SYMPOSIUM: INTENSIVE CARE
Acute kidney injury (AKI)
in paediatric critical care
Rupesh Raina
Abigail Chauvin
Akash Deep
Abstract
Incidence of acute kidney injury (AKI) is gradually increasing in children
admitted to critical care units partly because of increased awareness
of this entity. Though serum creatinine has been used in most defini-
tions, its inability to accurately reflect kidney function has resulted in
problems for clinical research in paediatric AKI. This has resulted in
the use of more than 35 definitions of AKI in clinical studies, ranging
from small changes in serum creatinine to requirement for dialysis.
Therefore, comparisons among studies are difficult, resulting in a
wide range of quoted epidemiology, morbidity, and mortality rates in
the AKI paediatric literature. Acute kidney injury may be precipitated
by critical illness, pre-existing medical conditions, and treatments
received both before and during ICU admission. In this review we
have attempted to outline the current definitions used for AKI, pres-
ence of AKI in various critical care conditions (bone marrow transplant,
liver, sepsis, cardiac, primary renal conditions leading to glomerulone-
phritis) and outline the basic management.
Keywords acute kidney injury; children; paediatric intensive care;
renal failure
Introduction
Acute kidney injury (AKI) is a complex condition with numerous
pathologies, in which there is sporadic failure and rapid loss of
renal function. It is fairly new terminology for what was previ-
ously referred to as “acute kidney failure”. AKI is detected by a
marked decrease in glomerular filtration rate (GFR), accompa-
nied by elevated levels of serum creatinine. This disease is
associated with a poor prognosis resulting in longer hospital and
intensive care stays and higher mortality rates. It is difficult to
present an accurate incidence of AKI since disease presentation
and definitions are variable, however it is estimated to vary be-
tween 8% and 30% in paediatric intensive care units. Prognosis
for these patients depends on the underlying aetiology, ranging
from full recovery to end-stage renal failure (ESRF).
Rupesh Raina MD is Consultant Nephrologist in the Department of
Pediatric Nephrology in Akron Children Hospital, Akron and Akron
General Medical Center, Cleveland Clinic Foundation, Akron, OH,
USA. Conflict of interest: none declared.
Abigail Chauvin is Second Year Medical Student at Northeast Ohio
Medical University of Rootstown, Ohio, USA. Conflict of interest:
none declared.
Akash Deep FRCPCH MD is Consultant Paediatric Intensivist at King’s
College Hospital, Denmark Hill, London, UK. Conflict of interest:
none declared.
PAEDIATRICS AND CHILD HEALTH 27:5
Epidemiology
The interpretation of AKI depends on which criterion is being
used, as well as the geographic location it is being diagnosed in.
The incidence of AKI in critical care environments diagnosed
using the Kidney Disease: Improving Global Outcomes (KDIGO)
criteria is approximately 40%.
The mortality rate in hospitalized patients with AKI was found
to be 14.7% greater than in hospitalized patients without AKI.
Increased incidence of AKI was found to be associated with male
sex, Afro-American ethnicity and being aged 15e18 years.
Additionally, neonates have a significantly higher mortality rate
and median length of stay in the hospital.
Aetiology and pathophysiology
The aetiology of AKI may be pre-renal, renal or post-renal. Pre-
renal AKI is due to renal ischaemia as a consequence of systemic
hypovolaemia. This occurs for a variety of reasons: diarrhoea,
haemorrhage, dehydration, decreased cardiac output/contrac-
tility, sepsis. Pre-renal AKI is the most common type of AKI in
children, and activates homoeostatic compensatory mechanisms
to restore renal perfusion.
Intrinsic-renal AKI occurs when internal renal structures are
damaged. Conditions causing intrinsic AKI include: ischaemia,
nephrotoxic drugs, glomerular disease, and microvascular dis-
ease (see below). Tubular cells of the straight segment of the
proximal tubule and the thick ascending limb of the loop of
Henle are especially susceptible to ischaemic insult, due to high
ATP demands and a naturally hypoxic environment, respec-
tively. Hypoxic and nephrotoxic drug-induced injury has been
found to lead to elevated risk of CKD long-term.
Post-renal AKI occurs due to obstruction after the level of the
kidneys. Typically, AKI is alleviated upon removal of the
obstruction. Additionally, if the individual has two functioning
kidneys the blockage must be bilateral in order to result in AKI;
otherwise, the functional kidney will compensate.
