Renal injury in endovascular aortic surgery

MARI cohort studyHYDRA-P trial

Athanasios Saratzis

NIHR Clinical Lecturer

NIHR Leicester Biomedical Research Centre, UK

Disclosures

Consulting & research support

• Medyria Medical

• General Electric Healthcare

• Amgen Inc

Other(s)

• Amgen Inc

• Novartis

Several potential mechanisms of short & long-term renal injury in EVAR

Adapted from: Saratzis A, et al. Kidney International 2018

AAASignificant inflammatory infiltrate

(not excised as in open repair)

Stent-GraftInflammatory response to

implantation (foreign body)

Renal arteriesCoverage of accessory arteries in 10%

Occlusion of orificeDissection or stenosis

Lower limbsIschaemic during the procedure (45-120 minutes)

Ischaemia reperfusion injury

Contrast

10 – 26% re-intervention rate over 5 yearsExisting co-morbidities & CKD

LONG TERM MECHANISMS

Rate: 20 - 25%

Saratzis et al. Ann Vasc Surg. 2016Saratzis et al. EJVES 2016Saratzis et al. CJASN 2015

Implications of AKI in EVAR

Impact on outcomesShort term mortality HR: 4.8 (95% CI: 2.3-5.6)

Long term mortality HR: 2.4 (95% CI: 1.4-3.1)

AKI after EVAR associated with:Short-term survivalLong-term survivalLong-term cardiovascular events£4.2 million extra treatment costs5,180 bed daysSaratzis et al. Kidney International 2018

Series of 950 EVARs with long-term FU

What does AKI do?

What about CKD?

cohort study

• 11 UK major centres

• All types of endo- & open aortic reconstruction

4 516 20

3964

96111

143163

185

217232 240

247

0

50

100

150

200

250

300

Tota

l n

um

be

r

Month-Year

MARI Recruitment - All Sites

Cumulative Total Cumulative Target

247 endovascular procedures for AAA (07/2018)

Interim analysis:

25.6% developed AKI within 1 week

All patients (4) who died had AKI

2 (both complex repairs) required filtration

Further results: end of 2018 – full risk factor analysis

cohort study

How can we prevent AKI in EVAR?

• Mechanisms of EVAR-related AKI very different to other interventions & surgery

• No RCT investigating AKI prevention specifically for EVAR

1) Create an EVAR specific AKI intervention:

Evidence review, patient input (interviews), national survey of anaesthetists

Delphi consensus:

• 10ml/kg/hr before & 2ml/kg/hr after (Hartmann’s)

• 8.4% NaHCO3 1ml/kg over 1 hour @ induction

2) RCT to test it

Pilot stage necessary

National survey of 131 anaesthetists

Methods:

FOLLOW-UP

48 hours: blood sample

24 hours: urine and blood sample

6 hours: urine sample

2 hours: urine sample

EVAR

GROUP 1: hydration

GROUP 2: hydration & bicarbonate 1mmol/kg bolus

Randomisation: 2 centresPILOT TRIAL

84% eligible patients recruited = 58 participants

Baseline characteristics

• Patients comparable in terms of:

Cardiovascular risk factors

Major established AKI risk-factors including eGFR

Contrast volume

Duration of procedure

97% of patients had a suprarenal fixation device

Results

• 84% recruitment rate

• No NaHCO3 AEs high-dose NaHCO3 safe

AKI incidence

Controls 33%

Intervention 7%

Major complications

Controls 10% (2 life-threatening)

Intervention 0

0

5

10

15

20

25

30

35

40

URINE

PLASMA

0

5

10

15

20

25

30

35

40

Control

Intervention

Markers of tubular ischaemia & inflammation

over 2 days

Conclusions

High-dose NaHCO3 promising AKI prevention strategy

• Safe

• Cheap

• Easily reproducible

• Acceptable by patients & clinicians

• Definitive RCT: currently in planning; 782 recruits

Acknowledgements

Clinicians & academics:

Taj Saran

Matthew Patteril

Nicholas Matharu

Jiffry Ahamed

Andrew Batchelder

David Sidloff

Camilla Gibson

Alexandra Meade

Dimitrios Grammatopoulos

NIHR Leicester BRC

Royal College of Surgeons

UNITED KINGDOMVASCULAR & ENDOVASCULAR RESEARCH NETWORK

£6,000 – 2 prizesOne specifically for new surgical technologies

Supported by industry & NIHR