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Acute kidney injury (AKI),
formerly known as acute renal failure (ARF) is an important contributor
to mortality and morbidity, especially in critically ill children.
Understanding the burden of AKI and its implication has been hampered by
the lack of a precise definition of AKI. More than 30 definitions in
literature have led to reporting of wide variation in incidence and
outcomes [1]. A minor acute reduction in kidney function (which may be
clinically not apparent and may be just a subtle rise in serum
creatinine) has been consistently shown to have an adverse prognosis.
Hence the term acute kidney injury (AKI) was proposed to encompass the
entire spectrum not limited to those who need renal replacement therapy
(RRT). Two similar definitions based on creatinine and urine output for
diagnosis and classification of AKI; the pediatric Risk, Injury,
Failure, Loss, End-Stage Renal Disease criteria (pRIFLE) and the Acute
Kidney Injury Network (AKIN) staging system have been proposed [2,3].
The spectrum and burden of AKI in developing
countries may be different from that of developed countries. The
patients from developing countries are younger, infection associated AKI
is more common and a significant proportion may have already developed
AKI at the time of hospitalization. In addition, resource limitations in
managing children who require RRT add to the burden.
Mehta and colleagues must be congratulated for taking
the first step toward understanding the natural history of AKI in
hospitalized children in our country using the AKIN criteria [4]. They
observed that one third of critically ill children developed AKI in
hospital and the incidence was four fold higher compared to the
non-critically ill. The authors have validated the findings from world
literature that AKI is common. They have shown that AKI occurs very
early in hospitalization, which may have important bearing on future
studies for early detection and treatment. AKI was associated with
longer stay in hospital and four fold increase in mortality as compared
to those who did not develop AKI reinforcing the importance of AKI as
one of the important factor affecting morbidity and mortality. Not
surprisingly, young age and sicker children were at increased risk of
AKI. Nearly half of survivors with AKI did not have complete recovery,
highlighting the importance of following up these children after
discharge.
The authors have stated that most common cause of AKI
is acute tubular necrosis (ATN). This may be an exaggeration as ATN is a
histopathological diagnosis and many of the conditions leading to AKI
may only affect glomerular filtration without compromising tubular
integrity. As seen in the study, one of the major limitations of AKIN
criteria is that children who do not have a baseline creatinine or who
have AKI at admission in whom serum creatinine is already elevated would
be missed. This will result in underestimating the incidence of AKI in a
country like ours where a significant proportion may have already
developed AKI at the time of hospitalization. Hence it would have been
valuable to evaluate pRIFLE in comparison to AKIN staging criteria and
their influence on outcome and risk factors for AKI. It is also known
that both the criteria identify somewhat different patients,
particularly in small children in whom small changes may have large
effect on AKI classification [5]. In order to overcome the lack of
baseline creatinine, it would have been interesting to use baseline
creatinine estimated by formula or use of age and gender specific norms
and compare it with measured baseline serum creatinine [6].
This study has shown that AKI is common and harmful.
As rightly pointed out by the authors, the study is underpowered to
examine the effect of AKI as an independent risk factor for mortality.
Adequately powered multicentre studies are required to generalize the
observations from the current study and also comprehensively identify
"at risk" population and evaluate short and long term outcomes. These
studies would also lay the foundation for evaluating more robust urine
and serum bio-markers in early identification and prognostication of
AKI, given the limitations of serum creatinine as a biomarker. The
initiation of nationwide AKI registry by Indian Society of Pediatric
Nephrology to capture the spectrum of AKI is a welcome step [7].
Competing interests: None stated. Funding:
Nil
References
1. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky
P; Acute Dialysis Quality Initiative workgroup. Acute renal failure:
Definition, outcome measures, animal models, fluid therapy and
information technology needs: The Second International Consensus
Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit
Care. 2004;8:R204-12.
2. Acute Kidney Injury Network. Mehta RL, Kellum JA,
Shah SV, Molitoris BA, Ronco C, Warnock DG, et al. Acute Kidney
Injury Network: Report of an initiative to improve outcomes in acute
kidney injury. Crit Care. 2007;11:R31.
3. Akcan-Arikan A, Zappitelli M, Loftis LL, Washburn
KK, Jefferson LS, Goldstein SL. Modified RIFLE criteria in critically
ill children with acute kidney injury. Kidney Int. 2007;71:1028-35.
4. Mehta P, Sinha A, Sami A, Hari P, Kalaivani M,
Gulati A, et al. Incidence of acute kidney injury in hospitalized
children. Indian Pediatr. 2012;49:537-42.
5. Joannidis M, Metnitz B, Bauer P, Schusterschitz N,
Moreno R, Druml W, et al. Acute kidney injury in critically ill
patients classified by AKIN versus RIFLE using the SAPS 3 database.
Intensive Care Med. 2009;35:1692-1702.
6. Alkandari O, Eddington KA, Hyder A, Gauvin F,
Ducruet T, Gottesman R, et al. Acute kidney injury is an
independent risk factor for pediatric intensive care unit mortality,
longer length of stay and prolonged mechanical ventilation in critically
ill children: a two-center retrospective cohort study. Crit Care. 2011;
15:R146.
7. Indian Society of Pediatric Nephrology. AKI
Registry Available from URL: http://124.247.216.178:8080/AKI. Accessed
April 17, 2012.
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