Diseases of intrinsic-renal AKI
Acute tubular necrosis (ATN) results from renal ischaemia-
reperfusion injury. Due to hypoxia, accumulation of metabolites,
and insufficient nutrition, tubular epithelial cells are damaged
and may progress to apoptosis or necrosis. Homoeostasis of
water, metabolic waste, and electrolytes is imbalanced. Small
arterioles in the outer medulla constrict and are obstructed by
leucocyte accumulation and complement activation in response
to inflammation, weakening the endothelium. Increased vascular
permeability causes fluid leak into the interstitium and oedema
ensues, causing further ischaemia. Additionally, the proximal
tubule is ineffective in ion transport. Therefore the macula densa
initiates further vasoconstriction of the afferent arteriole.
Acute cortical necrosis (ACN) constitutes 2% of all cases of
renal failure in adults and approximately 10% of all cases of ACN
are children. Common aetiologies of ACN in children include
placental abruptions, feto-maternal or twinetwin transfusion,
dehydration, trauma, sepsis, renal vein thrombosis, haemolytic
anaemia (severe), haemolytic uraemic syndrome, nephrotoxic
drugs and contrast substances.
Haemolytic uraemic syndrome (HUS) is a form of thrombotic
microangiopathy and occurs in two forms: typical and atypical. A
233 Ó 2017 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: INTENSIVE CARE

Shiga-toxin released from Escherichia coli causes typical HUS,

and atypical HUS (aHUS) can occur due to a variety of conditions AKIN guidelines; from Mehta et al 2007
including congenital or acquired complement system defects and Stage Serum creatinine Urine output
genetic mutations. Atypical HUS is differentiated from throm-
botic thrombocytopenic purpura (TTP) by levels of ADAMTS 1 [ SCr
0.3 mg/dL or 1.5 <0.5 mL/kg/hour for >6
activity, with aHUS indicated by more than 5% ADAMTS activ- e2.0 times baseline value hours
ity. If it is less than 5%, the patient will be classified with TTP. 2 [ SCr >2.0e3.0 times <0.5 mL/kg/hour for
baseline >12 hours
Diagnostic criteria 3a [ SCr
4.0 mg/dL with acute <0.3 mL/kg/hour for 24
increase of
0.5 mg/dL or [ hours or anuria for 12
AKI is a fairly new term that has replaced the nomenclature of
SCr >3.0 times baseline hours
“acute kidney failure”. Diagnosis of AKI is carried out using the
RIFLE or pRIFLE, AKIN, or KDIGO guidelines. These criteria have a
Any patients being treated with RRT automatically are placed into stage 3.
attempted to consolidate the varying definitions of AKI in order
to more consistently treat and evaluate patients. Table 2

RIFLE
In May of 2002, the Acute Dialysis Quality Initiative Group
(ADQI) met in Vicenza, Italy to establish a more concrete defi-
nition of AKI, as well as diagnostic guidelines. The criteria
established are known as “RIFLE”, an acronym for: ‘Risk of renal
dysfunction’, ‘Injury to the kidney’, ‘Failure of kidney function’,
‘Loss of kidney function’, and ‘End-stage kidney disease’. The
Risk, Injury, and Failure categories indicate stages of kidney
dysfunction, while the Loss and End-stage categories serve as
outcomes.
Serum creatinine (SCr) is used to estimate the GFR, and is
calculated as the change between current measurement and
baseline. One weakness of this model is that the baseline SCr is
frequently unknown, in which case the ‘modification of diet in
renal disease’ (MDRD) formula is utilized to estimate baseline
GFR. Table 1 summarizes these guidelines.
AKIN
Three years later in 2007, the AKI network (AKIN) published an
updated version of RIFLE, and this classification is known as
“AKIN” criteria. The three subcategories of AKIN are: ‘Risk’,
‘Injury’, and ‘Failure’. Data have shown that SCr changes in
smaller increments than accounted for in RIFLE guidelines may
correlate to adverse outcomes. Therefore, it is thought to be more
beneficial for AKI diagnostic criteria to be more sensitive to
recognize and treat as early as possible to avoid ESRD. Table 2
shows the AKIN criteria.
