Pediatric Annals

Special Issue Article 

Acute Kidney Injury in Hospitalized Pediatric Patients

Rajit K. Basu, MD, MS, FCCM

Abstract

Acute kidney injury (AKI) is pervasive, affecting a significant proportion of critically ill and noncritically ill children. Recent data demonstrate a clear independent association of escalating AKI severity with not only mortality, but also with longer-term disability and chronic kidney disease in children. The paradigm has shifted—patients are no longer dying with AKI, but rather from AKI. In this review, AKI is described in the paradigms of “past,” “present,” and “future” to stimulate a reassessment of our understanding of this organ dysfunction syndrome. Current treatment strategies as well as novel methodologies are discussed. A global effort is required to make progress in the fight against AKI and improve patient outcomes. [Pediatr Ann. 2018;47(7):e286–e291.]

Abstract

Acute kidney injury (AKI) is pervasive, affecting a significant proportion of critically ill and noncritically ill children. Recent data demonstrate a clear independent association of escalating AKI severity with not only mortality, but also with longer-term disability and chronic kidney disease in children. The paradigm has shifted—patients are no longer dying with AKI, but rather from AKI. In this review, AKI is described in the paradigms of “past,” “present,” and “future” to stimulate a reassessment of our understanding of this organ dysfunction syndrome. Current treatment strategies as well as novel methodologies are discussed. A global effort is required to make progress in the fight against AKI and improve patient outcomes. [Pediatr Ann. 2018;47(7):e286–e291.]

Prior to standardized definitions of acute kidney injury (AKI), broad-scale study of AKI in hospitalized patients was difficult. Few large population studies were published on the epidemiology of renal failure. In critically ill adult patients, a review of nearly 30 studies conducted over 25 years showed that no two studies used the same criteria to define AKI.1 The resulting heterogeneity of the data made direct or indirect extrapolation of conclusions about the impact of AKI on patient outcomes impossible. Pediatric data were even more sparse than adult data, especially in children outside of the pediatric intensive care unit (PICU). A meta-analysis of all reported PICU patients demonstrated a wide incidence and associated mortality, but also highlighted the paucity of reliable data, discrepancies in diagnostic criteria, and heterogeneity in consistent assessment for renal failure.2 In the early 2000s, a consensus panel of experts (Acute Dialysis and Quality Initiative) published the first guideline to unify diagnostic strata used to diagnose acute renal failure (ARF) and renamed the disease process “acute kidney injury.”3 This stratification process allowed clinicians to compare and contrast population data from across the world, making possible the identification of actual epidemiologic signal. Additionally, the name change underscored the message that kidney damage was not simply a binary perturbation; rather, the kidneys suffered incremental injury and degradation similar to dysfunction of other vital organ systems. The RIFLE (Risk, Injury, Loss, and End-Stage Kidney Disease) staging criteria were updated with a time-to-elevation component and modified for pediatric use (pRIFLE).3,4 In 2012, a governing body of critical care nephrologists (Kidney Diseases Improving Global Outcomes [KDIGO]) published the most inclusive classification criteria for AKI diagnosis.5 These criteria are now the standard for AKI diagnosis in clinical care and epidemiologic research5 (Table 1).

Standardized Diagnostic Criteria of Acute Kidney Injury

Table 1:

Standardized Diagnostic Criteria of Acute Kidney Injury

The Past: Epidemiology of an Epidemic

Standardization of disease classification has facilitated an explosion of epidemiologic data about AKI in critical illness and has reshaped the understanding of disease prevalence and associated outcomes. A meta-analysis of more than 3.5 million critically ill adult patients from 154 publications reported an incidence of all-stage AKI of 23.2% with 8.8% having stage 2 or 3 AKI in the first 7 days of intensive care unit (ICU) admission.6 The report also highlighted the independent association of AKI with mortality. Adjusting for age, comorbidities, and severity of illness, escalating AKI severity was associated with escalating mortality. Stage 2 or 3 AKI was associated with 28.5% and 47.8% mortality, respectively. A study from 2015 of more than 2,000 critically ill adults from 214 centers reported an AKI incidence of greater than 50% in the first 7 days after admission, with a severe AKI-associated mortality rate of greater than 50%.7 A global pediatric epidemiologic assessment of AKI reported a strikingly parallel set of data. In 4,683 critically ill children, 26.9% suffered some degree of AKI within 7 days of PICU admission (11.6% with Stage 2 or 3 AKI).8 Just as in adults, escalating AKI severity in pediatric patients was found to be associated in step-wise fashion with increased mortality, independent of severity of illness.8 Even more striking, an epidemiologic survey of neonatal patients identified a nearly identical AKI incidence signal in premature infants.9 In a sample of 2,162 neonatal ICU patients, 30% suffered some form of AKI and those with severe AKI had increased mortality.9 The association of mortality with AKI is not just limited to the PICU environment; analysis of more than 29,000 admissions to general pediatrics wards demonstrated an increased rate of mortality for those with AKI.10 Aside from mortality, resource use and overall patient outcomes are worse for critically ill patients with AKI, including lengths of stay, duration of ventilation, and rates of infection. Compared to those without AKI, neurodevelopmental outcomes are worse for patients with AKI in the setting of sepsis.11 Even more distressing for the general pediatrician are data indicating the high incidence of chronic kidney disease (CKD) after AKI. Data from AKI in adults demonstrated a high rate of residual decrease in estimated glomerular filtration rate in surviving patients after AKI.12 Small, single-center data demonstrated persistent signs of kidney dysfunction after AKI in children.13 More recently, new data demonstrated a clear association of AKI after cardiopulmonary bypass with long-term signs of CKD.14

