ACUTE KIDNEY INJURY

Presenter: Dr Deepti Verma

Dr Varun Anand
Moderator: Dr. Virendra Kumar
 OUTLINE
• Introduction • Clinical Presentation
• History • Predisposing Factors
• Definitions • Investigations
• Epidemiology • New Biomarkers
• Pathophysiology • Management
• Classification • Dialysis
• Causes • Prognosis
 AKI
Acute Kidney Injury

Or

ARF
Acute Renal Failure
 INTRODUCTION
• AKI is characterized by rapid deterioration of
renal functions resulting in
– Retention of nitrogenous wastes
– Loss of H2O & electrolyte regulation
– Loss of acid-base regulation

• Many terminologies have been used so far to

describe this renal impairment
 HISTORY
Year Scientist Terminology

1802 William Heberden Ischuria renalis

1909 William Osler Acute Bright’s disease

1914-1918 War Nephritis

1939-1945 Bywaters & Beall Crush syndrome

• Homer W. Smith is credited for introduction of
the term ‘‘acute renal failure’’ in 1951

• No single consensus definition of acute renal

failure
• A recent survey revealed the use of at least 35
definitions in literature
Kellum JA, Levin ,et al. Curr Opin
Crit Care 2002
 Drawbacks of “ARF”
• Epidemiology of ARF was not valid due to lack
of precise biochemical definition

• No severity grading was made in definition of

ARF

• Diagnosis was usually delayed due to

imprecise criteria
New Nomenclature is……..

ACUTE KIDNEY INJURY (AKI)

– AKI IS NOT JUST RENAL FAILURE

– It encompasses the entire spectrum from minor
changes in renal function to requirement for renal
replacement therapy
 DEFINITIONS
• RIFLE criteria in 2002
• Modified for pediatric age : pRIFLE criteria
• AKIN classification in 2007
• KDIGO definition in 2012
 RIFLE Criteria
• In 2002,the Acute Dialysis Quality Initiative
(ADQI), developed the RIFLE criteria for AKI

• RIFLE :
R: Risk for renal dysfunction
I : Injury to the kidney Severity Classes
F: Failure of kidney function
L: Loss of kidney function
Outcome Classes
E: End-stage renal disease
 p-RIFLE criteria
• For children,
RIFLE criteria was modified to pRIFLE to reflect changes in
estimated GFR (instead of serum creatinine)

• Estimated GFR calculated by Schwartz formula

• Estimated GFR(ml/min/1.73m2)
=k x Height/serum creatinine

Age k values
LBW during 1st yr of life 0.33
Term AGA during 1st yr of life 0.45
Children and adolescent girls 0.55
Adolescent boys 0.70
 AKIN Classification
• In September 2007, the Acute Kidney Injury Network
(AKIN), an international network of AKI researchers
endorsed the RIFLE criteria with a small modification
to include small changes in Serum creatinine levels
and developed the

AKIN classification
 AKIN Classification
STAGE Serum creatinine criteria Urine output criteria

1 Increase in S. creatinine of ≥ 0.3 mg/dl Less than 0.5 ml/kg per

(≥ 26.4 μmol/l) or increase to ≥150% to 200% hour for > 6 hours
(1.5- to 2-fold) from baseline

2 Increase in S. creatinine to >200% to 300% Less than 0.5 ml/kg per

(> 2- to 3-fold) from baseline hour for > 12 hours

3 Increase in S. creatinine to >300% (>3fold) Less than 0.3 ml/kg per

from baseline (or S. creatinine of ≥4.0mg/dl hour for 24 hours or
[≥ 354 μmol/l] with an acute increase of at anuria for 12 hours
least 0.5 mg/dl [44 μmol/l])

For AKIN classification , an acute reduction (within 48 hrs is required)

KDIGO (Kidney Diseases: Improving Global Outcomes)
guidelines 2012

• AKI is defined as any of the following:

Increase in SCr by ≥ 0.3 mg/dl (≥ 26.5 μmol/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/hr for 6 hours

