Management of Acute Kidney Injury in Critically Ill Children

Indian Journal of Pediatrics https://doi.org/10.1007/s12098-023-04483-2 REVIEW ARTICLE Management of Acute Kidney Injury in Critically Ill Children Sudarsan Krishnasamy1 · Aditi Sinha2 · Arvind Bagga2 Received: 17 July 2022 / Accepted: 9 January 2023 © The Author(s), under exclusive licence to Dr. K C Chaudhuri Foundation 2023 Abstract Acute kidney injury (AKI) is common in critically ill patients, affecting almost one in four critically ill children and one in three neonates. Higher stages of AKI portend worse outcomes. Identifying AKI timely and instituting appropriate measures to prevent and manage severe AKI is important, since it is independently associated with mortality. Methods to predict severe AKI should be applied to all critically ill patients. Assessment of volume status to prevent the development of fluid overload is useful to prevent adverse outcomes. Patients with metabolic or clinical complications of AKI need prompt kidney replacement therapy (KRT). Various modes of KRT are available, and the choice of modality depends most on the technical competence of the center, patient size, and hemodynamic stability. Given the significant risk of chronic kidney disease, patients with AKI require long-term follow-up. It is important to focus on improving awareness about AKI, incorporate AKI prevention as a quality initiative, and improve detection, prevention, and management of AKI with the aim of reducing acute and long-term morbidity and mortality. Keywords Kidney replacement therapy · Dialysis · Pediatric · AKI Introduction Acute kidney injury (AKI) is a clinical syndrome characterized by an abrupt decrease in kidney function, resulting in the accumulation of waste products and critical imbalances in fluid and electrolyte homeostasis. The term ‘AKI’ replaced ‘acute renal failure’ to encompass kidney dysfunction ranging from mildly elevated serum creatinine to severe forms requiring kidney replacement therapy (KRT) [1], emphasizing that even small increments in creatinine are associated with adverse short- and long-term outcomes. Definitions and Staging AKI has conventionally been defined and staged for severity based on serum creatinine and urine output (Table 1). The KDIGO criteria, which harmonize the AKIN with the RIFLE criteria, are most commonly used in adults and children [2]. The pediatric reference change value optimized criterion for AKI (pROCK), which is based on paired creatinine values in Chinese children admitted with nonrenal morbidities [3], might be more specific than KDIGO criteria in detecting ‘true’ AKI, but requires validation. Neonatal AKI is more difficult to identify. Serum creatinine at birth reflects maternal serum levels. Levels decline in the first few weeks, making ‘baseline’ creatinine dynamic. While sensitive, urine output is difficult to measure and is often preserved despite AKI due to tubular immaturity. The RIFLE and KDIGO definitions were adapted for neonates but require validation (Supplementary Table S1). In practice, an increase in creatinine by ≥ 0.3 mg/dL detects AKI better than a 50% rise in creatinine. A peak creatinine value of ≥ 2.5 mg/dL (~eGFR < 10 mL/min/1.73 m2) indicates severe AKI, and values ≥ 0.5 mg/dL at discharge are of concern [4]. Epidemiology * Aditi Sinha 1 Department of Pediatrics, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India 2 Division of Nephrology, Department of Pediatrics, All India Institute of Medical Sciences, New Delhi, India In a prospective report, AKI affected ~5% of hospitalized patients and ~30% of patients in the pediatric intensive care unit (PICU) [5]. Three multicenter studies inform on the global epidemiology of pediatric AKI. Using KDIGO criteria, the Assessment of Worldwide Acute Kidney Injury, Renal Angina, and Epidemiology (AWARE) study reported AKI in 26.9% of critically ill 13 Vol.:(0123456789) Indian Journal of Pediatrics Table 1  Definitions and staging of acute kidney injury (AKI) Stage pRIFLE eCrCla AKIN Serum creatinine KDIGO Serum creatinine pROCK Serum creatinineb 1 ↓ by 25% (risk) ↑ by ≥ 0.3 mg/dL in ≤ 48 h or to ≥ 1.5 times the baseline 2 ↓ by 50% (injury) ↑ to 2 to < 3 times baseline ↑ by ≥ 0.3 mg/dL in ≤ 48 h or to 1.5–1.9 times the baseline within 7 d ↑ to 2.0–2.9 times the baseline within 7 d 3 ↓ by 75% (failure) ≥ 3 times the baseline, or ≥ 3 times the baseline, or to ≥ 4 mg/dL, or initiation to ≥ 4 mg/dL with an acute rise of KRT of ≥ 0.5 mg/dL, or initiation of KRT ↑ by ≥ 20 µmol/L (0.23 mg/dL) and a relative increase by ≥ 30% within 7 d ↑ by ≥ 40 µmol/L (0.45 mg/dL) and a relative increase by ≥ 60% within 7 d ↑ by ≥ 80 µmol/L (0.91 mg/ dL) and a relative increase by ≥ 120% within 7 d Stage pRIFLE Urine output AKIN Urine output KDIGO Urine output pROCK 1 2 3 < 0.5 mL/kg/h for 8 h (risk) < 0.5 mL/kg/h for 16 h (injury) < 0.3 mL/kg/h for 24 h or anuria for 12 h (failure) < 0.5 mL/kg/h for 6 h < 0.5 mL/kg/h for 12 h < 0.3 mL/kg/h for ≥ 24 h, or anuria ≥ 12 h < 0.5 mL/kg/h for 6–12 h < 0.5 mL/kg/h for ≥ 12 h < 0.3 mL/kg/h for ≥ 24 h, or anuria for ≥ 12 h No recommendation ↓ decrease, ↑ increase, AKIN Acute kidney injury network, KDIGO Kidney disease improving global outcomes, KRT Kidney replacement therapy, pRIFLE Pediatric risk injury failure loss and end-stage, pROCK Pediatric reference change values optimized for AKI in children a Terms in parentheses indicate the stage in the pRIFLE criteria. The terms ‘loss’ and ‘end-stage’ in the pRIFLE criteria, referring to persistent AKI for > 4 wk and > 3 mo, respectively, do not have corresponding stages in the AKIN, KDIGO, and pROCK criteria. Estimated creatinine clearance calculated from Schwartz formula; with the lowest serum creatinine value in the preceding 3 mo taken as baseline b Based on an absolute serum creatinine increase beyond the reference change value (RCV) and a relative % increase from baseline within 7 d; pROCK criteria do not have the urine output criterion patients [6]. The Assessment of Worldwide Acute Kidney Injury Epidemiology in Neonates (AWAKEN) study reported AKI in 29.9% newborns, most commonly in those born at < 29 wk of gestation [7]. In the 0by25 Global Snapshot study, similar proportions of hospitalized patients had community-acquired and incident AKI [8]. Patients with AKI in low- and middle-income countries were older than their counterparts in high-income countries, usually had community-acquired AKI, and commonly had severe AKI [8]. Etiology and Risk Factors Based on pathophysiology, AKI is categorized as prerenal or functional, renal or intrinsic, and postrenal or obstructive. The Acute Dialysis Quality Initiative network summarized the risk factors into environmental, socioeconomic/ cultural, process of care, acute exposures, and inherent factors [9]. Risk factors, etiology, and outcomes of AKI differ between resource-limited and resource-sufficient regions and for community-acquired and hospital- (...truncated)