To date, no single effective therapy for AKI has been discovered. Many randomized, controlled clinical trials have described specific populations and have assessed for the impact of steroids, diuretics, vasoactive medications, and immune-modulating agents, all with negative results. Taken together, the entire history of AKI therapeutics has been narrowly focused on late, severe kidney injury and on trials conducted by consultant nephrologists, often after the diagnosis of AKI or ARF has been made.15

The global scope and impact of AKI should not be underestimated. Data from developing nations are rare, but one would assume that AKI rates and associated negative outcomes would be no different, if not worse, in those parts of the world.6 Further, appreciation of the AKI problem has lagged and is now catching up. A longitudinal study from Thailand lasting more than 2 decades provided an apt example: as appreciation of the disease process has grown (along with incorporation of standardized assessment metrics), the relative percentage of AKI in the population of admitted children has also increased.16

In total, AKI occurs frequently and makes outcomes worse, both in the short and long term. All pediatricians must shoulder the burden of caring for children recovering from AKI, as they are at high risk for CKD. General pediatricians and subspecialists should ask who will observe the kidney function of children after AKI as they grow into young adults? Unfortunately, a knowledge gap regarding AKI is widespread in the field of pediatric AKI.17 The first step forward for clinicians is to recognize the current state of diagnostics and treatable AKI-related complications.

The Present: Diagnosis and Management

Management guidelines for patients with AKI exist. Published in 2012, the KDIGO governing body promulgated a series of checklist items for directing clinicians to address for each stage of AKI in a hospitalized patient.18 Although pediatric-specific KDIGO guidelines are not yet published, many of the concepts can be generalized and applied to children (Table 2). Adherence to the guidelines in adults has been shown to mitigate not only AKI-associated negative patient outcomes, but also the progression of AKI in individual patients.17 Most guideline recommendations are currently part of routine clinical practice, including removal of offending agents (nonsteroidal anti-inflammatory medications and nephrotoxins) and optimization of supportive care. Of note, the guidelines have delineated action steps for patients at risk for AKI, but they offer no guidance toward how these at-risk patients should be identified.18

Acute Kidney Injury Management Guidelines: A Pediatric Modification to KDIGO Criteria

Table 2:

Acute Kidney Injury Management Guidelines: A Pediatric Modification to KDIGO Criteria

Given the lack of therapeutic options for established AKI, clinicians often struggle to identify modifiable aspects of the disease. A known complication of AKI is fluid accumulation. The management of fluid accumulation has long been recognized as important for end-organ function. Net negative and positive fluid states in hospitalized patients have been shown to affect the overall outcomes of patients with pneumonia and ARDS, septic shock, and congestive heart failure.19,20 It remains unclear whether AKI is a risk factor for fluid accumulation or whether fluid accumulation is a risk factor for AKI. The significant accumulation of fluid, or fluid overload, is increasingly associated with negative patient outcomes. The most prominent adult data emerged from the Fluid and Catheter Treatment Trial (FACCT)19,20 in which patients were randomized to liberal or conservative fluid management in the treatment of acute lung injury. Despite no impact on mortality, a major conclusion from this trial was that excessive net total positive fluid balance was associated with worse clinical outcomes. More data regarding fluid overload and associated outcomes now exist. In recent years, many single-center studies21 have described the negative impact of fluid overload on clinical outcomes in children, including after cardiac surgery, with respiratory failure, and with sepsis. A recent meta-analysis incorporating all available evidence from pediatrics concluded that excessive fluid overload is associated with negative patient outcomes, independent of severity of illness.21

Fluid balance is a modifiable aspect of critical illness and an intense focus of patient management in the PICU. Total fluid delivery and removal is addressed multiple times daily in critically ill patients. Failure to account for subtle daily changes in the net balance of fluids for a given patient leads to exaggerated fluid accumulation and likely does not account for the shifting fluid needs for a hospitalized patient. This is particularly important in pediatrics, as neonates, children, and young adults have a varied proportion of total body water as compared to the relative consistency that exists in adults.22,23 Proper adjudication of a patient's daily fluid needs, targets for net fluid balance, and initiation of fluid removal therapy (medical or mechanical) are basic steps toward alleviating the problem of fluid accumulation and overload, but this practice is not standardized.