KDIGO Staging of AKI
 RIFLE vs AKIN KDIGO vs RIFLE
• Retrospective analysis of • Prospective study 1,050
prospectively collected data people in first 7 days after
of 1,20,123 patients to hospitalisation
compare the RIFLE & AKIN
definition of AKI • AKI defined by RIFLE in 14.8%
and KDIGO 36.6%
• Compared to the RIFLE • People diagnosed as not
criteria, AKIN criteria does not having AKI by RIFLE, but AKI by
materially improve the KDIGO had increased risk of
sensitivity, robustness and death
predictive ability of definition
and classification of AKI
Bagshaw et al. Nephrol Dial Rodrigues et. al. PLOS One2013
Transplant 2008
 EPIDEMIOLOGY
• Reported incidence of AKI in different regions of
the world is widely variable

• Increasing trend in the overall incidence of AKI

• Current pediatric literature lacks extensive

studies

• Incidence of AKI is higher in PICU than in ward

patients
• Study from AIIMS (2012) n=486
– Incidence of AKI 36.1% among children in PICU
– Incidence of AKI 9% among children in ward
Mehta et al. Indian Pediatr. 2012 Jul;49(7)
• Study from JIPMER (2013) n=215
– Incidence of 25.1% in PICU with a mortality rate of
46.3% Krishnamurthy et al. Indian J Crit Care Med. 2013

• AWARE is an ongoing study of critically ill children

that will inform the prevalence and associations
of AKI across the globe.
Basu et al. BMC Nephrology (2015) 16:24
• In a prospective, observational study with 200 children
aged between 1-12 years, admitted in PICU (Nov 2012 to
Nov 2013)

• Incidence of AKI in children admitted to PICU was 17.5%

(35 out of 165)

• Morality rate was 28.57% in children with AKI (10 out of 35)

• Risk factors for AKI include: younger age, sepsis and shock
with multi-organ dysfunction and need for mechanical
ventilation

• Need for dialysis - 34.2% of children with AKI (12 out of 35)
Prabhakar et al. International journal of food and nutritional sciences , Vol.4,
Iss.3, Apr-Jun, 2015
• In a retrospective, observational study with
252 children (1 month to 18 years) admitted in
PICU
– Incidence was 40.9% (103 out of 252)
– 37.9% patients reached pRIFLE max of Risk
(39 out of 103)
– 35.9% patients reached Injury (37 out of 103)
– 26.2% had Failure (27 out of 103)

Naik S et al. Indian J Crit Care Med. 2014 Mar; 18(3):129-133.

• The incidence of AKI in newborns in a
developing county was 3.9/1,000 live births
and 34.5/1,000 newborns admitted to the
neonatal unit
Aggarwal A et al. Evaluation of Renal Function in Asphyxiated Newborns. J
Trop Pediatr 2005;51:295

• Other studies have demonstrated that VLBW, a low

Apgar Score, a PDA and maternal administration of
antibiotics and NSAID was associated with the
development of AKI

Cataldi L et al. Potential risk factors for the development of acute renal
failure in preterm newborn infants: a case controlled study. Arch Dis Child
Fetal Neonatal Ed 2005;90:514–519
 Epidemiologic Studies of AKI in children
AUTHOR YEAR POPUL. AKI STUDY DESIGN NUM AKI INCIDENCE
Defin.
Bailey et al. 2007 ICU 2x S Cr Prospective cohort 985 4.5%

Akan-Arikan et 2007 ICU pRIFLE Prospective cohort 150 82%

al.
Plotz et al. 2008 ICU pRIFLE Retrospective cohort 103 58%

Ozeakar et al. 2008 ICU AKIN Retrospective cohort 100 Stage 1: 25%
Stage 2: 36%
Stage 3: 39%
Zappitelli et al 2009 Cardiac pRIFLE Retrospective cohort 390 35.9%
Sur

Palmieri et al 2009 ICU pRIFLE Retrospective cohort 123 45.5%

(Burns)

Pediatr Nephrol (2010) 25:2401-2412

EVOLUTION of STAGES of AKI

Clin J Am Soc Nephrol 2008; 3: 864–868

PATHOPHYSIOLOGIC MECHANISMS in AKI

• Renal Blood Flow Autoregulation

• The Classic Theory of Ischemic Renal Injury
– Response to Hypoxia and Ischemia
– Free Radical Injury
• Renal Tubule Obstruction and Backflow
• Inflammation
 ISCHEMIC/HYPOXIC INJURY

In eNOS Endothelin ATP depletion

in iNOS
function peptides

Reactive 02
Vasoconstriction
and N
Loss of apical Loss of polarity
molecules
brush border with
mislocation of
SIRS
Na+K+ATPase
Activation of inflammatory resp.

