RESUMEN
BACKGROUND: Rapid correction of dysnatremias can result in neurological complications. Therefore, various formulas are available to predict changes in plasma sodium concentration ([Na+]) after treatment, but these have been shown to be inaccurate. This could be explained by sodium acumulation in skin and muscle tissue, which is not explicitly considered in these formulas. We assessed the association between clinical and biochemical factors related to tissue sodium accumulation and the discrepancy between predicted and measured plasma [Na+]. METHODS: We used data from an intensive care unit (ICU) cohort with complete data on sodium, potassium, and water balance. The predicted plasma [Na+] was calculated using the Barsoum-Levine (BL) and the Nguyen-Kurtz (NK) formula. We calculated the discrepancy between predicted and measured plasma sodium and fitted a linear mixed-effect model to investigate its association with factors related to tissue sodium accumulation. RESULTS: We included 594 ICU days of sixty-three patients in our analysis. The mean plasma [Na+] at baseline was 147±6 mmol/L. The median (IQR) discrepancy between predicted and measured plasma [Na+] was 3.14 mmol/L (1.48, 5.55) and 3.53 mmol/L (1.81, 6.44) for the BL and NK formulas, respectively. For both formulas, estimated total body water (p=0.027), initial plasma [Na+] (p<0.001) and plasma [Na+] change (p<0.001) were associated with the discrepancy between predicted and measured plasma [Na+]. CONCLUSION: In this ICU cohort, initial plasma [Na+], total body water, and plasma [Na+] changes, all factors that are related to tissue sodium accumulation, were associated with the inaccurateness of plasma [Na+] prediction.
RESUMEN
Therapeutic plasma exchange (TPE) is an effective treatment for several renal disorders, including renal transplant rejection. However, repeated plasma exchanges can result in various metabolic disturbances and complications. 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 prior to presentation. The patient was hospitalized with an antibody-mediated transplant rejection for which treatment with methylprednisolone, TPE with a 40 g/L albumin solution as a replacement fluid, and intravenous immunoglobulins was initiated. After four TPE treatments, the patient developed gastrointestinal complaints and muscle weakness. Despite daily oral bicarbonate supplementation, laboratory tests revealed a hyperchloremic metabolic acidosis: bicarbonate 11.7 mmol/L, chloride 111 mmol/L, and 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 solution showed a chloride concentration of 132 mmol/L. This is the first case that describes severe metabolic acidosis after multiple sessions of TPE with an albumin solution in a patient with impaired renal function. The hyperchloremic metabolic acidosis is the result of administration of large volumes of an albumin solution with high chloride concentrations. Special attention should be paid to the acid-base balance during TPE in patients with impaired renal function. Future research should investigate the incidence of hyperchloremic metabolic acidosis during TPE in patients with impaired renal function.