KDIGO
The most recent model for AKI diagnosis is by the Kidney Disease
Improving Global Outcomes (KDIGO) Work Group. Established
in 2012, this classification is designed to further expand upon the
AKIN definition. KDIGO defines AKI with the following criteria:
at least 1.5-fold elevated SCr within the past 7 days, elevated SCr
by
0.3 mg/dL within 48 hours, or UO equal to or less than 0.5
mL/kg/hour over 6 hours. See Table 3 for guidelines.
pRIFLE
In children specifically, a paediatric adaptation of RIFLE was
created, known as pRIFLE. pRIFLE differs from typical RIFLE clas-
sifications in that the classification is based on changes in estimated
creatinine clearance or UO, instead of change in SCr which is used in
adult RIFLE. There are three classifications: ‘Risk’, ‘Injury’, and
‘Failure’. This is because children are rapidly growing, which can
lead to changes in SCr independent of actual onset of AKI.
AKI in sepsis
Studies report 45e70% of AKI to be induced by sepsis. AKI and
sepsis independently increase mortality, but combined sepsis and
AKI shows a staggering mortality of 57e66%. Septic AKI occurs
due to a combination of alterations in microvascular blood flow,
ion balance, oxidative stress, and inflammation. Traditionally,
the ideology that renal ischaemia is the major cause of AKI lead
to the thought that restored perfusion via increased RBF would

RIFLE guidelines; from Bellomo et al 2004

RIFLE Glomerular Filtration Rate (GFR) Urine Output (UO) Sensitivity vs.
Specificity

Categories of kidney
dysfunction
Clinical outcomes
Risk SCr 1.5 times baseline or Y GFR >25% <0.5 mL/kg/hour for 6 hours Highly sensitive
Injury SCr 2 times baseline or Y GFR >50% <0.5 mL/kg/hour for 12 hours
Failure SCr 3 times baseline or
4 mg/dL; Y GFR <0.3 mL/kg/hour (oliguria) for Highly specific
75% 24 hours (or anuria for 12
hours)
Loss of Persistent AKI
function Renal Replacement Therapy (RRT) >4 weeks
ESRD End stage renal disease
Dialysis >3 months

Table 1

PAEDIATRICS AND CHILD HEALTH 27:5 234 Ó 2017 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: INTENSIVE CARE
Kidney Disease for Improving Global Outcomes (KDIGO)
guidelines; from KDIGO AKI Work Group 2012
Stage Serum creatinine (SCr) Urine output
1 [ SCr
0.3 mg/dL or 1.5 <0.5 mL/kg/hour, 6e12
e1.9 times baseline value hours
2 [ SCr 2.0e2.9 times <0.5 mL/kg/hour,
12 hours
baseline
3a [ SCr
4.0 mg/dL or 3.0 <0.3 mL/kg/hr,
24 hours or
times baseline or in patients anuria for
12 hours
under 18 years, Y eGFR to
<35 mL/minute/1.73 m2
a
Any patients being treated with renal replacement therapy automatically
are placed into stage 3.
Table 3
resolve AKI, however studies have shown that is not the case;
RBF is not thought to significantly influence septic AKI in pae-
diatric patients.
Sepsis is marked by systemic arterial vasodilation, largely
mediated by nitric oxide (NO). Inflammatory cytokines elevate
production of inducible NO synthase, resulting in an increased
NO release and drop in arterial resistance. Also, vascular endo-
thelial cells are resistant to pressor hormones. ATP-sensitive
potassium channels are activated during sepsis due to elevated
plasma [Hþ] and [lactate], as well as depressed [ATP] in
smooth-muscle cells of the vasculature. Hyperpolarization due to
potassium efflux occurs, causing voltage-gated calcium channels
to close, leading to further resistance to vasopressors. Pressor
hormone receptors are also down regulated due to over-
production of the hormones, further impairing the vasculature.
Since angiotensin II and norepinephrine do not restore normal
vascular resistance, alternative treatments must be considered.
Currently the most promising agent for vasopressor resistant
sepsis is arginine vasopressin, which is thought to deactivate the
ATP-mediated potassium channels, decrease expression of NO
synthase, and reduce cGMP signalling with NO. Arginine vaso-
pressin has a vasoconstrictive effect by targeting the efferent
glomerular arteriole to increase intraglomerular pressure. How-
ever, caution must be used since arginine vasopressin lacks car-
diac ionotropic qualities and can lead to depressed cardiac output
(CO). Lastly, non-specific effects of arginine vasopressin can
cause myocardial infarction and reduced compliance of
splanchnic vessels, leading to noncardiogenic pulmonary oedema.