Cytokines & reactive O2 molecules Kidney

dysfunction
Oxidation of prot.DNA & lipids

Tissue injury
 ACUTE KIDNEY INJURY

GLOMERULAR
TUBULAR INJURY BOTH
INJURY

• Hematuria • pH • Features of
• Proteinuria abnormalities both
• Hypertension • Electrolyte glomerular and
abnormalities tubular injury
• Urinary casts
present
 CLASSIFICATION
• Traditional Classification
– Pre Renal AKI
– Renal AKI
– Post Renal AKI

• Other classification
– Primary
– Secondary
 Pre-Renal
• Also called pre renal azotemia, is characterized by
diminished effective circulating arterial volume,
leading to inadequate renal perfusion and decreased
GFR.
 Renal
• Includes a variety of disorders characterized
by renal parenchymal damage, including
sustained hypoperfusion, ischaemia and
nephrotoxins.
 Post Renal
• Includes variety of disorders characterized by
obstruction of the urinary tract.
• In a patient with 2 functioning kidneys,
obstruction must be bilateral to result in AKI
• Relief of obstruction usually results in
recovery of renal function except in patients
with associated renal dysplasia or prolonged
urinary tract obstruction.
Causes
 CLINICAL PRESENTATION
• PRE RENAL
– There may be history of volume loss from
vomiting, diarrhoea or blood loss
– May present with dehydration, tachycardia,
hypotension, pallor and decreased urine output.
• RENAL
– Hematuria, Oedema and hypertension: glomerular
etiology
– Dysentry, petechiae and pallor: HUS
– Sudden dark red urine, pallor and jaundice: acute
intravascular hemolysis
– Rash with arthritis: SLE or HSP
– History of exposure to nephrotoxic drugs: ATN
– Fever, rash, arthralgia and exposure to drugs like
NSAIDS or antibiotics: Allergic interstitial nephritis
• POST RENAL
– History of interrupted urinary stream and palpable
bladder or kidney suggest obstructive uropathy
– Abdominal colic, hematuria and dysuria suggest
urinary tract calculi
 In Neonates….
HISTORY:-
Prenatal conditions – oligo- or polyhydramnios
– renal abnormality noted on antenatal US
– maternal diabetes(a/w RVT)
Neonatal conditions – prematurity, perinatal asphyxia, RDS,
sepsis
– Umbilical artery catheterization (A/W Renal artery
thrombosis)
– Drugs
– delayed 1st passage of urine,
– abnormal urine stream in male
– Lethargy, poor feeding, vomiting, seizures
 Physical Examination
• Thorough physical examination
– Vitals
– Skin
– Eyes
– Ears
– CVS
– Abdominal
– Respiratory system
– CNS
• Vital signs: Weight change, temp, HR, BP, RR
• SKIN: Mucous membranes (dry/pale)
Petechiae, purpura (palpable), skin turgor,
capillary refill, jaundice
• EYES: Periorbital edema, Sunken
• EARS: Hearing deficiet, Mucosal or cartilagenous
ulcerations
• RS: Pulmonary oedema
• CVS: JVP, Murmurs
• Abdominal: Ascites, mass, tenderness, distended
bladder
• CNS: Altered mental status
 PREDISPOSING FACTORS

