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Acute Kidney Injury for Core Trainees
- 1. A C U T E K I D N E Y I N J U R Y J I M R I T C H I E
- 2. O B J E C T I V E S • Define, stage and manage AKI events • Appreciate the clinical relevance / pathology of AKI • Understand local and national referral criteria / pathways • Highlight less common, intrinsic renal pathology • Understand the long term implications of AKI
- 3. O U T L I N E • Perspectives - historical and current • Identification and definition of AKI • Pathogenesis • NICE guidelines, care bundles and CQUINs • The other 20% • Dialysis, long term outcomes and final thoughts
- 4. P E R C E P T I O N S Acute physician / nephrologist Acute physician / ICU Nephrologist / arse
- 5. R E A L I T Y J U N E 2 0 1 3 A U G / S E P T 2 0 0 9 M A Y / J U N E 2 0 0 9 P A T I E N T S W I T H A K I 1 8 1 5 1 1 P E R C E N T A G E R E C O G N I S E D 8 9 % 7 3 % 6 3 % R E P E A T B L O O D S 1 0 0 % 8 0 % 5 9 % D I P S T I C K 3 3 % 2 7 % 2 2 % I V I P R E S C R I B E D 8 8 % 7 3 % 6 8 % F L U I D B A L A N C E 4 4 % 2 0 % 1 8 % D R U G S R E V I E W 8 3 % 4 0 % 2 7 % Courtesy of Dr R Nipah - EAU. Salford Royal NHS Foundation Trust J U N E 2 0 1 3 A U G / S E P T 2 0 0 9 M A Y / J U N E 2 0 0 9 P A T I E N T S W I T H A K I 1 8 1 5 1 1 P E R C E N T A G E R E C O G N I S E D 8 9 % 7 3 % 6 3 % R E P E A T B L O O D S 1 0 0 % 8 0 % 5 9 % D I P S T I C K 3 3 % 2 7 % 2 2 % I V I P R E S C R I B E D 8 8 % 7 3 % 6 8 % F L U I D B A L A N C E 4 4 % 2 0 % 1 8 % D R U G S R E V I E W 8 3 % 4 0 % 2 7 %
- 6. B A C K G R O U N D
- 7. A K I V S . V T E VTE prevention: estimate 25,000 deaths /year Selby et al - DoH VTE Prevention Program. HES Annual report 2010
- 8. A K I O U T C O M E S Selby et al - cJASN. 2012;7(4):533-540
- 9. A K I O U T C O M E S Kane-Gill et al - Am J Kidney Dis. 2015;65(6):860-869
- 10. N H S E N G L A N D R E S P O N S E
- 11. C O N C E P T U A L P A T H W A Y F O R A K I N O R M A L R I S K D A M A G E G F R F A L L K I D N E Y F A I L U R E D E A T H What we see Where we define AKI
- 12. W H A T I S A K I ? AKI is potentially all of these things M E A S U R E M E N T C H A N G E A B S O L U T E C R E A T I N I N E > 1 3 0 - > 6 0 0 R E L A T I V E C R E A T I N I N E 1 0 % - 1 0 0 % U R I N E O U T P U T 0 - 3 0 M L / H O U R N E E D T O D I A L Y S I S ! ! !
- 13. W H A T I S A K I ? “A clinical syndrome characterised by a rapid reduction in renal excretory function due to several different causes.”
