Acute kidney injury (AKI), formerly known as ‘acute renal failure,’ is an important clinical entity accounting for about 3–5% of patients admitted to hospitals [
1], and 20% in pediatric, 30% in neonatal and 40–60% in cardiac intensive care units [
2,
3]. AKI in infants constitutes about 30% of total admitted children [
4]. In neonates, sepsis, hypoxic/ischemic injury, hypernatremic dehydration, posterior urethral valves and post-cardiac surgery are predominant etiologies [
5‐
7], while acute gastroenteritis causing hypovolemia, sepsis, hemolytic uremic syndrome, diabetic ketoacidosis, malaria and post-bone marrow or stem cell transplant are common in older infants and children [
8‐
11]. Serum creatinine is not a reliable marker to detect AKI as it rises when about 50% of the glomerular function is decreased and also is affected by height, gender, body mass and hydration status. Management strategy essentially includes correction of fluid and electrolyte imbalance, treatment of underlying conditions, avoidance of nephrotoxic medications and dialytic support, as and when needed. However, it is associated with higher mortality as well as being a potential risk factor for progression to acute kidney disease and residual kidney injury [
12]. Therefore, in clinical practice there is a need for early detection, institution of therapeutic measures and prevention of further kidney damage. …