*Pediatr Nephrol 2005 20:132–135

 Predisposing Factors…
• EXPOSURES • SUSCEPTIBILITIES
– Sepsis – Dehydration/ Volume
– Circulatory Shock depletion
– Burns – Female gender
– Trauma – Black race
– Cardiac Surgery – CKD
– Nephrotoxic drugs – Chronic diseases
– Radiocontrast Agents – Diabetes mellitus
– Envenomation – Cancer
– Anaemia
– Genetic predisposition
 Lab Investigations
• Serum creatinine
• Urea
• Electrolytes
• CBC
• Urine analysis & microscopy
• Imaging studies
• Serologic testing
• Early Biomarkers
• Renal Biopsy
• CBC:
– Anemia (dilutional, hemolytic, SLE)
– Leucopenia (SLE, Sepsis)
– Leucocytosis (Sepsis)
– Thrombocytopenia (HUS, DIC, SLE, sepsis)
• Serum Biochemistry:
– Hyponatremia (dilutional)
– Metabolic acidosis
– Elevated blood urea nitrogen, creatinine, uric acid,
potassium, and phosphate (diminished renal
function)
– Hypocalcemia (hyperphosphatemia)
• URINALYSIS
– Dysmorphic RBCs, RBC casts: Glomerulonephritis
– WBC casts: Pyelonephritis
– Blood but no RBCs: Rhabdomyolysis, hemolysis
– Eosinophils: Interstitial nephritis
– Hyaline casts: Proteinuria
– Granular urinary casts
 Urine Sediment

Monomorphic RBCs Dysmorphic RBCs

RBC cast Hyaline cast

Urine Sediment

Fatty cast
WBC cast

ATN
• SEROLOGIC TESTING
– Hypocomplementemia: PSGN, MPGN, SLE
– ASO, anti-DNAseB: PSGN
– ANA, anti-dsDNA: SLE
– ANCA: Wegener’s, MPA
– Anti-GBM Ab: Goodpasture’s disease
– ADAMTS-13: HUS
• IMAGING STUDIES
– CXR: cardiomegaly, pulmonary congestion (fluid
overload), or pleural effusions
– Renal ultrasonography: renal & bladder anatomy,
obstruction or mass, blood flow assessment.
– DMSA scan
– MCU : posterior urethral valve, VUR
– Renal doppler study: identify thrombosis/ stenosis
– CT scan: Identify sites and causes of urinary
obstruction, mass lesions
– MRI/MR angiography- Vasculature
 INDICATIONS OF RENAL BIOPSY
• Patients in whom etiology of renal failure is not identified
particularly in the context of a systemic disease.

• Unremitting renal failure lasting longer than 2-3 weeks, where

biopsy may be useful in diagnosis (eg-crescentic GN) or in
assessing the extent of renal damage (tubular necrosis or
cortical necrosis).

• Suspected drug –induced AKI in a patient receiving therapy

with a potentially nephrotoxic drug (eg. renal transplant
patient receiving cyclosporine)
Conventional Markers of AKI
 Concept of biomarker
• AKI -- cellular insult -- molecular injury

• Cells start producing markers of injury and clinical

syndrome develops subsequently

• Biolological clock precedes clinical clock

• Detection of biomarker may provide much needed

window of opportunity for earlier intervention
Specific Roles of Biomarkers
 New Biomarkers
• Use of biomarkers may enable earlier
detection of renal injury and aid in identifying
the time of occurrence of initial injury, the
nature of the injury, and duration of AKI
– Interleukin 18 (urine)
– Neutrophil Gelatinin-Associated Lipocalin (urine &
plasma)
– Kidney Injury Molecule-1 (urine)
– Cystatin C (plasma)
 Interleukin 18
• IL-18 is a proinflammatory cytokine produced in PCT
after AKI. The intracellular protease capsase-1 converts
IL-1b and IL-18 to their active forms. IL-18 then exits the
cell and enters the urine.
• Urinary levels of IL-18 have been shown to increase in
ischemic AKI
• Urinary IL-18 > 100 pg/mg were predictive of
development of AKI 24 hours before creatinine levels
increased.

