Acute Kidney Injury

1. AKI: DEFINITION
CLASSIFICATION
AND DIAGNOSIS
DR. DIBYENDU RAYCHAUDHURI

2. Definition
 Acute kidney injury (AKI) (previously called acute renal failure) is
characterized by a reversible increase in the blood concentration of
creatinine and nitrogenous waste products and the inability of the kidney
to regulate fluid and electrolyte homeostasis appropriately.

3. Introduction
 Acute Kidney injury has been defined as the abrupt loss of
kidney function within hours to days, that results in the retention
of urea creatinine and oliguria and leads to dysregulation of
extracellular volume and electrolytes.
 5% of children admitted to pediatric tertiary care centres
 8% of infants NICU and 30-40% in PICU

4. AKI DEFINITION
RIFLE
stage
RIFLE: Creatinine
increase
RIFLE and AKIN: Urine
output
KDIGO: Creatinine increase AKIN
stage
Risk 150-200% <0.5 ml/kg/hr for 6-12 hrs >=0.3mg/dl increase or 150-
200%
1
Injury 200-300% <0.5 ml/kg/hr for>12 hrs 200-300% 2
Failure >300% <0.3 ml/kg/hr for >24 hrs;
or anuria >=12 hrs
>300%;creatinine>=4mg%;
initiation of RRT; or
Egfr<35ml/min/1.73 sq. m(18
yrs)
3

5.  Other 2 stages of RIFLE are Loss(failure for>4 weeks); ESRD (failure for>3
months)
 Serum creatinine increase from baseline
 Urine output criteria are identical in RIFLE and AKIN stages
 Time frame for increase in serum creatinine :>=0.3 mg/dl within 48 hours;
> 1.5 times the baseline within 7 days
Source: KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2912; 2:8

6. Classification
 Prerenal azotemia – functional response of structurally
normal kidneys to hypo perfusion
 Intrinsic ARF (ATN)- structural damage to the renal
parenchyma from prolonged ischaemia, nephrotoxins,or
glomerulonephritis.
 Postrenal ARF from urinary tract obstructions

7. The Acute Dialysis Quality Initiative (ADQI) has proposed a
graded definition of ARF called the RIFLE criteria.

8. Pediatric Modified RIFLE (pRIFLE)
Ackan-Arikan et al: Kid Int 2007
Pediatric Modified RIFLE Criteria
CrCl Urine output
Risk GFR decrease by 25% <0.5ml/kg/hour for8 hours
Injury GFR decrease by 50% <0.5ml/kg/hour for 16 hours
Failure
GFR decrease by 75% or
GFR<35ml/min/1.73m2
<0.3 ml/kg/hour for24 hours or
anuric fo
r 12 hours
Loss Persistent ARF > 4 weeks
End
stage
End Stage Renal Disease (>3 months)
GFR per Schwartz equation: GFR= Ht (cm) X constant / serum creat (mg/dl)

9. KDIGO AKI criteria

10. DIAGNOSIS---A K I
 What is the cause
 Glomerular or Tubular
 Prerenal or Postrenal
 Need for dialysis –peritoneal/haemodialysis

11. WHAT TO LOOK FOR
 Assess the history –how long/drug intake/altered urine
frequency/thirst/UTI/Family history
 Is there growth retardation/stunting
 Evidence of rickets
 Evidence of fluid overload, hypertension
 Cardiomegaly, palpable bladder ,kidney

12. Evaluation of AKI
Etiological classification of AKI
 Pre-renal
 Renal
 Post-renal

13. Pre-renal AKI
Prerenal disease — Decreased kidney function due to prerenal
disease occurs in two settings
 When renal ischemia is part of a generalized decrease in tissue
perfusion
 When there is selective renal ischemia

15.  Selective renal ischemia — Bilateral renal artery stenosis or unilateral
stenosis in a solitary functioning kidney is frequently made worse by
treatment with angiotensin converting enzyme inhibitors, angiotensin II
receptor blockers, or direct renin inhibitors.
Pre-renal AKI

16. Drugs affecting glomerular hemodynamics
 NSAISD, -decreasing either afferent (preglomerular)
arteriolar dilatation
 ACEI or ARB-efferent (postglomerular) arteriolar constriction
 Effects of these drugs are pronounced in already
compromised kidneys.
Pre-renal AKI

17. ATN: Causes
 All causes of severe prerenal disease, particularly if
accompanied by hypotension, surgery, and/or sepsis,
can cause postischemic (also called ischemic) ATN.
 Sepsis — Sepsis-induced ATN is often associated with
prerenal factors such as decreased renal perfusion and
systemic hypotension. Other factors include release of
cytokines and activation of neutrophils by cytokines.
 Nephrotoxins- Aminoglycosides, Heme pigments,
cisplatin, radiocontrast media, pentamidine, foscarnet,
cidifovir, tenofovir, mannitol ,hetastarch ,cannabinoids.

18. EVALUATION AND DIAGNOSIS

19. Evaluation And Diagnosis
1. Careful history taking and physical examination.
2. Assessment of renal function by estimation of the glomerular
filtration rate (GFR)
3. Careful examination of the urine
4. Radiographic imaging of the kidneys.
5. Serologic testing and tissue diagnosis with renal biopsy
6. Disease duration - availability of older data for comparison and
to establish a trend.

25. Investigations in AKI
 Blood
o CBC, CRP
o Blood urea and creat
o Electrolytes
o Blood gas (pH, bicarb)
o Serum albumin, SGOT, SGPT, CPK

26.  Urine
 Urinanalysis (routine, ME, culture)
 FeNa
 Urine for hemoglobin, myoglobin
• Radiology
 CXR (fluid overload, cardiomegaly)
 USG (renal size, obstruction, dilatation, cystic kidneys)
 Renal doppler (suspected arterial or venous thrombosis)
 Micturitating cystourethrography (VUR/PUV)
 DTPA for obstructive uropathy
Investigations in AKI

27.  12 lead ECG (hyperkalemia)
 Investigations for cause
 PBS, platelets, retic count, LDH, stool culture (suspected HUS)
 Blood ASO, serum C3,C4, ANA, ANCA
 Renal biopsy
Investigations in AKI

28. Pre-Renal vs. Renal Failure
Prerenal Renal
BUN/Cr >20 <20
FENa <1% >2%
Renal Failure
Index
<1% >1%
UNa <20 mEq/L >40 mEq/L
Specific Gravity >1.020 <1.010
Uosm >500
mOsm/L
<350
mOsm/L
Uosm/Posm >1.3 <1.3

29. Renal biopsy in AKI
 Rapidly progressive glomerulonephritis
 Unremitting AKI lasting for more than 4 weeks especially of unknown
etiology
 AKI associated with systemic disease (eg lupus, HSP)
 Interstitial nephritis
 Prognostication especially in HUS
 Underlying cause not apparent on clinical features and investigations
 AKI in transplanted kidney

30. Biomarker discovery in AKI: bench to
bedside
 NGAL:
 Expressed in proximal and distal nephron
 Binds and transports iron-carrying molecules
 Role in injury and repair
 Rises very early (hours) after injury in animals,
 IL-18:
 Role in inflammation, activating macrophages and mediates ischemic renal injury
 IL-18 antiserum to animals protects against ischemic AKI
 Studied in several human models
 KIM-1:
 Epithelial transmembrane protein, ?cell-cell interaction.
 Appears to have strong relationship with severity of renal injury

31. THANK YOU