Acute Kidney Injury
Post-op: Kidney attack
Kianoush Kashani
5th Anesthesia and Critical Care Conference
Kuwait 2013
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Outlines
• Definition
• Epidemiology/outcome
• Pathophysiology
• Diagnosis
• Management Vs treatment
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RIFLE Criteria
GFR criteria
Risk
Increased creatinine x1.5
or GFR decrease >25%
Injury
Urine output criteria
UO <0.5 mL kg-1
h-1 x6 hr
Increased creatinine x2
or GFR decrease >50%
UO <0.5 mL kg-1
h-1 x12 hr
Increased creatinine x3
or GFR decrease >75%
or creatinine 4 mg/
100 mL (acute rise of
0.5 mg/100 mL dL)
UO <0.3 mL kg-1
h-1 x24 hr or anuria
x12 hr
Failure
Loss
ESRD
High sensitivity
High specificity
Persistent ARF = complete loss of
renal function >4 weeks
End-stage renal disease
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AKIN Definition for AKI
AKIN 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
<0.5 mL/kg/hr for >6 hr
<0.5 mL/kg/hr for >12 hr
• <0.3 mL/kg/hr for 24 hr
• Anuria for 12 hr
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Incidence of AKI
8
Reasons for  incidence
• Age
6
• Comorbid conditions
• CKD
% 4
• More sensitive criteria
2
0
1983
1996
Year
2002
Hou et al: Am J Med 74:243, 1983
Nash et al: JASN 7:376, 1996
Nash et al: AJKD 39:930, 2002
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AKI and Mortality
Mortality Risk vs Non-AKI
RR (random)
95% CI
Study or subcategory
Mortality Injury vs Non-AKI
RR (random)
95% CI
Mortality Failure vs Non-AKI
RR (random)
95% CI
01 General ICU (Cr and UO criteria)
Abosaif
Ahlstrom
Cruz
Hoste
02 General ICU (without UO criteria)
Lopes (HIV)
Lopes (sepsis)
Ostermann
03 Cardiosurgery
Kuitunen
Lin
04 Other ICU
Coca
Lopes (bmt)
Lopes (burns)
05 Not confined to ICU
Uchino
0.01
0.1
1
10
100
0.01
0.1
1
10
100
0.01
0.1
1
10
100
Ricci Z: Kidney Int 73:538, 2008
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AKI and Long-Term Mortality
Cumulative probability
of survival (%)
100
80
No AKI
AKIN I
AKIN II
AKIN III
60
40
20
Number at risk
782,222
601,772
52,338
37,234
19,771
13,692
10,602
7,173
0
0
1
443,730
25,798
9,210
4,639
296,128
16,441
5,712
2,723
2
3
138,820
7,758
2,633
1,200
No AKI
AKIN I
AKIN II
AKIN III
4
Follow-up (years)
Lafrance et al: JASN 21(2):345, 2010
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ESRD After AKI
0.16
P<0.0001, DF=1
AKI
0.06
0.04
0.02
No AKI
0.00
Probability of ESRD
Probability of ESRD
0.08
No AKI or CKD
CKD only
AKI only
AKI and CKD
0.14
0.12
0.10
0.08
P<0.0001, DF=3
0.06
0.04
0.02
0
100 200 300 400 500 600 700
Days from hospital discharge
0
100 200 300 400 500 600 700
Days from hospital discharge
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RRT epidemiology (NEFROINT data)
ICU admissions
(ESRD excluded)
576
No AKI on admission
57.3%
Never developed AKI
34.2%
AKI on admission
42.7%
New AKI
23.1%
Ever AKI
65.8%
Complete recovery
59.4%
Partial recovery
13.5%
Required RRT
8.3%
Never recovered
27.2%
Piccinni et al. Minerva anestheiology 2011; 77:1-2
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Etiology of Hospital-Acquired AKI
60
50
40
% 30
20
10
N
R
PG
ar
Va
sc
ul
bs
t
O
A
IN
ru
ct
iv
e
K
I
A
C
Pr
er
en
al
A
TN
0
Comprehensive Clinical Nephrology, Johnson 3rd edition
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Ischemia induced AKI
Abuelo et al, NEJM 2007, 357 (8)
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Symptoms
•
•
•
•
•
Polyuria
Oliguria/anuria
Hematuria
Dysuria
Azotemia
• Mental status changes
•
•
•
•
Acidosis ( respiratory rate)
Hypervolemia/hypertension
Hyperkalemia
Pericarditis
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Urinary Index
Prerenal
azotemia
ATN
Urine osmolality (mOsm/kg)
>500
<400
Urine sodium level (mEq/L)
<20
>40
Urine/plasma creatinine ratio
>40
<20
<1
>2
<35
>35
Normal;
occasional hyaline
or fine granular
casts
Renal tubular
epithelial cells;
granular and
muddy brown
casts
Laboratory test
Fractional excretion of sodium (%)
Fractional excretion of urea (%)
Urinary sediment
Schrier: J Clin Invest 114(1):5, 2004
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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
