acute kidney injury berdasarkan kdigo 2012

pe jekasan detail aki, mari pelajari bersama

1. Dr. dr. Yenny Kandarini, SpPD-KGH, FINASIM

2. •Acute Kidney Injury (AKI)
Life-threatening disease process
•AKI occurs in
•
≈
7% of hospitalized patients.
•36 – 67% of critically ill patients
(depending on the definition).
•5-6% of ICU patients with AKI require RRT.
Nash K, Hafeez A, Hou S: Hospital-acquired renal insufficiency. American Journal of Kidney
Diseases 2002; 39:930-936.
Hoste E, Clermont G, Kersten A, et al.: RIFLE criteria for acute kidney injury are associated with
hospital mortality in critically ill patients: A cohort analysis. Critical Care 2006; 10:R73.
Osterman M, Chang R: Acute Kidney Injury in the Intensive Care Unit according to RIFLE. Critical
Care Medicine 2007; 35:1837-1843.

3. Definition of AKI
There are more than 35 definitions of AKI
(formerly acute renal failure) in literature!

4. ACUTE KIDNEY INJURY (AKI)
(Cedera Ginjal Akut)
DEFINITION :
AKI is an abrupt (less then 7 days) and sustained decrease in
kidney function.
•changes in blood biochemistry : increased of serum
creatinine, blood urea nitrogen
•decreased of urine out put in 80-90% cases (10-20%
normal or increase) or both
•kidney function used to be normal
When the patient has a previous episode of kidney disease,
the term is : Acute on Chronic Kidney Disease (ACKD)

5. Definition

6. Definition of Acute Kidney Injury (AKI) based on “Acute
Kidney Injury Network”
Stage Increase in Serum
Creatinine
Urine Output
1 1.5-2 times baseline
OR
0.3 mg/dl increase
from baseline
<0.5 ml/kg/h for >6 h
2 2-3 times baseline <0.5 ml/kg/h for >12 h
3 3 times baseline
OR
0.5 mg/dl increase if
baseline>4mg/dl
OR
Any RRT given
<0.3 ml/kg/h for >24 h
OR
Anuria for >12 h

7. Established renal failure (loss of
function > 3 months)
Loss of kidney function > 4 weeks but
< 3 months
Three-fold increase in creatinine
or > 75% decrease in GFR or
creatinine > 350 (acute rise)
Urine output < 0.3 ml/kg/hr
for 24 hours (or anuria for
12 hours)
Two-fold increase in
creatinine or > 50%
decrease in GFR
Urine output < 0.5 ml/kg/hr for at
least 12 hours
50% decrease in creatinine or
> 25% decrease in GFR
Urine output < 0.5 ml/kg/hr for at
least 6 hours
GFR Criteria Urine output CriteriaAND/OR
Failure of
kidney function
Loss of kidney
function
ERF
Risk of renal
dysfunction
Injury to the
kidney
AKI classified according to degree and outcome by RIFLE criteria

8. CAUSES OF AKI
Causes of AKI divided into three matter :
1.Prerenal :
Decreased of renal perfusion (hypoperfusion)
2.Renal (Intrinsic)
Damage of parenchyma of the kidney (glomeruli,
tubules, intra-renal vasculature, interstitial nephritis)

3.Post-renal
Obstruction of urinary tract

9. Major Disease Categories Causing AKI
Disease Category Incidence
Prerenal azotemia caused by acute renal
hypoperfusion
55-60%
Intrinsic renal azotemia caused by acute diseases of
renal parenchyma:
-Large renal vessels dis.
-Small renal vessels and glomerular dis.
-ATN (ischemic and toxic)
-Tubulo-interestitial dis.
-Intratubular obstruccttion
35-40%
*>90%*
Postrenal azotemia caused by acute obstruction of
the urinary tract
<5%

11. Prerenal Azotemia
The most common cause of AKI (30-50% of all cases)
A rapidly reversible process
A diminished renal blood flow  efective arterial
↓
blood flow
Absolute reduction in the volume of ECF (eg.
hypovolemia)
Effective circulating volume is reduced (eg. CHF)
Need additional information beyond the physical
examination to ascertain a measure organ perfusion
(invasive cardiac monitoring & FE
Na+
)