Am J Kidney Dis.2004;43:405-414.
J Am Soc Nephrol.2005;16:3046-3052.
 Neutrophil Gelatinin-Associated
Lipocalin
• Normally present at low levels in several human tissues
• NGAL expression is markedly elevated in injured
epithelium
• Easily detected in urine and blood after ischemic or
nephrotoxic injury
• Serum NGAL at the start of RRT were predictive of
survival in critically ill patients with AKI
• Biomarker of AKI in transplantation

Crit Care. 2010;14(1):R9

Pediatr Nephrol.2006;21(6):856-863
 Kidney Injury Molecule-1
• Highly overexpressed in proximal tubular cells after
ischemic or nephrotoxic AKI
• Urinary KIM-1 could be used to distinguish ischemic
AKI from prerenal azotemia & chronic diseases
• More specific to ischemic or nephrotoxic kidney
injury and is not markedly altered by CKD or UTIs.

Crit CareMed.2008;36(4)
Am JMed.1998;104(4):343-348
 Cystatin-C
• Cystatin C is a 13.3-kDa protein that is fully
catabolized in PCT and not returned to blood
• Serum Cys C is not affected by gender, age, race,
protein intake, and muscle mass
• Cys C was shown to detect AKI 1-2 days earlier than
creatinine in critically ill patients, and postoperative
Cys C was more effective at predicting AKI in
pediatric cardiac surgery patients
Kidney Int. 2004;66:1115–22.
Kidney Int. 2011;80:655–62.
Trend of Rise of Various Biomarkers

McIlroy DR et al. Biomarkers of acute kidney injury: an evolving

domain. Anesthesiology 112(4), 998–1004 (2010).
MANAGEMENT
 General Management
• Fluids
• Withdrawal/ dose reduction of nephrotoxic
drugs
• Role of diuretics
• Role of Vasopressors
• Management of complications
• Nutrition
• Management of specific conditions
• Renal replacement therapy
 Sick hospitalized children

WITH KIDNEY INJURY WITHOUT KIDNEY INJURY

Identify severity and

degree of renal injury
Biomarker + Biomarker -
• pRIFLE
•AKIN
• KDIGO
•Keep surveillance Take
for progression of preventive
PRE-RENAL RENAL POST-RENAL kidney injury measures
•Prevent further
injury

•IV BOLUS NO BOLUS

•FLUIDS
•URINE OUTPUT
•DIURETIC
FLUID
•REASSESSMENT
RESTRICTION
GENERAL GUIDELINES (KDIGO 2012)
• Once the diagnosis of AKI is made, we should
stage it
• Both urine output & creatinine is used as
measures of acute change in GFR
• In the absence of hemorrhagic shock, isotonic
crystalloids are preferred over colloids as
initial management for expansion of
intravascular volume
• Use of ionotrops with fluids is recommended
in patients with vasomotor shock
• In critically ill patients, insulin therapy can be
started targeting a plasma glucose of 110-149
mg/dL
• Diuretics are not recommended to prevent or
to treat AKI except in management of volume
overload
• Low dose dopamine is not recommended to
prevent or treat AKI
 Management
Assess volume status – clinically or CVP monitoring

VOL ?PRE RENAL

OVERLOAD / CAUSE
CARDIAC
FAILURE

Blood loss or Fluid

hypoproteinemia depletion
Fluid restriction
DIURETIC
VOIDS CRYSTALLOID
COLLOID 20 mL/kg over 30
URINE
min

RENAL / POST NOT VOID Repeat NS bolus

RENAL AKI URINE if not void urine
 NOT VOID
URINE

Voids urine Monitoing and prevention for

DIURETIC
further renal damage

Not voids urine

Voids urine
400 mL/m2/24 hr
(insensible losses)
+ RENAL
UO REPLACEMENT
+ Not voids urine
THERAPY
blood, git losses
HYPERKALEMIA (> 6 mEq/L)- cardiac arrhythmia, cardiac arrest and
death
• Earliest ECG change - peaked T waves
• Later - widening of the QRS intervals, ventricular
arrhythmias, and cardiac arrest
• Exogenous sources of potassium (dietary, IVF, TPN) should be
stopped
• Specific treatment of hyperkalemia

