Acute Kidney Injury

Acute kidney injury (AKI) is broadly defined as an abrupt decline in renal function with or without decreased urine output. In critically ill patients, AKI is frequently associated with increased morbidity, mortality, and length of hospitalization. AKI in neonates is also associated with increased mortality and longer hospital stay. Although AKI may be an isolated event, up to 30% of children have ongoing renal dysfunction and can be at higher risk for developing hypertension.

Classification Criteria

Several classification criteria for AKI have been developed primarily for research purposes to standardize the definition of AKI across clinical settings:

• RIFLE criteria: developed in 2004 by the Acute Dialysis Quality Initiative group and modified in 2007 for use in children (Pediatric Risk, Injury, Failure, Loss, End-Stage Renal Disease, or pRIFLE)

• AKIN criteria: developed in 2007 by the Acute Dialysis Quality Initiative group to modify the RIFLE criteria to reflect increases in serum creatinine of 0.3 mg/dL in a 48-hour period in adults

• KDIGO AKI criteria: developed in 2012 by the Kidney Disease Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group; integrates RIFLE, pRIFLE, and AKIN definitions for pediatric AKI; these criteria are the most frequently used in clinical practice; KDIGO is in the process of updating the 2012 guideline

(Source: Acute Kidney Injury in Children: An Update on Diagnosis and Treatment. Pediatr Clin North Am 2013.)

The bedside Schwartz equation is used to estimate a patient’s glomerular filtration rate (GFR). The estimated glomerular filtration rate (eGFR), applicable to children ages 1 to 18 years, is based on creatinine values verified by isotope-dilution mass spectrometry. The present pediatric equation was derived from data obtained from baseline visits of 349 children in the Chronic Kidney Disease Study in Children (CKiD) and was simplified in 2009 to a formula that only includes only two variables (see also CKD/ESKD section in this rotation guide):

Bedside Schwartz Equation: eGFR (mL/min/1.73m²) = 0.413 x [patient height (cm)/serum creatinine (mg/dL)]

Caveats for the use of AKI criteria in children:

• Serum creatinine measurement at a given point in time will not reflect a steady-state GFR because AKI is a dynamic process.

• Creatinine is a natural waste product that is created through metabolism of muscle cells. Children have lower muscle mass and consequently lower baseline serum creatinine than adults. Therefore, smaller changes in serum creatinine may reflect mild or even moderate AKI, especially in younger children.

• Brief periods of oliguria are not necessarily indicative of AKI and can result from other causes (e.g., inadequate fluid resuscitation, urinary retention).

Risk Factors

Patients with reduced nephron endowment or who are exposed to nephrotoxic conditions are at risk of developing AKI. Therefore, the following categories of hospitalized children are at high risk of developing AKI:

• preterm infants

• children who undergo cardiac bypass

• children receiving chemotherapy or hematopoietic stem-cell transplantation

• children with underlying chronic kidney disease (CKD)

Etiology

Individual patients may have more than one cause underlying an AKI event. A useful framework is to classify causative factors as contributing to one of the following categories:

• prerenal factors (decreased renal perfusion)

  • third-spacing of fluids (e.g., hypoalbuminemia in nephrotic syndrome or protein-losing enteropathy)

  • hypotension

  • heart failure

  • liver dysfunction

  • renovascular disease (e.g., thrombus)

  • shock states (e.g., hypovolemic, septic, cardiogenic)

• intrinsic factors (intrinsic damage to the renal parenchyma)

  • acute tubular necrosis

  • glomerular disease

  • thrombotic microangiopathies (e.g., hemolytic uremic syndrome)

  • renal vasculitis

  • tubulointerstitial nephritis (e.g., drug exposure)

• postrenal/obstructive factors

  • congenital anomalies of the kidneys and urinary tract (CAKUT; e.g., posterior urethral valves, ureteropelvic junction obstruction)

  • nephrolithiasis

  • tumors and masses

Diagnosis

• history and physical exam to identify potential etiologies of AKI, including evaluation for:

  • dehydration

  • recent nephrotoxic exposures

  • findings suggestive of primary renal disease (e.g., gross hematuria, edema, hypertension) or systemic disease (e.g., recurrent fevers, joint pain, rash)

  • abnormal voiding pattern (e.g., urinary retention, weak urinary stream)

• urinalysis and microscopy

• lab evaluation: serum chemistries with blood urea nitrogen (BUN) and creatinine

• imaging: renal and bladder ultrasound

Management

• Alter medication dosing of renally cleared medications after calculating eGFR.

• Reduce or eliminate nephrotoxin exposures (e.g., antibiotics, contrast agents, nonsteroidal anti-inflammatory drugs [NSAIDs]).

• Maintain renal perfusion.

• Correct electrolyte abnormalities.

• Control volume status.

• Consider renal replacement therapy (e.g., dialysis).