#4178 HYPERCHLOREMIC METABOLIC ACIDOSIS AFTER PLASMAPHERESIS IN A PATIENT WITH RENAL TRANSPLANT REJECTION: A CASE REPORT

Abstract

Abstract Background and Aims Plasmapheresis is an effective therapeutic intervention for several renal disorders, including renal transplant rejection. However, repeated plasmapheresis can cause various side effects and complications. Method We present a 61-year-old male with a medical history of type 2 diabetes, hypertension, successfully treated multiple myeloma and a post-mortem kidney transplantation 7 months ago. The patient was hospitalized because of rapid deterioration of his renal function (eGFR CKD-EPI 15 ml/min/1.73m2). Renal biopsy of the transplanted kidney confirmed the diagnosis of antibody-mediated transplant rejection. Treatment with methylprednisolone, plasmapheresis with a 40 g/L albumin solution as a replacement fluid and intravenous immunoglobulins was initiated. After 4 plasmapheresis treatments, the patient developed gastrointestinal complaints and muscle weakness. Despite the patient's use of 3 grams of oral sodium bicarbonate supplements a day, laboratory tests revealed a hyperchloremic metabolic acidosis: bicarbonate 11.7 mmol/L, chloride 111 mmol/L, sodium 138 mmol/L. Metabolic acidosis due to citrate accumulation was ruled out with a normal total-to-ionized calcium ratio. After treatment with intravenous bicarbonate supplementation, the symptoms disappeared. Analysis of the albumin plasmapheresis solution showed a chloride concentration of 132 mmol/L. Results This is the first case that describes metabolic acidosis after albumin plasmapheresis in a patient with impaired renal function. The observed hyperchloremic metabolic acidosis is most likely the result of the administration of large volumes (3.5 litres per session) of a 4% albumin solution with high chloride concentrations. We hypothesize that patients with renal impairment are more prone to develop metabolic acidosis after plasmapheresis with albumin-saline replacement fluids due to their reduced renal capacity to excrete excess acid and chloride. Conclusion Special attention should be paid to the acid-base balance during plasmapheresis in patients with impaired renal function. Future research should investigate the incidence of hyperchloremic metabolic acidosis during albumin plasmapheresis in different eGFR categories.