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FeNa More than 3%
Tubular dysfunction
• ATN
• Chronic renal disease
• Diuretics/concentrating defects
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Urinary Sediments
Sediment
Differential diagnosis
Normal or few
Red blood cells
White blood cells
Prerenal azotemia
Arterial thrombosis or embolism
Preglomerular vasculitis
HUS or TTP
Scleroderma crisis
Postrenal azotemia
Granular casts
ATN (muddy brown)
Glomerulonephritis or vasculitis
Interstitial nephritis
Red blood cell casts
Glomerulonephritis or vasculitis
Malignant hypertension
Rarely interstitial nephritis
White blood cell casts
Acute interstitial nephritis or exudative glomerulonephritis
Severe pyelonephritis
Marked leukemic or lymphomatous infiltration
Eosinophiluria (>5%)
Allergic interstitial nephritis (antibiotics > NSAIDs)
Atheroembolic disease
Crystalluria
Acute urate nephropathy
Calcium oxalate (ethylene glycol toxicity)
Acyclovir
Indinavir
Sulfonamides
Radiocontrast agents
Brenner and Rector: The Kidney, 8th edition
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Ultrasonography in AKI
Observation
Clue to diagnosis of
Shrunken kidneys
Chronic kidney disease
Normal size kidneys
Echogenic
Acute GN
Normal Echo
Prerenal
Acute renal artery
occlusion
Enlarged kidneys
Malignancy, renal vein thrombosis, diabetic
nephropathy, HIV
Hydronephrosis
Obstructive nephropathy
Comprehensive Clinical Nephrology, Johnson 3rd edition
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Pathology
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Pathology
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Renal Angina
Hazard Tranche 1
Very high risk patients
• Increase in 0.1 mg/dL over baseline
or
• 1 hour of oliguria in a appropriately
resuscitated subject
Hazard Tranche 2
High risk patients
• Increase in 0.3 mg/dL over baseline
or
• 3 hours of oliguria in a appropriately
resuscitated subject
Hazard Tranche 3
Moderate risk patients
• Increase in 0.4 mg/dL over baseline
or
• 5 hours of oliguria in a appropriately
resuscitated subject
Renal Angina Threshold
Hazard Tranche
#2
Hazard Tranche
#3
Hazard Tranche
#1
Hazard Tranche
#2
Hazard Tranche
#3
5
0.4
4
0.3
0.2
0.1
0.0
Risk of developing acute kidney injury
Oliguria (hr)
serum creatinine (mg/dL)
Hazard Tranche
#1
3
2
1
0
Risk of developing acute kidney injury
Goldstein et al: cJASN 5:943, 2010
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Biomarkers
• Cystatin C
• Functional marker in blood
• Tubular marker in urine
Stay tuned
new markers are
on the way
• NGAL
• In plasma less sensitive/specific than urine
• Others
•
•
•
•
•
IL-18
Kim-1
L-FABP
Netrin-1
Vimentin
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Risk prediction
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Risk prediction
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Risk prediction
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Management
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KDIGO guidelines
KI supplement, March 2012
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Mode of action
Compound
Development
stage
Increase HIF signalling/proteins
Prolyhydroxylase
inhibitors
Pre-clinical
Erythropoietin
Clinical, phase 3
Heat shock proteins
Pre-clinical
Geranylgeranylactone
Pre-clinical
Adenosine receptor
agonists
Pre-clinical
Ischaemic preconditioning
Clinical
Anti-CTLA-4
Pre-clinical
Anti-ICAM-1
Clinical, phase 1
Glitazones
Pre-clinical
Mesenchymal stem cells
Pre-clinical
Erythropoietin
Clinical
Endothelial progenitor
cells
Pre-clinical
Mesenchymal stem cells
Pre-clinical
Hepatocyte growth factor
Pre-clinical
Insulin-like growth factor
Pre-clinical
Epidermal growth factor
Pre-clinical
Protection against apoptosis
Reduce leucocyte adhesion in
PTCs
Increase re-endothelialization
PTCs
Increase tubular regeneration
Aydin, Z. et al. NDT. 2007
22:342-346
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‫شكرا‬
“The best interest of the patient is the only interest to be considered”
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Questions & Discussion
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