Ding X, Rosner MH, Ronco C (eds): Acute Kidney Injury ā Basic Research and Clinical Practice. Contrib Nephrol. Basel, Karger, 2018, vol 193, pp 1ā12 (DOI: 10.1159/000484956)
______________________
Acute Kidney Injury: Diagnosis and Classification in Adults and Children
Zaccaria Riccia Ā· Stefano Romagnolib
aDepartment of Cardiology and Cardiac Surgery, Pediatric Cardiac Intensive Care Unit, Bambino GesĆ¹ Childrenās Hospital, IRCCS, Rome, and bDepartment of Anesthesia and Intensive Care, Azienda Ospedaliero-Universitaria Careggi, Florence, Italy
______________________
Abstract
Background: The acute reduction of kidney function in critically and noncritically ill patients (regardless of their age) is one of the deadliest clinical conditions ever reported in modern medicine. Acute kidney injury (AKI) symptoms are sneaky and potentially difficult to be identified at the right time at the bedside. One of the greatest efforts of the recent history of critical care nephrology has been to find a common classification for AKI definition and staging with the purpose of allowing a timely diagnosis and push forward epidemiologic research. Summary: AKI is currently defined by the Kidney Disease Improving Global Outcomes (KDIGO) consensus classification that applies conventional serum creatinine and urine output (UO) criteria. According to a recent large epidemiologic study, this classification led to the confirmation that AKI occurs in about half of adult critically ill patients admitted to the intensive care unit and that a stepwise increase in mortality is associated with the severity of AKI along KDIGO stages. Both serum creatinine and UO have inherent limitations in accurately diagnosing abrupt decreases of renal function, but their common and easy application in routine clinical practice is currently considered the standard of care for AKI diagnosis. Pediatric and neonatal AKI have recently been described and specific staging with KDIGO modification has been proposed. Key Messages: AKI is frequent in critically ill patients and significantly affects intensive outcomes independent of other clinical factors. AKI can be diagnosed and its severity accurately staged by the KDIGO classification and its modification for pediatric patients. Serum creatinine and UO criteria are applied in order to diagnose and stage AKI. Despite some significant limitations of these commonly applied biomarkers, their application has made it possible to clearly appraise the importance of accurate AKI identification in clinical practice in several studies for prognostic and therapeutic purposes.
Ā© 2018 S. Karger AG, Basel
Introduction
Acute kidney injury (AKI) is one of the most common diseases among adult and pediatric critically ill patients admitted to the intensive care unit (ICU) and it is associated with severe short- and long-term complications, including increased mortality [1]. AKI is characterized by a rapid decline in kidney function mostly referred to a decrease in glomerular filtration rate (GFR). Since the (re)-establishment and optimization of hemodynamics with adequate intravascular volume, cardiac output and perfusion pressure are the only effective therapeutic interventions in patients with decreased GFR [2], early identification and diagnosis is crucial. This chapter reviews the evolution of diagnostic criteria of AKI, both in adult and pediatric setting, the currently recommended definition, and its major limitations.
