Purpose of ReviewAcute kidney injury (AKI) in children is a common and serious condition associated with significant morbidity, mortality and risk of long-term adverse outcomes. Although historically under-recognized, pediatric AKI is now better defined using standardized international criteria, including pRIFLE, AKIN and KDIGO, which have improved epidemiologic insights and early detection. However, despite the advances in AKI detection and management, there continues to be a high burden of both short and long term morbidity in AKI survivors.Recent FindingsKey developments in the sphere of AKI centre around earlier detection and institution of management. This has been advanced through novel biomarkers, including CysC, NGAL, TIMP-2 and IGFBP7. Furthermore, genetic susceptibility of AKI is an emerging field with recent genome-wide association studies. Timely recognition and supportive management remain the cornerstone of therapy, with escalation to kidney replacement therapy (KRT), particularly continuous modalities.SummaryThis review aims to highlight the important advances in pediatric AKI epidemiology, diagnosis, management and prognosis. Pediatric Acute Kidney Injury (AKI) management requires a comprehensive, targeted approach that takes into consideration the hemodynamic stability, metabolic and electrolyte derangements, and nutritional requirements to promote recovery. Fluid management is fundamental, noting resuscitation with isotonic crystalloids is warranted in hypovolemic patients. The clinical goal is for euvolemia while avoiding fluid overload, which can worsen the outcome. Dynamic clinical assessment, in combination with serum biomarkers, is key to effective therapy. Electrolyte abnormalities, notably hyperkalemia, hyponatremia and metabolic acidosis, necessitate prompt correction to prevent life-threatening complications. Supportive management includes potassium binders, bicarbonate therapy, judicious use of diuretics in volume overloaded states and avoidance of nephrotoxic medications. Nutritional support addresses the catabolic states of AKI. Increasing caloric intake and protein provision to at least 3g/kg/day in critically ill patients is essential to meet the high catabolic state and to maintain nitrogen balance despite elevated urea levels. Electrolyte restricted diet and binders may also be required for hyperkalemia and hyperphosphatemia. Kidney replacement therapy (KRT) is indicated for refractory hyperkalemia, severe acidosis, fluid overload unresponsive to diuretics, or overt uremic complications (e.g., encephalopathy, pericarditis).