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Children presenting with AKI may have signs of systemic fluid overload but be intravascularly dehydrated Electrolyte and acid–base abnormalities may be present upon presentation and may need to be emergently addressed Patients may require RRT if intrinsic renal function is unable to maintain fluid and electrolyte balance Consultation with a nephrologist will help guide evaluation and therapeutic choices Current Evidence AKI, previously termed acute renal failure, is an abrupt decrease in the GFR with impairment of creatinine clearance However, there may be a time lag between the onset of injury and clinically detectable changes in serum creatinine Depending on the severity of the injury, there may be altered water and electrolyte excretion as well as disturbances of metabolic and acid–base regulation In mild cases, nonoliguric AKI may be asymptomatic and only detected when serum laboratory studies are performed When severe, oliguric AKI may result in profound derangements of electrolyte and volume balance necessitating the initiation of RRT The Schwartz formula allows estimation of the GFR in children based on serum creatinine, patient length, age, and gender ( Table 100.13 ) It should be noted that this formula tends to overestimate GFR, and this overestimation increases with decreasing GFR AKI may be classified as prerenal, intrinsic renal, and postrenal Prerenal AKI can result from intravascular volume depletion or reduced effective circulating volume Volume depletion may occur in the setting of uncompensated fluid losses from a variety of sources including bleeding, urination, gastrointestinal output, and cutaneous losses from burns or excessive sweating Intravascular volume depletion may also develop when fluid shifts out of the vascular space into the interstitial space such as in the setting of hypoalbuminemia or during systemic inflammatory response syndrome (SIRS) Decreased effective circulating volume may be present in heart failure or distributive shock Intrinsic renal disease can result from