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SEPSIS‐INDUCED ACUTE BILATERAL RENAL CORTICAL NECROSIS

rhotic patients. There is no doubt that the patient had liver cirrhosis. But laboratory test showed no citrate accumulation. The following two factors may contribute to it. First, the patient’s liver function was improved from Child–Pugh class C to class A and at compensatory stage. Second, some reports indicated that kidney musculature also appears to remove citrate in blood. Besides citrate accumulation, there are high risks of hypocalcaemia, hypernatraemia and metabolic alkalosis in patients with liver cirrhosis and several remedial approaches were made. First, the dialysate sodium concentration was reduced to 130 mmol/L to avoid hypernatraemia and HCO3concentration was reduced to 26–28 mmol/L to avoid metabolic alkalosis. Second, electrolyte concentration was tested until the patient’s situation was stabilized. Third, symptoms of hypocalcaemia, such as tetany, muscle spasm and palpitation were carefully watched. If the symptoms were presented, the patient would be treated with 10 mL 5% CaCl2 i.v. for 5 min. According to our experience in this case, we think it is feasible and safe to use citrate anticoagulation in patients with compensated liver cirrhosis and liver function at Child– Pugh class A. It is necessary to perform point-of-care measurement of citrate concentration, electrolyte concentration, especially calcium during haemodialysis and then adjust the parameters of haemodialysis accordingly.