AKI biomarkers may allow for the prediction of AKI and also information on the specifics of AKI–the when,21 the where,24 and the why.22 Unfortunately kidney-specific biomarkers have not been incorporated into routine practice or gained widespread acceptance. Individual biomarkers have failed to demonstrate efficacy for AKI prediction outside of specific controlled populations in which they are derived and validated. The concept of renal angina, an AKI risk-stratification methodology combining risk factors with early signs of kidney dysfunction, has been tested in several populations25,26 to optimize the use of confirmatory biomarkers for the prediction of high risk for severe AKI.27 If risk can be identified prior to injury, clinicians would potentially have the advantage of mitigating incipient injury, initiating earlier supportive therapy or stopping therapy deleterious to kidney function. Additionally, for patients at higher risk, more stringent attention to net fluid balance would be possible. Further, a recently suggested change of the nomenclature of “pre-renal” and “intrinsic” AKI to “functional” and “damage-associated” AKI has been issued as a first step to improve diagnostic precision.22 In a study of nearly 350 children after cardiopulmonary bypass, biomarker “combinations” predicted AKI earlier than changes in creatinine and also increased the specificity for the AKI temporal “phenotype” (ie, duration, severity, and injury reversibility).28 Taken together, the use of context-driven, targeted biomarker testing is being studied presently and is yielding more data, suggesting the metaphorical needle for AKI diagnosis can be moved (Figure 1). In addition to biomarkers, functional testing of the kidney can be performed. A standardized assessment of the response to furosemide administration (ie, the furosemide stress test) in adults demonstrated that 2-hour urine production after a dose of furosemide was predictive of not only AKI progression, but also use of continuous renal replacement therapy and mortality.29

In the timeline of kidney injury, changes in SCr and UOP are late. Biomarker changes may detect incipient injury before changes in GFR can be detected. Renal angina may identify patients at risk even earlier. GFR, glomerular filtration rate; SCr, serum creatinine; UOP, urine output.

Figure 1.

In the timeline of kidney injury, changes in SCr and UOP are late. Biomarker changes may detect incipient injury before changes in GFR can be detected. Renal angina may identify patients at risk even earlier. GFR, glomerular filtration rate; SCr, serum creatinine; UOP, urine output.

The electronic health/medical record can be leveraged to study AKI. AKI “sniffers” embedded in several hospital EHR systems studying ward patients have been found to increase the rate of AKI diagnosis and, potentially more importantly, lessen the time to AKI detection.30 An EHR-based nephrotoxin detection system, studied first in pediatrics, can reduce not only medication exposure, but also AKI incidence.31 Use of these systems offers the advantage of lessening the burden on cumbersome human-driven and reliant chart screening, data extraction, and analysis.

In summary, the state-of-the-art treatment for AKI is changing. The current data demonstrate that the status quo is wholly inadequate. Through novel methodologies such as risk stratification, biomarker phenotyping, kidney stress testing, and integration of detection strategies into the EHR, the field of AKI may be on the verge of a paradigm shift. Appreciation of risk factors for disease and earlier recognition of incipient injury revolutionized the approach to acute coronary syndrome. Prior to any medical or surgical advance for therapy, the fundamental understanding of these facets of the disease process started to shift the tide and improve patient outcomes. The same is possible for AKI.

The Future of AKI

The understanding of AKI is on the verge of a complete paradigm shift. AKI has been misunderstood for generations, but current studies aim to properly inform clinicians treating this disease. Pediatricians have been on the forefront of the changing face of AKI, being the first to introduce the concept of fluid overload as a standardized measurement, ushering in the era of biomarkers, and introducing the concept of AKI risk stratification. Future AKI therapeutics will not just simply be randomizing patients into binary cohorts of “positive” or “negative” injury, but rather will be personalized incorporating risk, biomarkers tested in combination, changes in biomarkers over time, and stress testing (all very early in a patient's course) to yield true AKI and fluid overload phenotypes (Figure 2). The data show AKI in hospitalized patients occurs frequently and is associated with poor patient outcome. AKI increases the standardized mortality in adults by 3-fold7 and in children8 and neonates9 by up to 10-fold. The time is now to leverage this data into effort and resources, ultimately enabling the discovery of therapeutic advances. If the needle is to be moved, pediatricians must educate themselves and band together to study this disease syndrome and its long-lasting effects.

