Renal failure (urine output below 300 ml/day and serum creatinine above 300 pmol/l) despite adequate filling occurs in up to 70 per cent of patients with AHF. Hypovolemia and sepsis are important precipitating factors. In addition, altered levels of vasodilators and constrictors within the renal vasculature play an important role. Acetaminophen may cause direct renal toxicity as well as liver damage. The etiology of renal failure in AHF is usually multifactorial, comprising prerenal factors, hepatorenal failure, acute tubular necrosis, and direct nephrotoxicity.
Initial management consists of aggressive volume loading utilizing colloid and crystalloid as previously described. If oliguria persists, 'renal' dose dopamine (£ 2.5 Mg/kg/min) or a furosemide (frusemide) infusion (10 mg/h) may be tried. Current opinion suggests a very limited role for dopamine. Renal replacement therapy will be needed if acidosis, hyperkalemia, fluid overload, or a rising creatinine develop. It should be instituted in any oliguric patient showing signs of cerebral edema in order to remove fluid following mannitol administration. Continuous hemodiafiltration is the best form of renal replacement therapy in AHF. High-volume hemofiltration may also be utilized, but care must be taken in the choice of replacement fluid since patients will be unable to metabolize many of the standard solutions in which lactate and acetate are the predominant buffers. A bicarbonate-buffered solution will be well tolerated. Intermittent hemodialysis should be avoided since the frequent complication of hypotension may result in significant falls in cerebral perfusion pressure. However, it is useful in patients who have undergone transplantation or in those following AHF who are hemodynamically stable and no longer at risk of cerebral edema. Anticoagulation can be difficult since platelets are large and sticky and circuits may clot rapidly despite a coagulopathy. Heparin is used unless active bleeding is present or an intracranial bolt is in situ. However, heparin resistance is common owing to concurrent antithrombin III deficiency. Epoprostenol 5 ng/kg/min is an alternative anticoagulant.
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