Acute Kidney Injury Post-op: Kidney attack

©2012 MFMER | slide-1

Acute Kidney InjuryPost-op: Kidney attack

Kianoush Kashani

5th Anesthesia and Critical Care ConferenceKuwait 2013


Outlines

• Definition

• Epidemiology/outcome

• Pathophysiology

• Diagnosis

• Management Vs treatment


RIFLE CriteriaGFR criteria Urine output criteria

Risk

Injury

Failure

Loss

ESRD

High sensitivity

High specificity

Persistent ARF = complete loss of renal function >4 weeks

End-stage renal disease

Increased creatinine x3 or GFR decrease >75%

or creatinine 4 mg/100 mL (acute rise of 0.5 mg/100 mL dL)

Increased creatinine x2 or GFR decrease >50%

Increased creatinine x1.5 or GFR decrease >25%

UO <0.5 mL kg-1

h-1 x6 hr

UO <0.5 mL kg-1

h-1 x12 hr

UO <0.3 mL kg-1

h-1 x24 hr or anuriax12 hr O

ligur

ia


AKIN Definition for AKIAKIN Conference, Vancouver 2006

Stage I

Stage II

Stage III

• Inc Scr 0.3 mg/dL or >150-200% from baseline

• Inc Scr >200-300% from baseline

• Inc Scr >300%

• Scr >4 with acute min rise of 0.5 mg/dL

• Need for RRT

• <0.3 mL/kg/hr for 24 hr

• Anuria for 12 hr

<0.5 mL/kg/hr for >12 hr

<0.5 mL/kg/hr for >6 hr


Reasons for incidence

• Age

• Comorbid conditions

• CKD

• More sensitive criteria

Hou et al: Am J Med 74:243, 1983Nash et al: JASN 7:376, 1996Nash et al: AJKD 39:930, 2002

0

2

4

6

8

1983 1996 2002

Year

%

Incidence of AKI


AKI and Mortality

Ricci Z: Kidney Int 73:538, 2008

0.01 0.1 1 10 100

Study or subcategory

01 General ICU (Cr and UO criteria)AbosaifAhlstromCruzHoste

02 General ICU (without UO criteria)Lopes (HIV)Lopes (sepsis)Ostermann

03 CardiosurgeryKuitunenLin

04 Other ICUCocaLopes (bmt)Lopes (burns)

05 Not confined to ICUUchino

0.01 0.1 1 10 100 0.01 0.1 1 10 100

Mortality Risk vs Non-AKIRR (random)

95% CI

Mortality Injury vs Non-AKIRR (random)

95% CI

Mortality Failure vs Non-AKIRR (random)

95% CI


AKI and Long-Term Mortality

Lafrance et al: JASN 21(2):345, 2010

0

20

40

60

80

100

0 1 2 3 4

Cu

mu

lati

ve p

rob

abili

tyo

f su

rviv

al (

%)

Follow-up (years)

No AKI

AKIN IAKIN IIAKIN III

Number at risk782,222 601,772 443,730 296,128 138,820 No AKI 52,338 37,234 25,798 16,441 7,758 AKIN I 19,771 13,692 9,210 5,712 2,633 AKIN II 10,602 7,173 4,639 2,723 1,200 AKIN III


ESRD After AKI

0.00

0.02

0.04

0.06

0.08

0 100 200 300 400 500 600 700

Pro

bab

ilit

y o

f E

SR

D

Days from hospital discharge

0.02

0.04

0.06

0.08

0.10

0.12

0.14

0.16

0 100 200 300 400 500 600 700P

rob

abil

ity

of

ES

RD

Days from hospital discharge

No AKI

AKIP<0.0001, DF=1

P<0.0001, DF=3

No AKI or CKDCKD onlyAKI onlyAKI and CKD


RRT epidemiology (NEFROINT data)

Piccinni et al. Minerva anestheiology 2011; 77:1-2

ICU admissions (ESRD excluded)

576

No AKI on admission57.3%

AKI on admission42.7%

Never developed AKI34.2%

New AKI23.1%

Ever AKI65.8%

Never recovered27.2%

Partial recovery13.5%

Complete recovery59.4%

Required RRT8.3%


Etiology of Hospital-Acquired AKI

0

10

20

30

40

50

60

ATN

Prere

nal

ACKI

Obstru

ctiv

eAIN

Vascu

lar

RPGN

%

Comprehensive Clinical Nephrology, Johnson 3rd edition


Ischemia induced AKI

Abuelo et al, NEJM 2007, 357 (8)


Symptoms

• Polyuria• Oliguria/anuria• Hematuria• Dysuria• Azotemia

• Mental status changes• Acidosis ( respiratory rate)• Hypervolemia/hypertension• Hyperkalemia• Pericarditis