Changing the approach to treating AKI means improving the precision of diagnostics, appreciating the heterogeneity in patients, and leveraging novel methodology. Critically ill patients could be risk stratified by the RAI embedded within the EMR in automated fashion. Patients fulfilling renal angina would be directed toward biomarker testing (A-E) and yield unique biomarker phenotypes, with combinations of biomarkers providing information regarding the location, type, and severity of injury. An FST would be performed on oliguric patients, ultimately yielding specific and unique AKI phenotypes for each patient. These phenotypes would thus identify subpopulations of people with AKI that could be randomized for study into targeted therapy (X, Y, Z) and studied for epidemiologic outcomes. AKI, acute kidney injury; EMR, electronic medical record; FL, fluid overload; FST, furosemide stress test; ICU, intensive care unit; RAI, renal angina index.

Figure 2.

Changing the approach to treating AKI means improving the precision of diagnostics, appreciating the heterogeneity in patients, and leveraging novel methodology. Critically ill patients could be risk stratified by the RAI embedded within the EMR in automated fashion. Patients fulfilling renal angina would be directed toward biomarker testing (A-E) and yield unique biomarker phenotypes, with combinations of biomarkers providing information regarding the location, type, and severity of injury. An FST would be performed on oliguric patients, ultimately yielding specific and unique AKI phenotypes for each patient. These phenotypes would thus identify subpopulations of people with AKI that could be randomized for study into targeted therapy (X, Y, Z) and studied for epidemiologic outcomes. AKI, acute kidney injury; EMR, electronic medical record; FL, fluid overload; FST, furosemide stress test; ICU, intensive care unit; RAI, renal angina index.

References

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Standardized Diagnostic Criteria of Acute Kidney Injury

Scheme Stage Creatinine Criteria Urine Output Criteria
RIFLE GFR decrease ≥25% or sCr increase by 1.5x GFR decrease ≥50% or sCr increase by 2x GFR decrease ≥75% or sCr increase by 3x or >4 mg/dL Persistent failure >4 weeks Persistent failure >3 months <0.5 mL/kg/h for 8 h <0.5 mL/kg/h for 16 h <0.3 mL/kg/h for 24 h (anuria 12 h)
Pediatric RIFLE eCCl decrease >25% eCCl decrease >50% eCCl decrease >75% or eCCl <35 mL/min/1.73 m2 Persistent failure >4 weeks Persistent failure >3 months <0.5 mL/kg/h for 8 h <0.5 mL/kg/h for 16 h <0.3 mL/kg/h for 24 h (anuria 12 h)
AKIN 1 2 3 Increase >0.3 mg/dL or to 150%–200% baseline Increase to 200%–300% baseline Increase to >300% baseline or >4 mg/dL with an acute increase of 0.5 mg/dL <0.5 mL/kg/h for 6 h <0.5 mL/kg/h for 12 h <0.3 mL/kg/h 24 h (anuria 12 h)
KDIGO 1 2 3 Increase >1.5–1.9x baseline (or >0.3 mg/dL increase) Increase >2–2.9x baseline >3x baseline Initiation of CRRT Decrease in eGFR to <35 mL/min/1.73 m2 <0.5 mL/kg/h for 6–12 h <0.5 mL/kg/h for >12 h <0.3 mL/kg/h >24 h (anuria 12 h)

Acute Kidney Injury Management Guidelines: A Pediatric Modification to KDIGO Criteria

Stage 1 Stage 2 Stage 3
Stop nephrotoxins Noninvasive diagnostic testing Renal dose medications
Optimize hemodynamics Daily weights and strict intakes and outputs If oliguric, nephrology consultation
Serial serum creatinine measurements Early renal replacement therapy
Record urine output (Foley catheter)
Avoid glycemic extremes (<60, >250 mg/dL)
Weigh risk-benefit of radiocontrast
Authors

Rajit K. Basu, MD, MS, FCCM, is a Research Director, Division of Critical Care Medicine, Children's Healthcare of Atlanta; and an Associate Profesor, Department of Pediatrics, Emory University.

Address correspondence to Rajit K. Basu, MD, MS, FCCM, Division of Critical Care Medicine, Children's Healthcare of Atlanta, 1405 Clifton Avenue, Atlanta, GA 30322; email: Rajit.basu@choa.org.

Disclosure: The author has no relevant financial relationships to disclose.

10.3928/19382359-20180619-02

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