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A 26-year-old woman was admitted following a horse-riding accident. She had fractured her femur and suffered an intracranial hemorrhage. Postoperatively she required ventilation and then developed a respiratory tract infection, and on the third day of admission, her urine output had fallen to 0.5 mL/kg per hour, and her serum creatinine had risen from 0.5 mg/dL on admission to 1.24 mg/dL. At this stage her intracranial pressure (ICP), measured with an intraventricular catheter, remained elevated at 35 mm Hg, with a mean arterial blood pressure of 90 mm Hg. In view of the increase in creatinine and fall in urine output, a fluid challenge was given to try to prevent progression of acute kidney injury (AKI), to exclude a volume-responsive reversible cause of AKI (see Chapter 41). However, by the following day her urine output had fallen to 0.3 mL/kg per hour and her serum creatinine increased to 2.0 mg/dL.
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Timing of initiating renal replacement therapy
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As kidney function declines, the products of cellular metabolism accumulate, leading to retention of both the nitrogenous products of metabolism, typically assessed by the measurement of urea and creatinine but also potassium accumulation, and the development of a metabolic acidosis. Other potential toxins also accumulate,1 leading to the term azotemia rather than uremia. This patient has AKI, and as such the time course of the illness is short, and only a limited amount of toxins will have accumulated. However, patients with AKI may have to be started on renal replacement therapy (RRT) because of hyperkalemia refractory to standard medical therapy or increasing pulmonary edema compromising oxygenation, and brain hypoxia (Table 42-1).
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Historic data suggest that “early” initiation of RRT in AKI is associated with improved survival,2, 3, 4, 5, 6 but the evidence base is not sufficiently robust to allow a specific recommendation and the decision to initiate RRT should remain a clinical one. Whereas the decision to initiate RRT is straightforward in those ...