Acute kidney injury (AKI)

dan Renal Support

• Putu andrika
• AKI meningkatkan morbiditas dan mortalitas.
• Terjadi pada 3-50% perawatan di rumah sakit.
• Insiden tertinggi di ICU.
• Hospital-aquired AKI mortality 30-70%.
• The most common causes are sepsis, volume
depletion, haemodynamic instability, and nephrotoxic
injury.
Mortality in AKI patients admitted to the
intensive care unit.

the SHARF Study Group

Clin J Am Soc Nephrol 5: 1755–1762, 2010.
Incidence of AKI according to the KDIGO definition
across clinical settings.

Clin J Am Soc Nephrol 9: 12–20, 2014.

Mortality AKI (septic dan non-
septic)
35
29.70000076
30
25 21.60000038
Mortality %

19.79999924
20
15 13.39999962
12.60000038
10 7.5999999057.5
4.099999905
5
0
None Sepsis Non-septic AKI Septic AKI

ICU Hospital Trend 1 Trend 2

Bagshaw SM et al; Early acute kidney injury and sepsis:

a multicentre evaluation. Critical Care 2008
Major causes of acute kidney Injury
Lines S, Lewington A. Clin Med 2009;9:273–7.
• Septic shock remains the main cause of death in
intensive care units, and despite improved treatments,
mortality ranges from 30 to 70% (Angus et al. 2001;
Mori et al. 2010).

• Sepsis and septic shock are the most important causes

of acute kidney injury (AKI) in critically ill patients, and
account for 50% or more of cases of AKI in intensive
care units (Bagshaw et al. 2008).

• and mortality remains high despite improvements in our

ability to support vital organs.
 Definisi AKI
• Penurunan fungsi ginjal yang mendadak dalam
hitungan jam, hari, sampai dengan minggu
(sebelum lewat 3 bulan), diikuti
ketidakmampuan/ketidaksempurnaan ginjal
dalam melakukan fungsinya untuk eksresi sisa
metabolisme tubuh baik dengan atau tanpa
disertai gangguan cairan/elektrolit.
• Levels of AKI as defined by the Second International Consensus
Conference of the Acute Dialysis Quality Initiative Group: the RIFLE (Risk,
injury, failure, loss of function and end-stage kidney disease) criteria. UO =
urine output; GFR = glomerular filtration rate; SCreat = serum creatinine;
ARF = acute renal failure; ESKD = end-stage kidney disease. With open
access permission from Crit Care 2004;8(4):R204–12.
Acute kidney injury consensus definitions
Risk profile formation for AKI

Clinical Kidney Journal, 2015, vol. 8, no. 4, 405–414

Conceptual model of damage and function in AKI.
Modified

KDIGO clinical practice guideline for acute kidney

injury. Kidney Int Suppl. 2012; 2: 1–138
 Pathophysiology
• The kidneys receive around 20% of the cardiac output,
and renal oxygen extraction is low (approximately 10-
15%), yet they are very susceptible to tissue hypoxia,
especially during an acute illness.

• AKI develops due to a global decrease in renal

perfusion associated with a state of shock.

• In sepsis, animal models demonstrated that renal blood

flow (RBF) may be reduced, increased, or unchanged,
which implies that factors other than RBF play an
important role.

• ???????
Intrarenal Mechanisms for Autoregulation of the Glomerular Filtration Rate
under Decreased Perfusion Pressure and Reduction of the Glomerular
Filtration Rate by Drugs.
Pathophysiological Mechanisms of Ischemic Acute Tubular Necrosis.
• Pathophysiologic mechanisms of ischemic acute
tubular necrosis.

• Tubular injury is a direct consequence of metabolic

pathways activated by ischemia but is potentiated by
inflammation and microvascular compromise.

• The inset shows shedding of epithelial cells and

denudation of the basement membrane in the proximal
tubule, with back leak of filtrate (inset, left) and
obstruction by sloughed cells in the distal tubule (inset,
right).

• ATP = adenosine triphosphate; ATPase = adenosine

triphosphatase.

• With permission from N Engl J Med 2007;357:797–805

• mechanisms contribute, including regional variations in
perfusion and oxygen consumption, impaired
autoregulation, distortion of peritubular and glomerular
microcirculation, tubular cell injury, endothelial injury,
microvascular thrombosis, and arteriovenous shunting,
resulting in the activation of inflammatory processes.

• AKI is now considered a pro-inflammatory condition.

 Mechanism of AKI
Journal of Clinical Anesthesia 2015.27, 175-180

• 1. Ischemia/Reperfusion
• 2. Septic AKI
• 3. Hemodynamic causes of AKI
• 4. Inflammatory caused of AKI
• 5. Nephrotoxity as a cause of AKI
• Dellepiane et al. Critical Care (2016) 20:61
 TREATMENT
• Supportive focus on the optimisation of fluid and
haemodynamic status

• Treatment of the underlying illness

• Avoidance of Nephrotoxic Agents
• Exclusion of Obstruction
• AKI Care Bundles
• Prevention of Contrast-Induced Nephropathy
• Renal Replacement Therapy (Continuous RRT)
Renal replacement therapy in critically ill patients
with acute kidney injury
—when to start
• Renal replacement therapy (RRT) is a key
component of modern critical care.

• remain uncertain, including optimal indication and

timing.

• RRT is generally viewed as a organ support aimed

at achieving metabolic homeostasis and preventing
fluid overload and new organ failure.

• risks related to central venous access, infections

and anticoagulation
Indications and Contraindications for Continuous Renal-
Replacement Therapy in Critically Ill Patients with Acute Kidney
Injury.

Ashita Tolwani, CRRT

N Engl J Med 2012;367:2505-14.
Mehtha.WCN Berlin 2003
• SCUF – Ultra filtration

• CVVH – Ultra filtration + Convection

• CVVHD – Ultra filtration + Diffusion

• CVVHDF - Ultra filtration + Diffusion + Convection

 summary
• Among the several disorders encountered sepsis,
acute kidney injury (AKI) is one of the most important
because it is a life-threatening condition, increases the
complexity of care, and is an independent risk factor for
mortality.

• Screen patients who have undergone an exposure and

to continue monitoring highrisk patients..

• RRT is generally viewed as a organ support aimed at

achieving metabolic homeostasis and preventing fluid
overload and new organ failure.