- 14. H O W I S A K I D E F I N E D S T A G E C R E A T I N I N E U R I N E O U T P U T 1 1 . 5 - 1 . 9 X B A S L I N E > 2 6 U M O L / L I N C R E A S E < 0 . 5 M L / K G / H R F O R 6 - 1 2 H O U R S 2 2 . 0 - 2 . 9 X B A S E L I N E < 0 . 5 M L / K G / H R F O R > 1 2 H O U R S 3 3 . 0 X B A S E L I N E S C R > 3 5 3 U M O L / L R R T < 0 . 3 M L / K G / H O U R F O R > 2 4 H O U R S A N U R I A > 1 2 H O U R S
- 15. I N C I D E N C E O F A K I 5 - 15% of all non-elective admissions
- 16. N U M B E R S P E R 1 0 0 0 / B E D S • AKI 1 - 2727 / year [227 / month] • AKI 2 - 782 / year [65 / month] • AKI 3 - 636 / year [53 / month]
- 17. N U M B E R S I N C R I T I C A L C A R E Murugan et al - Nat Rev Nephrol 2012;7(4):209-217
- 18. N I C E G U I D E L I N E S • CG196 - Issued August 2013 • Areas covered - assessing risk - prevention - detection - management
- 19. N I C E G U I D E L I N E S - P R E V E N T I O N • Use of EWS triggers • Systems in place to monitor urine output • Caution around iodinated contrast - medication review - adequate hydration
- 20. R I S K F A C T O R A S S E S S M E N T • CKD • Age >65 • Heart failure • Liver disease • Diabetes • Previous AKI • Acute illness / sepsis • ‘Nephrotoxic’ drugs • Neuological / cognitive impairment • History of urological obstruction NICE- 2013; CG169
- 21. R I S K F A C T O R A S S E S S M E N T Kane-Gill et al - Am J Kidney Dis. 2015;65(6):860-869
- 22. I N V E S T I G A T I O N • Urine dipstick - consider renal referral if ‣ haematuria and proteinuria - without UTI - without catheter related trauma • Renal tract ultrasound - suspicion of obstruction / pyonephrosis (6 hours) - no identified cause for AKI (24 hours) NICE- 2013; CG169
- 23. T R E A T M E N T
- 24. C A U S E S O F A K I Pre - renal -25 - 60% Renal -35 - 70% -80 - 90% ischaemic Post - renal -5% (hospital) -20% (community)
- 25. A C U T E T U B U L A R N E C R O S I S Hypoperfusion / ischaemia Direct effect Haemodynamic changes Fall in GFR Fall in U/O Tubular damage Cells shed Casts form Backleak
- 26. I N T R I N S I C R E N A L D I S E A S E
- 27. F L U I D S Catecholamines -> PCT effect Pain / sepsis -> ADH stimulation Hypotension -> RAAS activation Can lead to salt / water retention Sepsis -> capillary leak Reduced hepatic synthetic activity Can lead to hypoalbuminaemia Hypo-oncotic ECF
- 28. E V I D E N C E F O R F L U I D S ? • Early Goal Directed Therapy - Surviving Sepsis • 30ml/kg crystalloid • No data have considered renal outcomes • Adverse effects of fluid overload?
- 29. E V I D E N C E F O R F L U I D S ? • There are no data to suggest that aggressive hydration improves outcomes in AKI - Obvious dehydration - Contrast mediated injury / crush injury E D G T E D G T ( F L U I D N E U T R A L ) V A S O A C T I V E N O V A S O A C T I V E S O D D S R A T I O 0 . 5 9 0 . 4 7 0 . 5 2 0 . 7 5 9 5 % C I 0 . 3 9 - 0 . 8 9 0 . 2 9 - 0 . 7 6 0 . 3 4 - 0 . 8 0 0 . 3 7 - 1 . 5 3 E D G T E D G T ( F L U I D N E U T R A L ) V A S O A C T I V E N O V A S O A C T I V E S O D D S R A T I O 0 . 5 9 0 . 4 7 0 . 5 2 0 . 7 5 9 5 % C I 0 . 3 9 - 0 . 8 9 0 . 2 9 - 0 . 7 6 0 . 3 4 - 0 . 8 0 0 . 3 7 - 1 . 5 3 Prowie et al - Crit Care 2012;16(4):230-245
- 30. E V I D E N C E F O R F L U I D S ? Prowie et al - Crit Care 2012;16(4):230-245
- 31. E V I D E N C E A G A I N S T F L U I D S … • 170 RRT requiring AKI secondary to ATN - primary end point of freedom from dialysis at 12 months - 61 (36%) recovered function (51 prior to discharge) - 1% increase in fluid overload associated with 3% reduction in chance of recovery Heung et al - Nephrol Dial Transplant 2012;27(3):956-61
- 32. E V I D E N C E A G A I N S T F L U I D S … • All AKI episodes in 618 patients over a 2-year period - fluid overload associated with mortality - dose dependent relationship - present in dialysed and non-dialysed patients Bouchard et al - Kid Int 2009;76:422-427 Dialysis AKI
- 33. W H I C H F L U I D - S T A R C H E S ? • Can deposit in the kidneys • No mortality benefit in acutely unwell patient - n = 804, HR death 1.17 [95% CI 1.01 - 1.36], p=0.03 - n = 7000, RR death 1.06 [95% CI 0.96 - 1.18], p=0.26 • 20% increased risk for RRT Perner et al - NEJM 20012;367:124-134 Myburgh et al - NEJM 2012;367:1901-11
- 34. W H I C H F L U I D - A L B U M I N ? SAFE Investigators - NEJM 2004;350:2247-56
- 35. W H I C H F L U I D - C R Y S T A L L O I D S ? Chowdhury et al - Ann Surg 2012;256:18-24 Yunos et al - JAMA. 2012;308(15):1566-1572
- 36. R E N A L R E P L A C E M E N T T H E R A P Y • Refractory hyperkalaemia • Profound acidaemia • Uraemic symptoms - pericarditis - encephalopathy • Fluid overload and pulmonary oedema
- 37. E V I D E N C E F O R R R T T I M I N G “Beliefs about when to initiate dialysis in patients with AKI are passionately held, and are - on the whole - unsupported by reliable evidence” Wilson et al - cJASN 2014;9:1510-1512 When is early Who will progress Recovery between early / late timings