Urinary Index

Schrier: J Clin Invest 114(1):5, 2004

PrerenalLaboratory test azotemia ATN

Urine osmolality (mOsm/kg) >500 <400

Urine sodium level (mEq/L) <20 >40

Urine/plasma creatinine ratio >40 <20

Fractional excretion of sodium (%) <1 >2

Fractional excretion of urea (%) <35 >35

Urinary sediment Normal; Renal tubularoccasional hyaline epithelial cells;

or fine granular granular andcasts muddy brown

casts


FeNa Less than 1%

Decreased renal perfusion• Decreased intravascular volume• NSAID• ACE inhibitor/ARB• Pigmenturia• Hepatorenal syndrome• Acute contrast nephropathy• Acute (early) GN• Early obstruction• Acute embolic event


FeNa More than 3%

Tubular dysfunction• ATN• Chronic renal disease• Diuretics/concentrating defects


Urinary Sediments

Brenner and Rector: The Kidney, 8th edition

Sediment Differential diagnosis

Normal or few Prerenal azotemiaRed blood cells Arterial thrombosis or embolismWhite blood cells Preglomerular vasculitis

HUS or TTPScleroderma crisisPostrenal azotemia

Granular casts ATN (muddy brown)Glomerulonephritis or vasculitisInterstitial nephritis

Red blood cell casts Glomerulonephritis or vasculitisMalignant hypertensionRarely interstitial nephritis

White blood cell casts Acute interstitial nephritis or exudative glomerulonephritisSevere pyelonephritisMarked leukemic or lymphomatous infiltration

Eosinophiluria (>5%) Allergic interstitial nephritis (antibiotics > NSAIDs)Atheroembolic disease

Crystalluria Acute urate nephropathyCalcium oxalate (ethylene glycol toxicity)AcyclovirIndinavirSulfonamidesRadiocontrast agents


Ultrasonography in AKI

Comprehensive Clinical Nephrology, Johnson 3rd edition

Observation Clue to diagnosis of

Shrunken kidneys Chronic kidney disease

Normal size kidneys Echogenic Acute GN

Normal Echo Prerenal

Acute renal arteryocclusion

Enlarged kidneys Malignancy, renal vein thrombosis, diabeticnephropathy, HIV

Hydronephrosis Obstructive nephropathy


Pathology


0

1

2

3

4

5

Hazard Tranche 1Very high risk patients

• Increase in 0.1 mg/dL over baselineor

• 1 hour of oliguria in a appropriately resuscitated subject

Hazard Tranche 2High risk patients


• 3 hours of oliguria in a appropriately resuscitated subject

Hazard Tranche 3Moderate risk patients


• 5 hours of oliguria in a appropriately resuscitated subject

Renal Angina

Goldstein et al: cJASN 5:943, 2010

Renal Angina Threshold

s

eru

m c

rea

tin

ine

(m

g/d

L)

Olig

uri

a (h

r)

Hazard Tranche#1

Hazard Tranche#2

Hazard Tranche#3

Hazard Tranche#1

Hazard Tranche#2

Hazard Tranche#3

Risk of developing acute kidney injury0.0

0.1

0.2

0.3

0.4

Risk of developing acute kidney injury


Biomarkers

• Cystatin C• Functional marker in blood• Tubular marker in urine

• NGAL• In plasma less sensitive/specific than urine

• Others• IL-18• Kim-1• L-FABP• Netrin-1• Vimentin

Stay tuned new markers are

on the way


Risk prediction


Management


KDIGO guidelines

KI supplement, March 2012


Mode of action CompoundDevelopment

stage

Increase HIF signalling/proteins

Prolyhydroxylase inhibitors Pre-clinical

Erythropoietin Clinical, phase 3

Protection against apoptosis

Heat shock proteins Pre-clinical

Geranylgeranylactone Pre-clinical

Adenosine receptor agonists Pre-clinical

Ischaemic pre-conditioning Clinical

Reduce leucocyte adhesion in PTCs

Anti-CTLA-4 Pre-clinical

Anti-ICAM-1 Clinical, phase 1

Glitazones Pre-clinical

Mesenchymal stem cells Pre-clinical

Increase re-endothelialization PTCs

Erythropoietin Clinical

Endothelial progenitor cells Pre-clinical

Increase tubular regeneration

Mesenchymal stem cells Pre-clinical

Hepatocyte growth factor Pre-clinical

Insulin-like growth factor Pre-clinical

Epidermal growth factor Pre-clinicalAydin, Z. et al. NDT. 2007 22:342-346


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Acute Kidney Injury Post-op: Kidney attack

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