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INTRODUCTION
Acute Kidney Injury (AKI) : the entire spectrum of the
syndrome from minor changes in markers of renal function
to requirement for Renal Replacement Therapy (RRT)
(KDIGO, 2012)
DEFINITION AKI
RIFLE criteria (ADQI, 2004) & AKIN criteria (AKIN, 2007)
DEFINITION AKI
Staging AKI (KDIGO, 2012)
AKI is defined as any of the following (Not Graded):
Increase in SCr by 0.3 mg/dl ( 26.5 lmol/l) within 48 hours;
or
Increase in SCr to 1.5 times baseline, which is known or
presumed to have occurred within the prior 7 days; or
Urine volume < 0.5 ml/kg/h for 6 hours.
CAUSES OF AKI
CAUSES OF AKI
Prerenal AKI Postrenal
AKI
Renal AKI
Secondary to
underperfusio
n
renal or
extrarenal
losses
Heart failure
Cirrhosis
Sepsis.
Urinary tract
obstructions
Stones
tumor
PATHOGENESIS OF AKI IN
SEPSIS
1.Renal Hemodynamics
2.Renal Apoptosis
3.Endothelial Damage
4.Tubular Damage
Renal Hemodynamics
New study
RBF ????
Increase
or
decrease
??
(Ricci,2009; Rajapakase, 2009)
Renal Hemodynamics
New Hypotesis
Hyperdynamic sepsis
Renal Apoptosis
Endothelial Damage
sepsis
IL-1b, TNF and PAF
increase the neutrophil
aggregation and toxic
substance release
glomerular capillaries
microthrombi
Tubular Damage
Necrosis or apoptosis
Tubular epithelium lose basal
membrane adhesion quality
Excreted to the tubular lumen
Tubular epithelium cylinders or
granular cylinders In urine
Microobstruction
(Kockara, 2013)
New Biomarker
Biological marker of the inflammatory process : Cystatin C,
neutrophil gelatinase-associated lipocalin (NGAL) and
IL-18
Tubular protein : kidney injury molecule-1 (KIM-1), Urine
sodium/hydrogen exchanger isoform 3 (NHE3) and Liver
fatty acid-binding protein (L-FABP)
Biological markers of tubular disease : 1-microglobulin,
2-microglobulin, N-acetyl--D-glucosaminidase, etc
Edelstein, 2008; Parikh, 2008; Roesli, 2008
Sepsis or
ICU Setting
Kidney
Transplant
(tx)
NGAL
Urine
2 hrs post-CPB
4 hrs
48 hrs
postcontra before AKI
st
1224 hrs
post-tx
IL-18
Urine
Not tested
48 hrs
before AKI
1224 hrs
post-tx
KIM-1
Urine
Not tested
Not tested
NGAL
Plasm
a
2 hrs post-CPB
2 hrs
48 hrs
postcontra before AKI
st
Not tested
12 hrs postCPB
8 hrs
48 hrs
Variable
postcontra before AKI
Edelstein, 2008; Parikh, 2008; Roesli, 2008
st
Cystatin Plasm
C
a
AKI EVALUATION
AKI
Clinical evaluation and
physical examination.
Clinical Test
Lab values
AKI stage
KDIGO, 2012
Stage-based management
of AKI
KDIGO, 2012
AKI management
A.Maintain hemodynamic status
a. Status Volume Optimalization
b. Vasopressor use
c. Diuretic use
B. Avoid nephrotoxic drugs
C. Avoid nephrotoxic contrast media
D. Glycemic Control
E. Nutrition
F. Renal Replacement Therapy
b. Vasopressor use
c. Diuretic use
KDIGO, 2012
D. Glycemic Control
E. Nutrition
E. Nutrition
CONCLUSION
AKI in Sepsis, a commonly condition in an
ICU
The patophysiology AKI in sepsis not fully
understood
A better understanding of AKI in sepsis is
required to implement prevention strategies
and appropriate therapy
Risk factors identification, evaluation and
appropriate management are important in
septic condition to prevent AKI
THANK YOU
Schematic representation of the inflammatory response to sepsis and resulting kidney injury. (Modified from205; reprinted with
permission.
Jaber BL et al: Blood Purif 22: 101111, 2004). Abbreviations are: GFR, glomerular filtration rate; NAG, N-acetyl- -D-glucosaminidase; KIM,
kidney injury molecule 1.
dopamin
At low doses (0.5-3.0 g/kg/min), dopamine acts predominantly on
D1 receptors in the renal, mesenteric, cerebral and coronary beds
resulting in selective vasodilation. Some reports suggest that
dopamine increases urine output by augmenting renal blood flow
and glomerular filtration rate and natriuresis by inhibiting
aldosterone and renal tubular transport [2]. But the clinical
significance of renal-dose dopamine is somewhat controversial
because a renal protective effect has not been demonstrated.
At intermediate doses (3-10 g/kg/min), dopamine also stimulates
1 receptor and increases cardiac output (CO), predominantly by
increasing stroke volume with variable effect on heart rate.
At higher dose (10-20 g/kg/min), the predominant effect of
dopamine is to stimulate 1-adrenergic receptors and produce
vasoconstriction with an increased systemic vascular resistance
(SVR), and the sum of these effects is an increase in mean arterial
pressure (MAP)
NE
Noradrenaline (also known as norepinephrine) is a potent 1adrenergic receptor agonist with modest -agonist activity
because of which it is incorrectly labelled as a pure vasopressor
However, it has shown effects on contractility in critical illness
[9].
It primarily increases systolic, diastolic and pulse pressure and
has a minimal net impact on CO. It has minimal chronotropic
effects because of which it is a drug of choice in settings where
heart rate stimulation is undesirable. Coronary flow is
maintained to certain extent because of its vasoconstrictor
effects [10]. Due to relative scarcity of cerebral vascular
adrenergic receptor, high doses of noradrenaline can be safely
used to maintain cerebral perfusion pressure without
significantly compromising the circulatory flow
AIN
The mechanism of drug-induced AIN is unknown, but an
immunological basis is suspected. Drugs can elicit an
immune response leading to AIN in different ways. The
drug can bind to a normal component of the tubular
basement membrane (TBM) and act as a hapten or the
drug can mimic an antigen normally present within the
TBM or the interstitium and induce an immune response
that will also be directed against this antigen. Other ways
to evoke an immune response include the drug binding
to the TBM or deposit within the interstitium and act as a
planted (trapped) antigen. The drug can also elicit the
production of antibodies and become deposited in the
interstitium as circulating immune complexes