Abstract

Acute kidney injury (AKI) is characterized by a sudden deterioration in kidney function that results in the accumulation of nitrogenous waste products (e.g., urea) and alters the regulation of extracellular fluid volume, electrolytes, and acid-base homeostasis. Although the criteria for neonatal acute kidney injury have varied, a frequently used definition is a serum creatinine level of more than 1.5 mg/dL.The causes of neonatal acute kidney injury are multiple and can be divided into prerenal, renal, and postrenal categories. Prerenal azotemia is the most common type of acute kidney injury in the neonate and may account for up to 85% of all cases. There are currently no specific medical therapies to treat AKI. The basic approach in management of AKI should be planned according to the underlying etiology. To maximize the chance for survival, the clinician must support the cardiorespiratory system, maintain maximal nutrition, balance homeostasis, and manage the consequences of AKI. The prognosis for neonates with acute kidney injury is variable, and largely related to the infant’s underlying medical condition, with mortality rates ranging from 14% to 73%. (JAREM 2013; 3: 53-9)

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