AGENT DOSE MECHANISM ONSET OF

ACTION

K >6 Sodium polystyrene 1 g/kg orally or by exchanges sodium 30-60 min

sulfonate resin retention enema , q 2 hr for potassium and
(Kayexalate) can take several hr
to take effect

K >7 Calcium gluconate 1.0 mL/kg IV, over 3-5 counteracts the k- immediate
+/- 10% min induced ↑ in
ECG myocardial
irritability but not
lower the S. K level
Sodium bicarbonate 1-2 mEq/kg IV, over 5- Shifts K+ into cells 15-30 min
10 min

Regular insulin + 0.1 units/kg + 1 mL/kg, Shifts K+ into cells 30-120 min
glucose 50% sol over 1 hr
Mild metabolic acidosis - rarely requires treatment

SEVERE METABOLIC ACIDOSIS (arterial pH < 7.15;

serum bicarbonate < 8 mEq/L) IV bicarbonate to
raise the arterial pH to 7.20

• The remainder of the correction may be

accomplished by oral sodium bicarbonate after
normalization of the serum calcium and
phosphorus levels

• Rapid correction of acidosis reduces the ionized

calcium concentration and may precipitate tetany
HYPOCALCEMIA - treated by lowering the serum
phosphorus

• Calcium should not be given intravenously, except in

cases of tetany, to avoid deposition of calcium salts
into tissues

• Low-phosphorus diet, and phosphate binders should

be orally administered to bind any ingested phosphate
and increase GI phosphate excretion

• Common agents include sevelamer (Renagel), calcium

carbonate (Tums tablets or Titralac suspension), and
calcium acetate (PhosLo)
• HYPONATREMIA is most commonly a dilutional
disturbance , corrected by fluid restriction rather
than NaCl administration
MODALITY INDICATION

Hypertonic (3%) saline symptomatic hyponatremia

(seizures, lethargy)

S. Na <120 mEq/L

• Acute correction of the serum sodium to 125

mEq/L (mmol/L) should be accomplished using
the following formula:
= 0.6 × wt (kg) ×(125− serum sodium in mEq/L)
 NUTRITION
• AKI assoc w/ marked catabolism and negative
nitrogen balance
• Enteral preferred over parenteral
• High-biologic value protein, low P, low K diet should
be used
• A total energy intake of age appropriate calories in
patients with any stage of AKI is suggested
• Protein restriction should be avoided
– 0.8–1.0 g/kg/d of protein in AKI patients without need for
dialysis,
– 1.0–1.5 g/kg/d in patients with AKI on RRT, and
– up to a maximum of 1.7 g/kg/d in patients on CRRT
 Supportive Management
• Infections: Antibiotics (renal adjusted doses)
• Hypertension: Due to hyperreninemia or ECF volume
expansion. BP Monitoring and antihypertensive use.
• Anemia: generally mild (hemodilutional) Children
with HUS, SLE, active bleeding, or prolonged AKI can
require transfusion of PRBC if Hb<7 g/dL
• Neurologic symptoms: headache, seizures, lethargy,
and confusion. Benzodiazepams are the most
effective.
 MANAGEMENT OF COMMON
CONDITIONS CAUSING AKI
• Prerenal AKI
Administer crystalloids; stop diuretics, NSAIDs,
ACE inhibitors; Inotropes (for cardiac failure)
pressor agents
• Acute tubular necrosis
Discontinue drug or toxin; treat cause of
circulatory failure, supportive care.
• Vasculitis
Immunosupressive medications ;plasma
exchange

• Interstitial nephritis
Discontinue offending drug ;consider steroid
therapy

• Renal artery,vein occlusion

Anticoagulation; thrombolysis or surgery
• Intrarenal obstruction
Discontinue offending drug; alkaline diuresis
for rhabdomylosis, hemoglobinuria or urate
nephropathy

• Urinary tract obstruction

Bladder catheter or nephrostomy;radiologic or
surgical treatment of obstruction.
• Glomerulonephritis
Supportive care if postinfectious; antibiotics
(for shunt infection or endocarditis) ;
immunosupressive medications (IgA
nephropathy, rapidly progressive GN)