Endothelin is a potent vasoconstrictor that has also been
shown to play an active role in the complex pathophysiology of
sepsis. TNF-a causes endothelin release, which acts on vascular
endothelial cells and causes microvascular fluid leakage.
Inflammation also plays a central role in septic AKI. Inflamma-
tory cytokines lead to heterogeneous up-regulation of inducible
NO synthase, damaging various regions of the microvasculature.
Rapidly progressive glomerulonephritis
Rapidly progressive glomerulonephritis (RPGN) is indicated by
decreased renal function and is often associated with haema-
turia, proteinuria, and decreased UO. This condition is frequently
PAEDIATRICS AND CHILD HEALTH 27:5
referred to as crescentic glomerulonephritis (CGN), since it is
marked by development of glomerular crescents. Glomerular
crescents are a non-specific response to glomerular injury,
appearing as
2 layers of cells in the Bowman’s space of the
glomerulus, constricting the glomerular capillary tuft. Crescent
formation is initiated by holes in the glomerular basement
membrane (GBM), Bowman’s capsule, and walls of glomerular
capillaries allowing macrophages and coagulation factors to
trigger cleavage of fibrinogen to fibrin. Earlier commencement of
medical intervention will help to avoid long-term damage.
Nephrotoxic AKI
Nephrotoxic medications are a substantial cause of AKI, reported
as 16% of AKI in hospitalized paediatric patients. Certain anti-
biotics, antivirals, antifungals, angiotensin converting enzyme
inhibitors (ACEI), non-steroidal anti-inflammatory drugs
(NSAIDs), calcineurin inhibitors, chemotherapeutic agents, and
radiographic contrast substances induce nephrotoxic AKI.
Cisplatin is a platinum-based chemotherapeutic agent typically
utilized in the management and treatment of solid, malignant
neoplasms. One in every three patients treated with cisplatin ex-
periences nephrotoxicity. Proximal tubule injury, consequent
oxidative stress and inflammation, and direct toxicity to renal
vascular endothelial cells cause AKI. Currently, supportive therapy
is the typical intervention. Contrast substances are the third most
common aetiology of AKI in hospitals. Presentation is typically
non-oliguric, with transient loss in renal function. The pathological
mechanism consists of increased renal blood flow (RBF) initially,
followed by decreased RBF and eGFR. The fall in eGFR is also
contributed to by constriction of the vasa recta, medullary
ischaemia, reactive oxygen species (ROS) generation, and injury to
tubular epithelial cells.
Recently, a retrospective cohort study of 100 children with
AKI due to exposure to high levels of nephrotoxic medications in
a non-critical setting was performed at Cincinnati Children’s
Hospital Medical Center. Researchers found that patients with
nephrotoxin-induced AKI were 3.84 times more likely to develop
1þ signs of CKD. Additionally, the AKI cohort was found to have
significantly decreased eGFR and higher likelihood for hyper-
tension and proteinuria at 6-months.
To manage paediatric nephrotoxic AKI, cease treatment with
the toxic agent as soon as possible and prevent exposure to
future nephrotoxins to preserve renal function. Fluid therapy
should target restitution of renal perfusion. In severe cases, renal
replacement therapy (RRT) may be utilized for the purpose of
toxic solute removal.
AKI in bone marrow transplantation
AKI is a common complication of haematopoietic stem cell
transplantation (HSCT), otherwise commonly known as bone
marrow transplants. Patients with HSCT-induced AKI requiring
renal replacement therapy have a disappointingly low survival
rate of 42%. It is reported that the incidence of paediatric HSCT-
induced AKI is between 25% and 30%. Pheresis may contribute
to graft versus host disease (GVHD) due to differing immuno-
logical composition to marrow. GVHD accompanied by renal
disturbance is reported to occur in 11e41% of paediatric patients
who receive HLA-matched BMT. However, peripheral HSCT
235 Ó 2017 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: INTENSIVE CARE
collection leads to reduced rates of sepsis, cytopaenia, and need
for nephrotoxic antibiotic therapy after transplantation.
