DESCRIPTION

• Acute kidney injury (AKI) is defined as an abrupt (within 48 hours) reduction in kidney function with an absolute increase in serum creatinine of ≥0.3 mg/dL or a 1.5-fold increase from baseline or a reduction in urine output (documented oliguria of <0.5 mL/kg/h for >6 hours).
• In AKI, the urine output is variable: Anuria, oliguria, and, in some cases, polyuria can all be observed at presentation.

EPIDEMIOLOGY

• The epidemiology of AKI has changed from primary kidney disease to a syndrome secondary to other systemic illness or associated treatment.
  • Only 7–10% of AKI is secondary to primary isolated kidney disease.
• AKI may be seen in up to 10% of all hospitalized children.
  • The incidence is higher in intensive care unit (ICU) admissions and with increasing multiorgan disease severity.
  • AKI is seen in 27% of children admitted to a PICU or NICU.

ETIOLOGY

Previously, AKI was subcategorized into three groups: prerenal, renal, and postrenal. The differentiation between “prerenal” and “intrinsic” causes can be difficult because renal hypoperfusion may coexist with any stage of AKI. For that reason, “functional” has replaced prerenal, and “structural” has replaced intrinsic in the terminology.

• Functional
  • Decreased glomerular filtration rate (GFR) resulting from renal hypoperfusion in a structurally intact kidney
  • Often reversible when the underlying cause is corrected (e.g., rehydration)
• Structural
  • Disorders that directly affect the kidney
  • Acute tubular necrosis (ATN) was used in the past to describe a form of intrinsic AKI from severe and persistent hypoperfusion of the kidneys. However, the histologic diagnosis of tubular necrosis is rarely confirmed by biopsy.
  • Glomerular disorders include the various forms of acute glomerulonephritis (AGN) (e.g., postinfectious, rapidly progressive [crescentic]).
  • Vascular lesions compromise glomerular blood flow. Hemolytic uremic syndrome (HUS) is the most common vascular disorder that causes intrinsic AKI in children.
  • Acute interstitial nephritis (AIN) most often occurs as a result of exposure to medications such as nonsteroidal anti-inflammatory drugs (NSAIDs). It may also be associated with infections (e.g., pyelonephritis), systemic diseases, or tumor infiltrates.
• Postrenal
  • Obstructive process (either structural or functional)
  • Obstruction can be in the lower tract or bilaterally in the upper tracts (unless the patient has a single kidney).
  • More common in newborns

PATHOPHYSIOLOGY

The pathogenesis of AKI is multifactorial. It may be initiated by ischemia or toxins, and the subsequent injury involves a complex interplay between vasoconstriction, leukostasis, vascular congestion, cell death, and abnormal immune modulators.