AKI Definition and Classification in Adult Patients
The field of critical care nephrology and AKI has been hampered by the long-standing lack of a standardized system to diagnose and classify this syndrome. Over the years, a number of different definitions have been applied without well-defined terms identifying āacute renal failureā or āacute tubular necrosis.ā As a demonstration of the confusion that reigned around renal failure in the past, a survey conducted in 2004 during an international meeting on Critical Care Nephrology showed that more than 200 different definitions of AKI were provided by the involved clinicians [3]. The first innovative and revolutionary step in the AKI definition was performed by the Dialysis Quality Initiative (ADQI) Group in 2004 [4]. The ADQI consensus founded the Risk, Injury, Failure, Loss and End-stage Kidney (RIFLE) criteria identifying the following categories: āat Riskā is the least severe category of AKI, followed by āInjury,ā āFailure,ā āLossā and āEnd-stage renal diseaseā (Table 1). Diagnosis and staging severity were based on two āstrategicā parameters: a rise in serum creatinine level (SCr) from a baseline value and/or a decrease in urine output (UO) per kilogram of body weight over a specified time period (7 days) as surrogates for GFR. This first classification did not aim to predict mortality or adverse outcomes; it also did not aim to trigger standardized therapeutic interventions but was conceived to start a fundamental process for AKI definition and āexactā detection, at least for epidemiologic purposes. Furthermore, a primary message was clearly stated: AKI is not a āyesā or ānoā condition but is characterized by a progressive disease severity, where the more advanced the renal dysfunction is the worse the clinical picture and therefore the outcomes would be. In 2007, the AKI definition evolved from the RIFLE criteria into the AKI Network classification, known as the Acute Kidney Injury Network (AKIN) criteria [5] (Table 1). According to the AKIN criteria, AKI severity has been divided into 3 stages of escalating severity (1, 2, and 3), while the old RIFLE-Loss and end-stage renal disease were eliminated, since considered prognostic classes, without classification purposes. Another relevant difference between the RIFLE and AKIN criteria is the 48-h time-frame within which the diagnosis of AKI must be made to fulfill the AKIN criteria. The last classification released in 2012 was born in an attempt of reconciling all previous ones: The Kidney Disease Improving Global Outcomes (KDIGO) consensus classification [6] (Table 1). According to the KDIGO criteria, AKI is diagnosed if SCr increases by 0.3 mg/dL (or ā„26.5 Ī¼mol/L) in ā¤48 h, or rises to ā„1.5-fold from baseline within the prior 7 days and/or a decrease in UO <0.5 mL/kg/h for 6ā12 h. This initial dysfunction identifies the stage 1 of AKI. AKI stage 2 is reached when there is an increase in SCr 2.0ā2.9 times from baseline and/or UO <0.5 mL/kg/h for ā„12 h. Finally, stage 3 occurs when there is an increase in SCr 3.0 times from baseline or to 4 mg/dL (or ā„353.6 Ī¼mol/L), or initiation of renal replacement therapy irrespective of SCr and/or UO <0.3 mL/kg/h for ā„24 h, or anuria for ā„12 h. In patients <18 years, there is a decrease in estimated GFR (eGFR) to <35 mL/min/1.73 m2.
Table 1. RIFLE, pRIFLE, AKIN, KDIGO, neonatal KDIGO criteria for acute kidney injury
System | SCr criteria | UO criteria |
RIFLE criteria |
Risk | SCr increase to 1.5-fold or GFR decrease >25% from baseline | <0.5 mL/kg/h for 6 h |
Injury | SCr increase to 2.0-fold or GFR decrease >50% from baseline | <0.5 mL/kg/h for 12 h |
Failure | SCr increase to 3.0-fold or GFR decrease >75% from baseline or SCr ā„4 mg/dL (ā„354 Ī¼mol/L) with an acute increase of at least 0.5 mg/Dl (44 Ī¼mol/L) | ā¤0.3 mL/kg/h Ć 24 h or anuria Ć 12 h |
Loss | Persistent AKI = complete loss of kidney function >4 weeks | |
End-stage renal disease | End stage kidney disease (>3 months) | |
pRIFLE criteria | | |
Risk | eCCl decrease by 25% | <0.5 mL/kg/h for 8 h |
Injury | eCCl decrease by 50% | <0.5 mL/kg/h for 16 h |
Failure | eCCl decrease by 75% or eCCl <35 mL/min/1.73 m2 | ā¤0.3 mL/kg/h Ć 24 h or anuria Ć 12 h |
Loss | Persistent complete loss of kidney function >4 weeks | |
End-stage renal disease | End stage kidney disease (>3 months) | |
AKIN criteria | | |
Stage 1 | SCr increase ā„0.3 mg/dL (ā„26.5 Ī¼mol/L) or increase to 1.5- to 2.0-fold from Baseline | <0.5 ml/kg/h for 6 h |
Stage 2 | SCr increase >2.0- to 3.0-fold from baseline | <0.5 mL/kg/h for 12 h |
Stage 3 | SCr increase >3.0-fold from baseline or serum creatinine ā„4.0 mg/dL (ā„354 Ī¼mol/L) with an acute increase of at least 0.5 mg/dL (44 Ī¼mol/L) or need for RRT | <0.3 mL/kg/h for 24 h or anuria for 12 h or need for RRT |
KDIGO criteria | | |
Stage 1 | SCr increase ā„0.3 mg/dL... |