Sinusiodal obstruction syndrome (SOS), also referred to as
veno-occlusive disease (VOD), commonly occurs with BMT. The
exact pathophysiology is not yet known, but current literature
points to injury to hepatic sinuosoids. Despite lack of empirical
evidence about SOS induced paediatric AKI in BMT, it is well
known that SOS/VOD is a significant risk factor for AKI devel-
opment. AKI in SOS is thought to pathologically behave similarly
to hepatorenal syndrome (HRS) with regards to haemodynamic
shifts, as well as liver impairment resulting in hypoalbuminemia,
fluid leakage from capillaries, splanchnic vasodilation, and
hypovolaemia in the intravascular compartment. Chemothera-
peutic drugs commonly utilized in BMT are also a source of AKI
due to nephrotoxicity. Norepinephrine from the activated hep-
atorenal sympathetic nervous system constricts the afferent renal
arteriole, depressing GFR and retaining salt. The prognosis of
SOS-AKI is poor, and thus treatment usually is supportive:
treatment for the kidneys mirrors treatment of HRS, and defib-
rotide tends to be the drug of choice.
AKI in liver disease
AKI in liver disease can occur in patients with acute liver failure
(ALF), chronic liver disease, acute on chronic liver failure and
post-transplantation. The most important point to bear in mind is
that AKI in these patients is not always hepatorenal syndrome
(HRS). In fact of all the causes of AKI in patients with liver dis-
ease, majority are caused by pre-renal or acute tubular necrosis
and HRS constitutes only a small part. ALF is a rare condition,
indicated by new onset liver dysfunction with coagulopathy
which in children may or may not be accompanied by enceph-
alopathy, AKI and ALF often occur concurrently, especially with
specific etiologies: nephrotoxic medications, acetaminophen
overdose, HRS, sepsis, and hypovolaemia.
As liver disease progresses, there are severe vascular haemo-
dynamic complications that disturb renal processes, leading to
imbalanced electrolyte levels and ascites. Frequently, changes in
vascular compliance and renal perfusion culminate in AKI, com-
mon in patients with chronic liver disease (CLD). CLD causes
haemodynamic fluctuations, unbalancing fluids and electrolytes,
and leaving the kidneys highly susceptible to damage. Ascites is an
indicator of this disease state in both children and adults, and
serves as a mortality predictor. However, the pathophysiology of
ascites in children is not completely understood at this point in
time, so children must be treated based on adult models of disease.
AKI in cirrhotic patients tends to be either pre-renal or intra-
renal. Depending on the aetiology, fluid management will differ:
in pre-renal AKI, fluid supplementation is necessary to elevate the
intravascular volume while in intra-renal AKI decreasing fluids
may be necessary. If ascites is severe, abdominal compartment
syndrome could be the cause. Many traditional biomarkers will
overestimate renal function due to problems rooted in declining
hepatic function, and more accurate markers such as inulin are
unrealistic in practice due to high cost and feasibility of use.
However, the Modification of Diet in Renal Disease Study (MDRD)
equation can be used in patients with liver cirrhosis.
HRS causes pre-renal acute kidney injury in patients with
ascites and cirrhosis of the liver. The whole process is
PAEDIATRICS AND CHILD HEALTH 27:5
precipitated by portal hypertension which causes bacterial
translocation and release of vasodilators especially nitric oxide.
The kidneys will attempt to salvage as much perfusion as
possible by arteriole vasodilation via prostaglandins. However
with low cardiac output state, activation of Renal Angiotensin
Aldosterone system leads to renal vasoconstriction and eventual
ascites due to sodium and water retention.
AKI in cardiac disease
AKI commonly occurs in patients undergoing cardiac surgeries,
with increased mortality and morbidity, as well as increasing costs
of healthcare overall. Incidence of AKI after cardiac surgery ranges
from 3% to 30%. A large retrospective cohort study seeking to
determine the incidence of AKI in the cardiac postoperative paedi-
atric population found that patients with AKI were more likely to
have had a more complex surgery requiring lengthier cardiopul-
monary bypass, cyanosis, and requirement of mechanical ventila-
tion. Of this subset of patients, 1e5% required RRT for AKI, and
those patients additionally have a heightened mortality rate of 60%.
In one study by MacDonald et al, it was found that AKI
occurred in 73% of subjects, with 95% occurring within the first
three days post-transplant. Significant risk factors for AKI within
this paediatric group included ventilation at the time of trans-
plant (p ¼ 0.01) and elevated baseline eCCl (p ¼ 0.03). Preop-
erative inotrope usage was found to significantly reduce the odds
of AKI incidence (p ¼ 0.02). Multivariate analysis demonstrated
an independent correlation between AKI and longer paediatric
intensive care unit stay. Patients with a day 3 postoperative
tacrolimus level exceeding 15 mg/litre were significantly more
likely to develop AKI. The authors of this study believe that
children receiving heart transplants should be classified as ‘high-
risk’ for AKI and should be closely monitored. Studies have also
found creatinine kinase-MB (CK-MB) and heart-type fatty acid
binding protein (h-FABP) independently and strongly projected
postoperative AKI incidence.