- 38. E V I D E N C E F O R R R T T I M I N G • 102 patients - prospective study • Single center in India • Early start; sCr >620 • 80% volume depletion Jamale et al - Am J Kidney Dis 2013;62(6):1030-1033 Vaara et al - cJASN 2014;5(9):1577-1585 • 986 patients - retrospective study • Multi-centre study • 4 patient groups (propensity matched) • Possible benefit from early RRT 27% vs. 49%
- 39. R E F E R R A L C R I T E R I A • AKI with no clear cause • AKI 3 • Possible diagnosis of vasculitis / GN… • AKI in CKD 4 / 5 • AKI in renal transplant • Inadequate response to treatment / complications of AKI NICE- 2013; CG169
- 40. S A F E T R A N S F E R S
- 41. L O N G T E R M O U T C O M E S CKD ESKD Coca et al - Kidney Int 2012;81(5):442-448
- 42. L O N G T E R M O U T C O M E S “Dose dependent” effect Interaction with pre-existing CKD
- 43. G F R D E C L I N E P O S T - A K I Ritchie, Asar, Kalra et al - Unpublished data. Under review Stat Med No AKI AKI 1 AKI 2/3 Recovery period ~1 month. 78% / year increase 8% 4%
- 44. B I O M A R K E R S F O R A K I N O R M A L R I S K D A M A G E G F R F A L L K I D N E Y F A I L U R E D E A T H What we see Where we define AKI M A R K E R A C T I O N • NGAL • IL-18 • KIM-1 • L-FABP • Cystatin-C
- 45. B I O M A R K E R S • All can predict AKI • None have led to an intervention to prevent AKI developing • None have a clear role above established markers
- 46. B I O M A R K E R S - E V E N T S Perianayagam et al - Am J Kidney Dis 2009;54(6):1025-1033
- 47. B I O M A R K E R S - O U T C O M E M O R T A L I T Y R O C A U C L - F A B P 0 . 8 9 N G A L 0 . 8 3 I L - 1 8 0 . 8 3 C R 0 . 7 3 A P A C H E I I 0 . 9 0 Doi et al - Crit Care Med 2011;39(11)
- 48. C Q U I N • Commissioning for Quality and Innovation Payment Framework • Links income to achieving quality improvement plans
- 49. A K I C Q U I N • Discharge summary information for patients coded as having an AKI ‣ stage ‣ evidence of medication review ‣ follow up blood tests - type - frequency
- 50. T H A N K S
Editor's Notes
- Where’s the fluid balance Repeat bloods Actions?
- 2009 NCEPOD report Only 50% of AKI care considered good Poor assessment of risk factors Unacceptable delay in recognition of post-admission in AKI in 43% 22 patients died with a primary diagnosis of post-admission AKI which was predictable and avoidable Complications missed (13%), avoidable (17%) or badly managed (22%) NCEPOD recommendation - initial clerking for all emergency admission should include AKI risk factor. All emergency patients should have electrolytes checked on admission and appropriately thereafter. Unacceptable delay in recognition of post admission AKI in 43% Complication missed (13%), avoidable (17%), badly managed (22%) 33% inadequate investigations 29% inadequacies in management Poor recognition of acute illness, hypovolaemia, sepsis
- AKI does not discriminate by age
- All trusts must comply
- AKI is a consequence of disease
- The pattern and burden of AKI appears to be particularly significant in developing countries [3] and therefore the recently published Kidney Disease Improving Global Guidelines (KDIGO) Clinical Practice Guidelines for Acute AKI Definition A key recommendation is that clinicians effectively adopt the previously published AKI Network definition of AKI [5] as one of the following: • An increase in serum creatinine by ≥0.3 mg/dl (≥26.5 µmol/l) within 48 h • An increase in serum creatinine to ≥1.5 times baseline within the previous 7 days • Urine volume ≤0.5 ml/kg/h for 6 h Furthermore, KDIGO suggests that AKI should be staged according to severity as outlined in table Kidney Injury provides a welcome and timely synthesis of the evidence base to support the management of AKI . AKI Definition A key recommendation is that clinicians effectively adopt the previously published AKI Network definition of AKI [5] as one of the following: • An increase in serum creatinine by ≥0.3 mg/dl (≥26.5 µmol/l) within 48 h • An increase in serum creatinine to ≥1.5 times baseline within the previous 7 days • Urine volume ≤0.5 ml/kg/h for 6 h Furthermore, KDIGO suggests that AKI should be staged according to severity as outlined in table
- SRFT audit data 62% of AKI 1 occurred in our hospital 177 AKI 1 51% did not progress 27% -> AKI2 21% -> AKI 3
- 3198 adults, 198 European ICU Chart shows rates of organ dysfunction in admitted patients Irrespective of reasons for critical care admission, ~50% of patients with develop AKI
- As age increases, models using other factors function less well Age is a dominant factor Limitation of this study is that is represents a US ICU population
- Discussion slide
- Causes of aki depend on where acquired ATN often seen as the number 1 cause. Debabteable….
