Update in Acute Kidney Injury Mark Devonald Consultant Nephrologist
If you stay awake you might hear about Why AKI is important Some cases to illustrate some specific points A couple of updates on AKI Comprehensive review of AKI and everything
AKI is important because it is: Common Serious Expensive
AKI is expensive The Economic Impact of Acute Kidney Injury Marion Kerr NHS Kidney Care
AKI is common and serious: mortality RIFLE stage Incidence (%) In-hospital mortality (%) 0 82.0 4.4 Risk 9.1 15.1 Injury 5.2 29.2 Failure 3.7 41.4 All AKI 18.0 24.6 KDIGO stage Incidence (%) In-hospital mortality (%) 0 83.4 2.2 1 10.4 15.4 2 3.5 28.9 3 2.1 35.3 3D 0.6 38.7 All AKI 16.6 22.0 Uchino et al, Crit Care Med 2006 Porter et al, Nottingham University Hospitals n=20,126 n=140,190
AKI is serious: length of stay AKI stage No. of pts Median Age LoS(days) 0 3 1 10,557 74 9 2 3,105 76 9 3 1,888 74 10 1-3 15,550 74 9 Porter et al, NDT 2014
AKI is serious: effect on renal function Cerdá J et al. CJASN 2008;3:881-886 2008 by American Society of Nephrology
risk AKI CKD risk
Case 1:
Porcine model of IR-AKI Gardner and Devonald, in preparation
Sham surgery (control) No AKI Healthy young (7-8/52) pig 5 weeks AKI stage 1 Ischaemia Reperfusion (40 min) Gardner and Devonald, in preparation
AKI is common RIFLE stage Incidence (%) 0 82.0 Risk 9.1 Injury 5.2 Failure 3.7 All 18.0 KDIGO stage Incidence (%) 0 83.4 1 10.4 2 3.5 3 2.1 3D 0.6 All 16.6 Uchino et al, Crit Care Med 2006 n=20,126 Porter et al, Nottingham University Hospitals (unpublished) n=140,190
Detection of AKI
KDIGO 2012 First identify AKI (rise in SCr 1-5-1.9 x baseline within 7d or rise 26 µmol/l <48 h). Thenstage: Stage SCr criteria U/O criteria 1 1.5 1.9 x baseline OR 26 µmol/l increase <0.5mL/kg/h for 6 12 h 2 2.0 2.9 x baseline <0.5mL/kg/h for 12 h 3 3.0 x baseline OR Increase in SCr to 354 µmol/l OR Initiation of RRT OR In patients <18 years, decrease in egfr to <35 ml/min per 1.73 m 2 <0.3mL/kg/h for 24 h OR anuria for 12 h
2009 The advisors judged there to be an unacceptable delay in recognising post-admission AKI in 43% of patients. June 2009
AKI e-alerts Tell you that SCr has risen (if you haven t worked that out for yourself) Stage the AKI (KDIGO or similar) passive, active, interruptive
What is AKI e-alerting? Algorithm-based DETECTION Clinical ALERT SCr based standard criteria RIFLE, AKIN, KDIGO Passive alert Message with SCr result SCr based non-standard criteria >75% increase, SCr Active alert Phone call, text Non-SCr based Urine output Interruptive alert Compulsory action
Continuous assessment and staging of AKI 1st SCr during admission Subsequent SCr measured Pt admitted Time 1 year 7 days Identify and stage AKI KDIGO Baseline If no actual baseline SCr, use imputed SCr assuming egfr 75 ml/min
Why do we need AKI e-alerting? Request SCr Look up RESULT ACTION KDIGO RIFLE AKIN Frequent failure to notice small (or large) ΔSCr Delayed detection of AKI e.g. NCEPOD 2009 Failure to document AKI Increased mortality Wilson FP et al Clin Nephrol 2013
Apologies for stating the obvious but You will not get an AKI e-alert if you haven t checked the SCr
Does e-alerting improve outcomes? Lancet 2015
Wilson FP et al, Lancet 2015
Wilson FP et al, Lancet 2015
Summary so far: AKI is common, serious and expensive AKI (even stage 1?) leads to CKD e-alerts useful but effects uncertain
DetecKon Diagnosis AKI is a syndrome not a diagnosis
AKI is easy, isn t it? Case 2A: 52F 1/52 malaise, mild fever, R loin pain ABs for UTI from GP Admitted SCr 420uM (BL 80) Urinalysis Bld++ Prot++ Nit+ IV Abs, IVI Stage 3 AKI Case 2B: 78M 1/52 post-op TKR Peri-op hypotension, N+V Post-op SCr rises to 650uM (BL 140) Urinalysis Bld- Prot+ Nit- Oliguric, K 6.8 Stage 3 AKI Temporary HD then IVI Good U/O, feels well SCr 400 380.370 Good U/O, feels well SCr 500 460.420