• Hemolytic uremic syndrome

Supportive care; plasma infusions, plasma
exchange
RENAL REPLACEMENT THERAPY
DIALYSIS
 Dialysis
Indications for dialysis in AKI:

• Vol overload + hypertension and/or pul edema refractory to diuretic

therapy

• Persistent hyperkalemia

• Severe metabolic acidosis unresponsive to medical management

• Uremia (encephalopathy, pericarditis, neuropathy)

• Blood urea nitrogen >100-150 mg/dL (or lower if rapidly rising)

• Calcium:phosphorus imbalance, with hypocalcemic tetany that

cannot be controlled by other measures
 Dialysis Modalities
• Intermittent Hemodialysis (IHD)

• Peritoneal Dialysis (PD)

• Continuous Renal Replacement Therapies (CRRT)

– CVVHD (predominantly diffusive clearance)
– CVVH (convective clearance)
– CVVHDF (both convective &diffusive clearance)
PERITONEAL DIALYSIS
 INDICATION OF PD (NICE GUIDELINES 2011)
Children 2 years old or younger
Patient with residual renal function

• Though rates of PD use have ↓ in PICU, it is still the most

commonly used method of RRT in children in the world
J. Cerd´a, A. Bagga, V. Kher, and R. M. Chakravarthi, “The contrasting characteristics of AKI in
developed and developing countries,” Nature Clinical Practice Nephrology, vol. 4, no. 3, pp. 138–
153, 2008.

• The use of PD is favored in the neonates who often have

difficult vascular access, low tolerance to volume shifts,
and thermodynamic instability
S. Subramanian, R. Agarwal, A. K. Deorari, V. K. Paul, and A. Bagga, “Acute renal failure in
neonates,” Indian Journal of Pediatrics, vol. 75, no. 4, pp. 385–391, 2008.
Intermittent hemodialysis
(IHD)

• Technical expertise & trained personnel

• Hemodynamic stability of the patient
• Vascular access in large vessel
• Problematic in children for whom obtaining
access is a chronic problem
J. M. Symons, P. D. Brophy, M. J. Gregory et al., “Continuous renal replacement therapy
in children up to 10 kg,” American Journal of Kidney Diseases, vol. 41, no. 5, pp. 984–
989, 2003.
• IHD, unfeasible in hemodynamically unstable and
small infants, who do not tolerate the large
volume shifts that occur during dialysis

• IHD is ideal for patients with acute electrolyte

abnormalities and those that would benefit from
and can tolerate high doses of dialysis in a short
time frame

S. P. Andreoli, “Acute renal failure in the newborn,” Seminars in

Perinatology, vol. 28, no. 2, pp. 112–123, 2004.
 CRRT - Continuous renal replacement therapy
• Extracorporeal blood purification therapy
intended to substitute for impaired renal
function over an extended period of time
 • CRRT is of 3 types :

THERAPY MECHANISM

Continuous Venovenous Ultrafiltration produced is replaced completely or

Hemofiltration in part by sterile filter replacement fluid

Continuous Venovenous •Fluid replacement is not routinely administered.

Hemodialysis •Solute clearance is diffusive.

Continuous Venovenous Solute removal is both diffusive and convective.

Hemodiafiltration
S. Walters et al, “Dialysis and pediatric AKI: choice of renal support modality,” Pediatric
Nephrology, vol. 24, no. 1, pp. 37–48, 2009.
 Prevention
• Conditions causing AKI can be prevented
• Avoidance of nephrotoxic drugs
• Prompt rehydration therapy in acute
diarrhoea.
• Avoid radiological contrast agents
• Proper hydration for patients undergoing
procedures with radiocontrast media
• Adequate hydration, diuresis along with use of
Allopurinol for TLS
SPECIAL CONDITIONS RELATED
TO AKI
Uric Acid Nephropathy and Tumor Lysis Syndrome
Tumor lysis syndrome - as ↑ Serum potassium
tumor cells are lysed ↑BUN
↑Purine metabolite products
↑Phosphorus
↓Serum calcium