- Direct glomerular effects - mesangial contraction reducing effective surface area Vasocontriction - RAAS activation, increased AII, reduced prostocyclin levels Tubular damage - neuohormonal effeects (eNOS) alterirng heamdynamics Dead tubular cells shed into lumen forming casts - local obstruction, opposed filration pressure, decreased gfr This also causes backleak - ie filtrate back into the cirulcation - reduces effective GFR and urine vol
- 2/3 body weight is water 1/3 of this is extracellular - mainly interstitial; some plasma; some transcellular Changes in fluid balance when acutely unwell lead to a tendency to retain fluids but also to re-distribute to the ‘wrong’ compartments Explains often poor response to fluids etc in terms of a diuresis
- CIN / rhabdomyolysis are exceptions Meta-analysis of EGDT in prevention of post-operative AKI For all EDGT ~555 ml extra fluid in non-aki group Better result in EDGT with equal fluids (ie. vasoactives) Similar result if just stratified by ionotropes No between group difference if no ionotropes in study
- Patients at a tertiary renal center over a 12 month period Percent fluid overload was calculated based on the following formula: [(Weight at dialysis initiation – Baseline weight)/Baseline weight] × 100%. Recognizing that weight changes (gain or loss) may begin to occur pre-hospitalization, we defined baseline weight as the average outpatient weight recorded within 3 months preceding hospitalization. KM plot suggests that this is an early modifiable factor (i.e. separation does not continue)
- Not just RRT dependent AKI 30 day mortality 37% vs. 25%; 60 day 46% vs. 32%; discharge 48% vs. 35% Dialysis needing patient OR death 2.07 if overloaded Non-dialysis patients OR death 3.14 if overloaded KM shows survival Bar chart shows dose dependent relationship - hypovolaemia and hypervolaemia bad Also - volume overload at time of peak sCr - less likely to recover renal function
- Low molecular weight hydroxyethyl starches Hence not recommended in acutely ill patients of any real nature
- 6997 patient Albumin vs. crystalloid Death - RR 0.99 ICU stay 6.5 vs 6.2 days Same for LOS, LO ventilation, RRT, days RRT
- Hyperchloridaemia can cause afferent arteriolar constriction and therefore theoretically reduce GFR Randomised trial of 12 healthy volunteers - 2L saline or plasmalye: reduced renal perfusion seen in saline group ICU trial (pre/post intervention by year) 760 vs 773 patients. 694 mol vs 496 chloride RIFLE-defined AKI (odds ratio, 0.52 [95% CI, 0.37-0.75]; P.001) and use of RRT (odds ratio, 0.52 [95% CI, 0.33-0.81]; P = .004)
- Even in CKD there is no absolute definition for when RRT should start Several RCT have shown no survival benefit from early start in CKD There is no “optimal” form of RRT in AKI - not going to cover this
- INDIA - signal to increased death in early start group FINNAKI - RRT within 12 hours (conventional indications) >12 hours (conventional indication; before convention indicatoin; no rat Ongoing - Staart-AKI (Standard vs accelerated initiation of RRT in AKI). 90 day mortality in 100 patients being randomised to RRT within 12 hours or study criteria / based on clinical need. Excellent overall survival! IDEAL-ICU - 864 septic AKI in France. Early vs/late RRT Questions are also about selection / AKI cause etc
- These are criteria for discussion. They do not equate to transfer
- Meta-analysis of 36 studies AKI associated with excess risk for development of CKD (HR 8) and ESRD (HR 3) In addition, long term increased risk for death (HR 2) - ie risk increased after AKI recovery
- Dose effect shows biological plausibility - worse AKI associated with increased risk for both CKD and ESRD CKD is such a potent risk factor for ESRD. However, AKI episodes still increase risk (though not as much as in the non-CKD population). Raises questions of monitoring… Comparable data for proteinuria / non-proteinuria
- 3.3 = 28ml/min (28 -> 26.8 -> 25.8 ->24.7) 2.95 = 20ml/min Recover to ~22ml/min (28 -> 22 -> 20.2 -> 18.6)
- 200 patients in prospective cohort study No benefit of CC over existing markers
- Prediction of death - clinical scores outperform biomarkers
- What is a CQUIN