in high risk cardiac surgery  Continuous IVI in ICU for septic shock may lower rate of AKI  Early continuous IVI may help in treatment of AKI in critically ill pts  Ineffective for prevention of CI – AKI  Guidelines do not suggest its use yet, waiting for more evidence

22 1) AKI in renal transplant pt 2) AKI complications 3) AKI stage 3 4) AKI on CKD stages 3/4 5) Resolved AKI with residual impaired GFR, HTN or Proteinuria 6) AKI of unknown etiology 7) AKI not responding to therapy  Remember:  Density of physicians in many African countries is /1000  WHO recommend 2.3 professionals per 1000 population  Nephrologists cannot handle all cases everywhere  Shrinking number of nephrologists & increasing demand  Involve PC, ED & IM physicians & nurses Referral to Nephrologist

23 ISN 5 R’s Approach to AKI Management 4. Renal Replacement Therapy in AKI:  Timing of Initiation, Modality, Dose & Duration of RRT

24 Timing of RRT in AKI Urgent Indications 1) Severe  K not responding to therapy 2) Severe acidosis (pH <7.1) not fixed by NaHCO 3 used for volume restoration 3) Uremic Encephalopathy 4) Uremic Pericarditis 5) Severe pulmonary edema not responding to diuresis 6) Relative indication: Cr > 500 & / or Ur > 50  Non – Renal Indications for RRT:  Dialyzable toxins such as barbiturates, methanol, theophylline  Severe hyperthermia  Severe inflammatory response in septic unstable pt W/O severe AKI?

25  Timing of RRT in the absence of urgency is not clear  Early initiation does not improve pt’s survival or renal recovery  RRT induced hypotension & arrhythmias may delay recovery  Vascular access has complications  RRT requires anticoagulation  Do not delay RRT unnecessarily when benefit outweighs risks  Do not use diuretics to enhance renal recovery or reduce RRT dose  Consider likelihood of renal recovery, degree of dysfunction in other organs, need for fluid intake (nutrition, drugs, blood) Timing of RRT in AKI Non – Urgent Indications

26 RRT Modality for AKI  Outcome similar in critically ill AKI pts treated with CRRT & IHD  Mortality, Renal recovery & Length of hospitalization  CRRT is preferred for hemodynamically unstable pts  SLED may be better than IHD for unstable pts  CRRT is preferred with acute brain injury or brain edema  IHD – induced hypotension may compromise cerebral perfusion  Fluid shift from rapid solute removal may induce disequilibrium

27 Conventional Intermittent HD Advantages 1) Cheap & low work load 2) Small amount of anticoagulation required 3) Intermittent nature allows diagnostic & therapeutic procedures  3-4 sessions per wk & 3-4 hrs per session 4) Adequate removal of excess fluid by UF 5) Clearance mainly by diffusion which is excellent for small solute  Excellent for severe hyperkalemia & severe acidosis  Clearance can be enhanced by:  Increasing dialysis duration & frequency  Increasing Qb (above ml/min) & Qd (above ml/min)  Using large (high efficiency) & porous (high flux) membrane

28  Skilled personnel required  Difficult fluid control with intermittent therapy  Rapid solute shift can cause cerebral edema  Avoid in head trauma, hepatic encephalopathy, brain edema, ↑ ICP  Not recommended in hemodynamically unstable pts  Tolerance in critically ill unstable pt is improved by:  Cooling dialysate to cool core T o to improve SVR & venous tone  Increasing time & frequency to slow down fluid & solute removal  Na profiling & UF profiling Conventional Intermittent HD Disadvantages

29 CRRT Advantages  Simple for ICU nurses to operate  Assures Hemodynamic stability in critically ill pts D/T:  Gentle fluid & solute removal W/O fluctuations  Improves gas exchange, fluid balance & biochemistry  Allows aggressive & early enteral / parenteral nutrition  Reduces risk of brain edema especially in pts with CLD  T o loss by dialysis circuit reduces core T o improves SVR/venous tone  Clearance = IHD with UF rate of 35ml/Kg/h (2L/h in 70 Kg pt) / 24h  ? Avoiding episodes of hypotension may enhance renal recovery  ? Filtration/adsorption of inflammatory cytokines/cardiac depressants