Fluid management
Fluid management plays a major role in prevention and subse-
quent treatment of AKI. When the balance between intravascular
and extracellular fluid compartments is disturbed; redistribution
of fluids may be hindered. The primary endpoint of fluid treat-
ment is to restore renal perfusion via increasing intravascular
volume. The general types of fluids are colloids, albumin, gelatin,
and crystalloids. The debate as to which type of fluid to use has
always been a matter of debate. Hypertonic fluids are more likely
to remain in the intravascular compartment, and most likely
prove to be more effective than hypotonic fluids in patients with
depleted intravascular volume. It is suggested that synthetic col-
loids are avoided in patients with AKI or at risk for AKI and that
balanced salines are the best mode of fluids for AKI treatment.
Fluid overload in patients with AKI
It is believed that AKI ensues due to systemic hypotension with
resultant renal ischaemia. Thus, traditionally many practitioners
have attempted to “cure” AKI by supplying the patient with
larges volumes of fluids to restore intravascular volume and
renal function. However, this course of treatment may cause
fluid overload (FO), especially when oligo-anuric. Although it is
236 Ó 2017 Elsevier Ltd. All rights reserved.
 SYMPOSIUM: INTENSIVE CARE
unclear whether oedema caused by FO has any direct causal
effect on AKI, oedema causing abdominal compartment syn-
drome can cause tubule compression, further retention of water
and salt, and diminished renal blood flow, inducing AKI.
To manage FO, the goal is to initiate a neutral or negative fluid
balance. Current treatment approaches include diuretics and
renal replacement therapy (RRT). However, each has its own
disadvantages. Patients may develop ‘diuretic resistance’,
imbalanced electrolytes, and further decline in renal integrity. In
terms of RRT, intermittent haemodialysis may trigger intra-
dialytic hypotension. Therefore continuous renal replacement
therapy (CRRT) is favoured in order to maintain haemodynamic
stability and prevent further renal injury.
Other possible treatment methods include adenosine receptor
antagonists such as theophylline. Although diuretics may restore
urine output, research suggests no significant difference in pre-
vention of renal damage. Additionally, diuretics such as furose-
mide have been found to inhibit NaeK ATPase, causing further
ischaemia. One experimental method of treatment includes ‘renal-
dose’ dopamine, a dosage of 0.5 to 3e5 mg/kg/minute. Dopamine
serves as a vasodilator to restore renal blood flow and urine output,
however this method of treatment has not been proven to be
effective in AKI for increasing survival and is no longer promoted.
Electrolyte balance
AKI frequently results in uraemia, characterized by elevated levels
of creatinine in plasma, metabolic acidosis, hyperkalemia, oliguria,
and reduced consciousness if AKI is severe enough during acute
phase of disease. Serum potassium and ECG should be monitored
closely for hyperkalemia and ensure levels over 6.5 mmol/litre are
quickly treated. Monitoring of acid-base balance is essential as
well, and one may administer IV bicarbonate for treatment of
acidosis in the face of persistence despite corrected hypovolemia/
hypotension. Lastly, ionized calcium should be monitored as well
and treated if levels reach less than 1.0 mmol/litre, especially since
treatment of acidosis could further decrease calcium levels.
Conclusion
AKI is a condition that adversely affects outcomes in critically ill
paediatric patients. Various complications may stem from this
complication both early and later in life. Early detection and
treatment of AKI result in better outcomes. The medical field has
come a long way in defining and treating AKI, but there is always
room to improve management strategies. A admitted to paediatric intensive care.
FURTHER READING
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Practice points
C Acute kidney injury (AKI) is relatively common in children
C The incidence of AKI in any setting depends upon the pre-
cise definition used but the presence of AKI is associated
with increases in morbidity and mortality.
C Sepsis is one of the important causes of AKI which leads to
increased duration of ventilation and ICU stay
C Use of low dose dopamine or diuretics does not appear to
improve outcomes although both may increase urine
output.
237 Ó 2017 Elsevier Ltd. All rights reserved.