Pediatr Nephrol (2009) 24:253–263 DOI 10.1007/s00467-008-1074-9 EDUCATIONAL REVIEW Acute kidney injury in children Sharon Phillips Andreoli Received: 19 November 2007 / Revised: 17 November 2008 / Accepted: 18 November 2008 / Published online: 13 December 2008 # IPNA 2008 Abstract Acute kidney injury (AKI) (previously called acute renal failure) is characterized by a reversible increase in the blood concentration of creatinine and nitrogenous waste products and by the inability of the kidney to regulate fluid and electrolyte homeostasis appropriately. The inci- dence of AKI in children appears to be increasing, and the etiology of AKI over the past decades has shifted from primary renal disease to multifactorial causes, particularly in hospitalized children. Genetic factors may predispose some children to AKI. Renal injury can be divided into pre- renal failure, intrinsic renal disease including vascular insults, and obstructive uropathies. The pathophysiology of hypoxia/ischemia-induced AKI is not well understood, but significant progress in elucidating the cellular, bio- chemical and molecular events has been made over the past several years. The history, physical examination, and laboratory studies, including urinalysis and radiographic studies, can establish the likely cause(s) of AKI. Many interventions such as ‘renal-dose dopamine’ and diuretic therapy have been shown not to alter the course of AKI. The prognosis of AKI is highly dependent on the underlying etiology of the AKI. Children who have suffered AKI from any cause are at risk for late develop- ment of kidney disease several years after the initial insult. Therapeutic interventions in AKI have been largely S. P. Andreoli Department of Pediatrics, James Whitcomb Riley Hospital for Children, Indiana University Medical Center, Indianapolis, IN, USA S. P. Andreoli (*) Riley Research Room 230, 699 West Street, Indianapolis, IN 46077, USA e-mail: sandreol@iupui.edu disappointing, likely due to the complex nature of the pathophysiology of AKI, the fact that the serum creatinine concentration is an insensitive measure of kidney function, and because of co-morbid factors in treated patients. Improved understanding of the pathophysiology of AKI, early biomarkers of AKI, and better classification of AKI are needed for the development of successful therapeutic strategies for the treatment of AKI. Keywords Acute renal failure . Acute kidney injury . Hypoxic/ischemic injury . Acute tubular necrosis Introduction Acute kidney injury (AKI) (previously called acute renal failure) is characterized by a reversible increase in the blood concentration of creatinine and nitrogenous waste products and by the inability of the kidney to regulate fluid and electrolyte homeostasis appropriately. There are many causes of AKI, and the more common ones are listed in Table 1. Some causes of AKI, such as rapidly progressive glomeru- lonephritis (RPGN), may present as AKI but rapidly evolve into chronic kidney disease (CKD). Several renal diseases, such as the hemolytic–uremic syndrome (HUS), Henoch– Schönlein purpura, and obstructive uropathy with associated renal dysplasia, may present as AKI with improvement of renal function to normal or near-normal levels, but the child’s renal function may slowly deteriorate, leading to CKD several months to years later. Children with AKI due to hypoxic/ischemic insults, HUS, acute glomerulonephritis and other causes are more likely to demonstrate oliguria or anuria (urine output less than 500 ml/24 h in older children or urine output less than 1 ml/kg per hour in younger children and infants). Children