Acute kidney injury (AKI) is common in critically ill children, and is associated with increased mortality and long-term renal sequelae. The definition of pediatric AKI was standardized based on elevation in serum creatinine levels or decrease in urine output; accordingly, epidemiological studies have ensued. Although new biomarkers appear to detect AKI earlier and predict prognosis more accurately than traditional markers, they are not frequently used in clinical setting. There is no validated pharmacological intervention for AKI, so prevention and early detection are the mainstays of treatment. For high risk or early stage AKI patients, optimization of volume status and blood pressure, avoidance of nephrotoxins, and sufficient nutritional support are necessary, and have been demonstrated to be effective in preventing the occurrence of AKI and improving prognosis. Nevertheless, renal replacement therapy is needed when conservative care fails.
Acute kidney injury (AKI) is characterized by an abrupt deterioration of kidney function, and is common in critically ill children and adults. It occurs in approximately 30% of pediatric intensive care unit (PICU) [
In 2012, the Kidney Disease: Improving Global Outcomes (KDIGO) criteria were established, and provided a standardized definition of AKI in children and adults [
Physicians sometimes, however, experience difficulty in diagnosing and staging AKI using the KDIGO definition. Many patients exhibit elevated serum creatinine levels without previous measurement. It is not integrated to set baseline value without available measurement data within 48 h, as specified by the KDIGO criteria. Some have used the lowest serum creatinine level measured before or after AKI as a baseline value. Others propose that the baseline serum creatinine level can calculate backward using an estimated glomerular filtration rate (eGFR) of 100–120mL/min/1.73 m2, assuming that previous kidney function was norma [
For neonates, the neonatal modified KDIGO definition was used in a recent large cohort (
Serum creatinine is currently widely used as a biomarker for AKI; however, it has some limitations. It is insensitive to small changes in GFR, and is not a real-time indicator. It may not change until up to 50% of kidney function is lost [
Serum cystatin C is produced by all nucleated cells and, is therefore, unaffected by clinical factors [
Despite the excellent performance of new biomarkers, they are not frequently used in clinical setting due to several concerns. First, they were validated for specific etiologies of AKI, such as pediatric patients undergoing cardiac surgery, and their efficacy cannot be reproduced in AKIs of different etiologies [
Two large, multinational epidemiological studies have been published in the pediatric and neonatal areas [
In the pediatric literature, AKI is consistently associated with poor outcomes, similar to adults. Many studies have demonstrated that AKI is an independent risk factor for prolonged stay in the PICU, longer duration of mechanical ventilation, and increased mortality among critically ill children [
There are no effective medications for established AKI. Therefore, prevention and early detection are the mainstays of management. Monitoring high-risk patients and reducing additional risk factors can prevent the occurrence of AKI and improve outcomes. Prematurity, and chronic diseases such as CKD render the host susceptible to AKI, and events such as volume depletion, exposure to nephrotoxins, sepsis, major surgery, and critical illness lead to AKI [
Despite its importance, physicians often do not devote attention to the accumulation of risk factors and early decline of kidney function as they perform or attend to other important aspects of care [
Supportive care comprises optimization of volume status, blood pressure, avoidance of nephrotoxic agents, and nutritional support. It is important to maintain adequate renal perfusion through fluid and hemodynamic management [
The proper type of fluid should be administered to prevent volume depletion. Crystalloids are the preferred solutions because data supporting the routine use of colloids for volume resuscitation are lacking [
Maintaining optimal blood pressure is crucial, although there is no currently definitive target value for pediatric AKI. For patients with hypotension, fluid resuscitation is initially considered if hypotension is due even partially to hypovolemia [
Nephrotoxin exposure is one of the most common causes of AKI in hospitalized children [
Nutritional support is important for improving outcomes in children with AKI. For critically ill children with AKI, nutritional requirements should be individualized and assessed frequently [
Many researchers have investigated candidate medications to prevent and treat AKI. Anti-inflammatory, antioxidative and antiapoptotic interventions are representative examples; however, their yield remains insignificant. Although a few medications have demonstrated effectiveness in certain situations, most have yielded negative or conflicting results. Medications advocated in the past were not proven to be effective. The KDIGO guideline recommend NAC to prevent contrast-induced AKI in high-risk patients [
RRT is required when conservative care fails. Indications for RRT include fluid overload (severe hypertension or pulmonary edema), severe hyperkalemia, metabolic acidosis, and severe uremia [
AKI has attracted attention because of its high prevalence and association with poor outcomes. Many studies have been conducted to identify new biomarkers and effective pharmacological interventions, and significant improvements have been achieved. Unfortunately, however, not many have been applied in actual clinical practice. Considering the gap between research achievements in adults and children, pediatric nephrologists have much to contribute to developments in understanding and treating AKI.
This research did not receive any specific grant from funding agencies in the public, commercial, or not-forprofit sectors.
No potential conflict of interest relevant to this article was reported.
Definitions and Staging of Kidney Disease: Improving Global Outcomes (KDIGO) and Neonatal Modified KDIGO Criteria for Acute Kidney Injury
Stage | Pediatric KDIGO criteria |
Neonatal modified KDIGO criteria |
||
---|---|---|---|---|
Serum creatinine | Urine output | Serum creatinine | Urine output | |
1 | 1.5–1.9 times baseline within 7 days | <0.5 mL/kg/h for 6–12 h | 1.5–1.9 times baseline |
>0.5 and ≤ 1 mL/kg/h |
OR | OR | over 24 h | ||
≥0.3 mg/dL increase within 48 h | ≥0.3 mg/dL increase within 48 h | |||
2 | 2.0–2.9 times baseline | <0.5 mL/kg/h for ≥12 h | 2.0–2.9 times baseline |
>0.3 and ≤0.5 mL/kg/h |
over 24 h | ||||
3 | ≥3.0 times baseline | <0.3 mL/kg/h for ≥24 h | ≥3.0 times baseline |
≤0.3 mL/kg/h over 24 h |
OR | OR | OR | ||
Increase in serum creatinine to ≥4.0 mg/dL | Anuria for ≥12 h | Increase in serum creatinine to ≥2.5 mg/dL | ||
OR | OR | |||
Initiation of renal replacement therapy | Initiation of renal replacement therapy | |||
OR | ||||
Decrease in eGFR to <35 mL/min per 1.73 m2 |
Baseline serum creatinine is the lowest previous value.
Abbreviation: eGFR, estimated glomerular filtration rate.