1 week later Case 2A: 52F Completed Abs Oral fluids SCr 370 390 420 Case 2B: 78M Well Oral fluids SCr 400 390 370.380 What would you do? ANCA + PR3>100 R renal vein thrombosis IgG paraprotein 28g/L Myeloma (cast nephropathy)
DetecKon Diagnosis Be prepared to reconsider your diagnosis (especially if AKI does not resolve as expected) IV fluid will often cause a transient fall in SCr (dilution not improvement in renal function)
Diuretics and the dark art of dialysis
Case 3: 58M Known IHD, CCF, CKD 3A Rx Ramipril 10 mg od, spironolactone 25mg od, furosemide 80mg bd etc Admitted grossly overloaded SCr 180uM (BL 130), urea 26mM, K 5.6mM Started on IV furosemide 160mg bd Minor improvement in overload after a week; furosemide 250mg bd IV SCr: 180 210 250 270 Urea: 26.34 46..54 You, yes YOU. Dialyse my patient would you? diuretic resistance bla bla
Cardiorenal Syndrome (CRS) CRS Type 1 Acute cardiorenalsyndrome CRS Type 2 Chronic cardiorenalsyndrome CRS Type 3 Acute renocardiacsyndrome CRS Type 4 Chronic renocardiacsyndrome Acute cardiac problem leads to AKI Chronic heart problem leads to CKD AKI leads to acute cardiac problem CKD leads to chronic cardiac problem CRS Type 5 Secondary cardiorenalsyndrome Systemic condition leads to cardiac and renal problems
What do you do? 2 comments Bad heart + bad kidneys = bad prognosis Cardiac status usually determines outcome A few suggestions Agree on realistic plan and goals Aim for volume offload by Remove spiro + ACEI temporarily to allow diuretic increase Thiazide + loop = synergistic Salt and water restriction MDT discussion about renal replacement therapy (would they tolerate long term RRT?)
AKI update: cardiorenal
AKI update: diuretic resistance Rao et al, JASN 2017
AKI update: diuretic resistance Rao et al, JASN 2017 Justifies addition of thiazide to loop diuretic in diuretic resistance
Contrasting cases
Case 4A: 80M 3/52 diarrhoea, jaundice, wt loss AKI SCr 320 (BL 100) U/S: ascites, possibility of metastases IVI SCr: 320 280 250 Case 4B: 56F Acute abdomen, unwell, hypotensive, guarding. Surgical hx. AKI: SCr 280 (BL 80), low Hb, high lactate. Poor U/O Physicians want CT with contrast Surgeons want CT with contrast What do you advise?
RISK? Risk factors CKD egfr<40 DM + CKD Heart failure Age >75 Hypovolaemia Large volume of contrast Intra-arterial route NICE CG169, 2013
Case 4A: 80M 3/52 diarrhoea, jaundice, wt loss AKI SCr 320 (BL 100) U/S: ascites, possibility of metastases IVI SCr: 320 280 250 Case 4B: 56F Acute abdomen, unwell, hypotensive, guarding. Surgical hx. AKI: SCr 280 (BL 80), low Hb, high lactate. Poor U/O Physicians want CT with contrast Surgeons want CT with contrast Could wait but risk is low Can t wait Ensure that risk assessment does not delay emergency imaging NICE CG169, 2013
Update: AKI biomarkers
Traditional AKI biomarkers are poor KDIGO SCr UO Marker of glomerular filtration NOT injury Can take 24-48h to rise after injury Need to know baseline Can be a normal physiological response Has to be measured continuously Has to be measured for >6 hours
AKI outreach: aims How does early detection change management? Early detection Fluid balance Medicines review Intensity of monitoring Specialist review Avoid dehydration or overload Avoid nephrotoxins; Adjust doses Frequency, extent, cost Transfer, escalation, discharge
Cystatin C NGAL KIM-1 Ideal Biomarker Accessible sample Sensitive Specific Stable Cheap IGFBP-7/ TIMP-2 NephroCheck
Fig 1. Mean corrected urinary Cd at different stages of AKI Fig 2. Mean corrected urinary Cu at different stages of AKI
Summary (1) AKI is common, serious and expensive AKI increases risk of CKD E-alerts help to detect AKI but benefits uncertain
DetecLon Diagnosis Summary (2) Cardiorenal syndrome needs realistic MDT approach If a contrast scan is important, do it SCr is a poor AKI biomarker but it s not been eclipsed yet
Thank You mark.devonald@nuh.nhs.uk