Acute kidney injury (AKI) is “an abrupt (within 48 hours) reduction in kidney function defined as an absolute increase in serum creatinine by > 0.3 mg/dL or a relative increase of > 50% from baseline, or oliguria of < 0.5 mL/kg/h for > 6 hours.” This definition has replaced the old term acute renal failure, classically hallmarked by a sudden and rapid decline in glomerular filtration rate (GFR), leading to accumulation of nitrogenous wastes such as blood urea nitrogen (BUN) and creatinine. This change has been the result of a deliberate campaign by experts in the field to underscore the association of even subtle disturbances in renal function with adverse outcomes, while emphasizing that AKI is a continuum on a spectrum from subclinical renal injury to full-blown complete failure with total loss of kidney function. Even small increases in serum creatinine are now recognized as contributing to poor outcomes. In adults, an increase in serum creatinine of only 0.3 mg/dL was associated with increased mortality rates, even when controlling for significant patient comorbidity. Similar results were noted in pediatric patients with acute decompensated heart failure, in whom a 0.3-mg/dL or greater rise in serum creatinine demonstrated a 7-fold increased risk of mortality. These findings highlight the need for a focus on earlier detection and treatment of AKI, well before the serum creatinine begins to rise and other nonrenal complications ensue. With improved understanding about incomplete recovery from AKI episodes leading to chronic kidney disease (CKD) and the independent mortality and morbidity risk that AKI poses in hospitalized adults and children, AKI is now seen as a public health threat. Unfortunately, there are no satisfactory therapeutic options.
During the last decade, the definition of AKI has been standardized by the proposition and subsequent validation of consensus criteria. Currently, there are 3 standardized definitions for AKI that have been modified for and validated in pediatric patients, pRIFLE (Pediatric Risk, Injury, Failure, Loss, End-Stage Renal Disease), Acute Kidney Injury Network (AKIN), and Kidney Disease: Improving Global Outcomes (KDIGO) in chronological order (Table 467-1). All of these definitions rely on relative changes in serum creatinine from baseline and varying degrees of oliguria. Based on these definitions, we now know that AKI is a common finding in critically ill children, seen in as many as 30% of all children admitted to intensive care units (ICUs) and 50% of patients with shock, and increases risk of death by approximately 15-fold independent of comorbidities. Furthermore, mortality and renal morbidity rates increase with increasing AKI severity.
TABLE 467-1CURRENT STANDARDIZED CLASSIFICATION OF PEDIATRIC ACUTE KIDNEY INJURY (AKI) |Favorite Table|Download (.pdf) TABLE 467-1 CURRENT STANDARDIZED CLASSIFICATION OF PEDIATRIC ACUTE KIDNEY INJURY (AKI)
|AKI Staging ||KDIGO ||Pediatric-Modified AKIN (pAKIN) ||AKI Staging ||Pediatric-Modified RIFLE (pRIFLE) |
|Serum Creatinine ||Urine Output ||Serum Creatinine ||Urine Output ||Serum Creatinine ||Urine Output |
|Stage 1 ||1.5–1.9 times baseline or ≥ 0.3 mg/dL increase ||< 0.5 mL/kg/h for 6 to < 12 h || |
≥ 125–200% (1.25- to 2-fold) from ...