Address For Correspondence:
R Bhimma, Department of Pediatrics & Child Health, Nelson R Mandela School of Medicine, University of Kwazulu-Natal, Private Bag 7, Congella, 4013, South Africa.
Email: bhimma@ukzn.ac.za

Introduction

Acute renal failure (ARF) is now being more often referred to as acute kidney injury (AKI) and will be done so for the rest of this paper. AKI is defined as an abrupt or rapid decline in glomerular filtration rate (GRF) usually accompanied by a rise in serum creatinine and blood urea nitrogen (azotaemia). It is important to note that a rise in creatinine and urea may not be present immediately after kidney injury and that the only sign of AKI may be decreased urine production. Other factors may result in increased creatinine levels due to inhibition of renal tubular secretion such as medication (e.g. cimetidine, trimethoprim). Similarly blood urea levels may rise from gastrointestinal or mucosal bleeding, steroid use, protein loading and rhabdomyolysis [1, 2].

Although the majority of children with AKI recover completely after appropriate therapy, children who have suffered AKI from any cause are at risk for late development of kidney disease several years after the initial insult [3]. Recent studies show that the incidence of AKI in hospitalised children is increasing worldwide [4-13] particularly in the setting of post-cardiac surgery and in children undergoing stem cell transplantation.

Paediatric retrospective studies have reported incidences of AKI in paediatric intensive care units of between 8-30% [4,5,12,14]. Most studies have shown that neonates have higher rates of AKI, especially following cardiac surgery, severe asphyxia, or premature birth [6,13]. Other factors linked to the development of AKI in neonates include very low birth weight (less than 1500g), a low Apgar score, a patent ductus arteriosus, and maternal receipt of antibiotics or non-steroidal anti-inflammatory drugs during pregnancy [9]. The incidence of AKI in newborns in a developing country was 3.9 /1000 live births and 34.5/1000 newborns admitted to the neonatal unit [10].

Children with AKI due to acute interstitial nephritis, nephrotoxic renal insults including aminoglycoside nephrotoxicity, and contrast nephropathy usually have normal urine output. On the other hand, oliguria (urine output less than 500ml per 24 hours in older children or urine output less than 1ml/kg per hour in younger children and infants) or anuria (urine output less than 100ml/day in older children or less than 0.5ml/kg per hour in younger children and infants) is more likely to be present in children with AKI due to hypoxia or ischemic insults, haemolytic uremic syndrome, acute glomerulonephritis and other causes [15].