12. Prerenal Azotemia

13. PRERENAL CAUSES OF AKI
1.Shock :
•cardiogenic ahock
•distributive shock (e.g.sepsis, anaphylactic)
2.Hypovolemia – hypovolemic shock
•haemorhage
•gastrointestinal loss (vomiting, diarrhea)
•cutaneous losses (e.g.burns)
3.Renal hypoperfusion
•renal artery stenosis
•hepatorenal syndrome
4.Changes of water distribution (oedema)
•congestive heart failiure
•hepatic failure
•nephrotic syndrome

14. Intrinsic causes of AKI

15. RENAL / INTRINSIC CAUSES OF AKI
1.Glomerular disease
•glomerulonephritis
2.Tubular injury
•prolonged renal hypoperfusion
•toxin (snake venom), drugs (aminoglycosides),
3.Vascular
•vasculitis
•arterial or venous thrombosis
4.Interstitial nephritis
•infiltrative malignancy
•toxin (alcohol, metal)
•infection (leptospiral)

17. POST-RENAL CAUSES OF AKI
BPH
Prostate cancer
Cervical cancer
Retroperitoneal fibrosis
Retroperitoneal lymphoma
Metastatic carcinoma
Nephrolithiasis
urethral stricture
Blood clots

18. Prerenal

19. Renal

20. Postrenal

21. Clinical Findings – Symptoms & Signs
Limited, non diagnostic, unrecognized  laboratory
necessary
Related to azotemia and due to underlying cause
Symptoms
Decrease in urine output and dark and cola-colored
urine
Azotemic  anorexia, nausea, malaise, metallic taste,
itching, confusion, fluid retention, hypertension
Physical examinations
Volume overload, pericardial friction rub, asterixis

22. Clinical Findings – Laboratory Findings
Elevations of the BUN and serum creatinine
Serum cyctatin C
Low FE
Na+
< 1  prerenal azotemia
High FE
Na+
 may not indicate ATN  CKD prior AKI 
falsely high
Ultrasound  obstruction

23. Clinical Findings – Laboratory Findings

24. DIAGNOSTIC
1.History of disease
•gastroenteritis, bleeding ?
•heart disease
•toxin ? post infection ?
•stone disease ?
2.Investigation
A. Physical examination.
•blood pressure (hypotension/shock)
•anemic, dehydration
•renal colic, ballotment, full vesica urinaria

25. B. Blood chemistry
•haemoglobine, white blood cell
•blood ureum, creatinine serum
•potassium (K), sodium (Na)
•blood gas analysis
C. Radiology
•plain photo abdomen
•ultrasonography

26. New Biomarkers in AKI
Alternatives to Serum Creatinine
Urinary Neutrophil Gelatinase-Associated
Lipocalin (NGAL)
Ann Intern Med 2008;148:810-819
Urinary Interleukin 18
Am J Kidney Dis 2004;43:405-414
Urinary Kidney Injury Molecule 1 (KIM-1)
J Am Soc Nephrol 2007;18:904-912

27. COMPLICATIONS
1.Volume overload
•acute pulmonary oedema
•acute left heart failure
2.Metabolic acidosis
3.Electrolyte imbalance
•hyperkalemia

28. 28
AKI
Zöllner,
Innere Medizin,
modified
Dialysis Treatments
Creatinine
M/l
Time / days
Urine
l/day
3. Polyuria
Uncontrolled
Urine
Quantities
(1 - 2 weeks)
1. Damage
Damage to
Renal Tissue
(minutes to
days)\
2. 2. Oliguria / Anuria
Complete Loss of
Renal Function
(up to 6 weeks))
4. Recovery
slow Recovery of
Renal Function
(several months)
Prevention/
Supportive
Prevention/
Maintenance
RISKINJURY FAILURE

29. Prevention
Recognition of the high risk patients
Elderly
DM
Volume depletion
Vascular surgery
Chronic renal failure
Multiple antibiotics
Multiple insults
Correction of volume depletion
The prevention of CIN
Prophylactic infusion of saline (1 ml/kg for 12 hours before and after
procedure)
N-acetylcysteine and sodium bicarbonate

30. Treatment

31. Treatment
Prerenal azotemia
Reversible on restoration of renal perfusion
Hemorrhage  corrected by PRC
Isotonic saline
Colloid  >> adverse outcomes & into question
Monitor serum potassium and acid-base status
Cardiac failure  Positive inotropes, preload- and afterload-
reducing agents, mechanical aids
Acute tubular necrosis
>> supportive
Loop diuretic (furosemide)
Restricting fluids
Dopamine  no propective clinical data

