©2012 mfmer | slide-1 acute kidney injury post-op: kidney attack kianoush kashani 5 th anesthesia...
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©2012 MFMER | slide-1
Acute Kidney InjuryPost-op: Kidney attack
Kianoush Kashani
5th Anesthesia and Critical Care ConferenceKuwait 2013
©2012 MFMER | slide-4
Outlines
• Definition
• Epidemiology/outcome
• Pathophysiology
• Diagnosis
• Management Vs treatment
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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
©2012 MFMER | slide-7
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
©2012 MFMER | slide-9
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
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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
©2012 MFMER | slide-12
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
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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
©2012 MFMER | slide-14
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%
©2012 MFMER | slide-16
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
©2012 MFMER | slide-19
Symptoms
• Polyuria• Oliguria/anuria• Hematuria• Dysuria• Azotemia
• Mental status changes• Acidosis ( respiratory rate)• Hypervolemia/hypertension• Hyperkalemia• Pericarditis
©2012 MFMER | slide-20
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
©2012 MFMER | slide-21
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
©2012 MFMER | slide-22
FeNa More than 3%
Tubular dysfunction• ATN• Chronic renal disease• Diuretics/concentrating defects
©2012 MFMER | slide-23
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
©2012 MFMER | slide-24
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
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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
• Increase in 0.3 mg/dL over baselineor
• 3 hours of oliguria in a appropriately resuscitated subject
Hazard Tranche 3Moderate risk patients
• Increase in 0.4 mg/dL over baselineor
• 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
©2012 MFMER | slide-28
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
©2012 MFMER | slide-34
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
©2012 MFMER | slide-35
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