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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 mechanical ventilation and then developed a respiratory tract infection. On the 3rd hospital day, her urine output had fallen to 0.5 mL/kg/h, 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 decrease in urine output, a fluid challenge was given to try and prevent progression of acute kidney injury (AKI), to exclude a volume-responsive reversible cause of AKI (Table 48-1). However, by the following day her urine output had fallen to 0.3 mL/kg/h, and the creatinine level had increased to 2.0 mg/dL.
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When should renal replacement therapy be instituted?
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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, and 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 acute kidney injury (AKI); 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 48-2).
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