32. Treatment
Role of RRT
Indications
Refractory fluid overload
Hyperkalemia
Severe metabolic acidosis
Azotemia
Signs of uremia
Overdose with a dialyzable drug/toxin
Hemodialysis
Frequent dialysis  daily hemodialysis

33. Treatment
Nutrition in AKI
Excessive catabolism
Increased gluneogenesis, protein degradation, reduced protein
synthesis
Insulin resistance, 2
nd
hyperparathyroidisme, increased glucagon,
metabolic acidosis  > malnutrition
RRT  increased metabolism, loss of nutrients
Diminished utilization of available nutrients
Anorexia or vomiting

34. Treatment
Nutrition in AKI
Protein intake
1.2-1.4 g/kg
Lipids
20-25% daily calories
Glucose
70% solution
Estimated energy requirement
30-40 kcal/kg normal body weight/day
Vitamin & mineral
Not well defined
Water-soluble vitamin

35. Proposed criteria for the initiation of renal replacement therapy
in adult critically ill patients
1.Oliguria (urine output < 200 ml/12 hr)
2.Anuria/extreme oliguria (urine output < 50 ml/12 hr)
3.Hyperkalemia ([K+] > 6.5 mmol/liter)
4.Severe acidemia (pH < 7.1)
5.Azotemia ([urea] > 30 mmol/liter)
6.Clinically significant organ (especially lung) edema
7.Uremic enchepalopathy
8.Uremic pericarditis
9.Uremic neuropathy/myopathy
10.Severe dysnatremia ([Na] > 160 or < 15 mmol/liter)
11.Hyperthermia/Hypothermia
12.Drug overdose with dialysable toxin
The presence of :
- one of the above criteria is sufficient to initiate renal replacement therapy in a critically ill
patients
- two of these criteria makes renal replacement urgent and mandatory.
- combined derangements suggest initiation of renal replacement therapy even before the above
mentioned limits have been reached.

36. Evaluation of
AKI

37. Evaluation of
AKI

38. AKI ACKD
History of kidney diseaseNo/unknown Yes
Physical examination
- hypertension rare mostly
- oedema rare mostly
Blood biochemistry :
- anaemic rare mostly
- hyperphosphatemia (PO4) rare mostly
Ultrasonographic normal small kidney
Deferential diagnosis between
Acute Kidney Injury (AKI) and
Acute on Chronic Kidney Disease (ACKD) :

39. Prognosis
50% survival rate
Prognosis of hospitalized patients  depend on the
site
Survival  influenced by the severity of underlying
illnesses & number of failed organs

40. Mortality increases proportionately with increasing
severity of AKI (using RIFLE).
AKI requiring RRT is an independent risk factor for
in-hospital mortality.
Mortality in pts with AKI requiring RRT 50-70%.
Even small changes in serum creatinine are
associated with increased mortality.
Hoste E, Clermont G, Kersten A, et al.: RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill
patients: A cohort analysis. Critical Care 2006; 10:R73.
Chertow G, Levy E, Hammermeister K, et al.: Independent association between acute renal failure and mortality following cardiac
surgery. American Journal of Medicine 1998; 104:343-348.
Uchino S, Kellum J, Bellomo R, et al.: Acute renal failure in critically ill patients: A multinational, multicenter study. JAMA 2005;
294:813-818.
Coca S, Peixoto A, Garg A, et al.: The prognostic importance of a small acute decrement in kidney function in hospitalized patients: a
systematic review and meta-analysis. American Journal of Kidney Diseases 2007; 50:712-720.

41. Pendidikan Kedokteran Berkelanjutan 2012

42. SELF ASSESSMENT
21 years old man, came with oligouria since 2 days ago.
His urine just 250 ml/24 hrs. Since days ago he has
profuse diarrhea and vomiting.
On physical examination the patient look severe ill,
dehydration, blood pressure 90/60 mmHg, pulse
118/mnt, temp. 38 C, body weight 50 kg, urine volume
120 ml/6 hrs
What is the assessment for this patient ?
What examination have we take more ?

43. Laboratory examination shows :
Hb. 16 mg%, WBC 14.000.
Urine: proteinuria +, eryth 1-2/HPF, lecocyt 1-3/HPF
BUN 45 mg%, creatinin 2.2 mg%, Kalium 5.7 meq/lt,
Na 140 mq/kt
What is the diagnosis for the patient ?
•Clinical diagnosis
•Etiology
•Complication

44. What is the management ?