• Allopurinol limit the increased excretion of uric acid with

chemotherapy but result in a markedly increased excretion of
uric acid precursors including hypoxanthine and xanthine
LaRosa C, Krishnamurti L et al. ARF from xanthine nephropathy during management of acute
leukemia. Pediatr Nephrol 2007;22:132–135

• Rasburicase , which is well tolerated in ped patients is a

recombinant form of urate oxidase that catalyzes uric acid to
allantion which is 5 times more soluble than uric acid

Rampello E et al. The management of TLS. Nat Clin Pract Oncol 2006;3:438–447
SNAKE AND SCORPION ENVENOMATION - AKI

• The incidence of AKI (using AKIN definition) in Russell’s

viper envenomation is 45.9%

Sriram krishnamurthy, kuralvanan gunasekaran et al, indian pediatrics, volume 52 july

15, 2015

• The incidence of snake bite-associated AKI in an adult

population from Karnataka using the AKIN definition
was 14.6%

Harshavardhan L, Lokesh AJ, Tejeshwari HL, Halesha BR, Metri SS. A study on the acute kidney injury in
snake bite victims in a tertiary care centre. J Clin Diagn Res. 2013;7:853-6.
Endogenous Toxin Induced AKI
• Hemolysis and rhabdomyolysis from any cause
can result in sufficient hemoglobinuria or
myoglobinuria to induce tubular injury and
precipitate acute kidney injury

Watanabe T. Rhabdomyolysis and ARF in children. Pediatr Nephrol 2001; 16:1072–

1075

Zededa-Orozco D et al. Factors associated with ARF in children with rhadomyolysis.

Pediatr Nephrol 2008;23:2281–2284.
 Contrast Induced AKI
• Defined as rise in SCr of >0.5 mg/dl or a 25%
increase from baseline value, assessed at 48
hr after a radiological procedure
• Alternative imaging methods in patients at
increased risk for CI-AKI should be considered
• Lowest possible dose of contrast medium in
patients at risk for CI-AKI should be used
• It is recommended using either iso-osmolar or
lowosmolar iodinated contrast media in
patients at increased risk of CI-AKI
• IV volume expansion with isotonic NaCl is
recommended in patients at increased risk for
CI-AKI
• Oral NAC with IVF has some role in prevention
of CI-AKI
Kidney International Supplements (2012) 2, 69–88

McCullough PA. Contrast-induced acute kidney injury. J Am

Coll Cardiol 2008; 51: 1419–1428.
 PROGNOSIS
• Serum creatinine
• Underlying etiology
• Presence or absence of insufficiency in other organs
• Choice/timing of therapy

Primary AKI was found to have improved survival compared to

secondary (90 vs 51%)
Foland JA et al. Crit Care Med 2004

Indian study reported acute mortality 35%,

Glomerulonephritis, Snakebite commonest etiologies

Sinha R, Nandi M, etal. Nephrol Dial Transplant 2009

 Long Term Prognosis
• Very little data esp. in children

• Children suffering substantial loss of nephrons – are

at risk for late dev. of renal failure.

• Studies show hypoxic/ischaemic & nephrotoxic

insults can also lead to chronic kidney disease

• Life-long RFT, urinanalysis & hypertension

monitoring required
• Askenazi et al, Kidney Int 2006
–174 pediatric patients with in-hospital AKI and survived to
discharge
–3-5 year survival after discharge was 79.9%
–68.5% of deaths were in the first year after discharge
–21% of survivors had at least one sign of persistent renal injury:
microalbuminuria, decreased GFR, hypertension, or glomerular
hyperfiltration
–9% developed end stage kidney disease

• Sinha R, et al.(2009) reported 25% of survivors had renal

morbidity after 10 years with one one of the following:
abnormal creatinine, hypertension, hematuria, proteinuria
 TAKE HOME MESSAGE
• The incidence and prevalence of AKI in
children may be underestimated
• Further studies are needed to clearly define
AKI and determine its burden in children
• Early detection of AKI will be beneficial, and
more sensitive biomarkers can be used
• Use of biomarkers to predict patients who are
at higher risk for AKI may help to decrease its
occurrence
THANK YOU