30 CRRT Disadvantages 1. Expensive with use large amounts of substitution fluids 2. High work load with 24h operation 3. Requires heavy anticoagulation 4. Pt immobilization 5. Downtime may cause loss of expensive disposables 6. Loss of nutrients, vitamins & trace elements 7. Different drug clearance & dosing & affected by downtime 8. Hypothermia? 9. ? Removal of useful anti-inflammatory molecules

31 Alternative Modalities 1) Extended Daily Dialysis (EDD):  Good IHD clearance plus gentle CRRT fluid & solute removal  Conventional dialysis machine with Qb 200ml/min & Qd 300ml/min  Runs for long periods (6-12hr/d) allowing investigations / procedures  Less anticoagulation & faster correction of acidosis than CRRT 2) Pulse high volume (HV) CVVHF:  CRRT for AKI in septic pts with MODS  Removes middle & large MW inflammatory mediators  UF rate of 85ml/kg/hr for 6-8hrs  Followed or preceded by UF rate of 35ml/kg/hr 3) Slow Continuous Ultrafiltration (SCUF):  No dialysate or replacement fluid is needed as no HD or HF  Safe & effective removal of fluid of up to 2L/hr

32 Dose of RRT in AKI  RRT dose should be prescribed before starting each session  Assess actual delivered dose to adjust the prescription  Delivered dose is frequently less than prescribed  Hemodynamic instability, access or filter problems, down time  Dose improved by more time, bigger filter, higher QB & QD & UFR  Recommended Kt/V is 3.9 / wk for IHD or SLED  Recommended effluent volume is ml/kg/h for CRRT – 42L/d

33 Peritoneal Dialysis  Pros:  Similar effectiveness to HD  Easy, safe & Cheap  Cons:  Higher risk of mechanical obstruction, protein loss in dialysate & ↑ BS

34 ISN 5 R’s Approach to AKI Management 5. Rehabilitation:  AKI is associated with late mortality & reduced QoL  F/U 3-6 months post discharge a) Document recovery or arrange regular F/U if pt has developed CKD b) Manage complications such as HTN

35 Conclusions  AKI is a common & serious medical emergency world wide  AKI has major impact on mortality, GFR recovery & health care cost  Apply ISN’s 5 Rs & KDIGO guidelines in prevention & management 1) Risk factors/exposing factors Identified/managed early to avoid AKI 2) Recognition of AKI early is essential to institute therapy early:  Volume resuscitation, Anemia correction, BP/O 2 sat optimization  Avoidance of nephrotoxins 3) Response to established AKI:  Correct volume status, Control BP/BS, Early nutrition, Sepsis treatment  Do not use diuretics to prevent or treat AKI but for volume control  Do not use dopamine to prevent or treat AKI 4) RRT:  Initiate when indicated & individualize modality (IHD/CRRT/PD) & dose 5) Rehabilitation post discharge with adequate long-term F/U

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38  Limitations of AKI Definitions / Staging:  Cannot calculate change in GFR in AKI W/O known baseline Cr  Cr is poor indicator of real GFR in unsteady state like AKI  Rise in Cr requires time & this delays diagnosis of early injury  Cr is affected by:  Muscle mass & muscle dietary supplements  Decreased Cr production in CLD  Lab techniques / errors  Drugs that inhibit tubular secretion (e.g., H2B)  Endogenous-Exogenous Chromogens may interfere with assay  Endogenous: Bilirubin, Uric Acid  Exogenous: Cephalosporins, Cimetidine, Trimethoprim  Cr might be affected by hemodilution D/T massive blood transfusion or fluid resuscitation & accumulation in acute illness  Estimation of U/O is difficult W/O urinary catheter  U/O criterion of 0.5 ml / kg / h for 6h is too sensitive  Rise in Cr is more predictive of mortality than this criterion  0.3 ml/kg/h for 6h correlate better with stage, RRT need & death  Morbidly obese pt may fulfill UO criteria W/O GFR change


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