A patient was recently seen on the consult service for evaluation of hyponatremia. She had a history of multiple myeloma and a previous bone marrow transplant and had significant cholestatic liver dysfunction related to GVHD. Her serum sodium at the time of presentation was 120 mmol/L. The initial thought was that she may have SIADH but her serum osmolarity came back at 290 suggesting that we were in fact dealing with a case of pseudohyponatremia.
The commonest causes of pseudohyponatremia are severe hypergammaglobulinemia and hypertriglyceridemia. Neither was present in this case. A previous case report in the NEJM in 2003 described pseudohyponatremia in a patient with cholestatic jaundice that was felt to be the result of accumulation of lipoprotein X. This is formed when there is reflux of cholesterol and phospholipids into the circulation from blocked biliary ducts. Because it is not soluble, it increases the solid portion of plasma and leads to pseudohyponatremia. A plasma sample confirmed to presence of lipoprotein X in this patient.
One point that was raised during the assessment was that the diagnosis of pseudohyponatremia cannot be made by measuring the serum osmolarity alone. It is important to confirm this by measuring the serum sodium with a direct ion sensitive electrode as this will measure the sodium concentration in the plasma water alone and therefore give a true result. This is because there are occasional cases where a patient with true hyponatremia will present after ingestion of a large quantity of alcohol. In this case, the serum sodium will be low, there will be a significant osmolar gap (suggesting that the patient has pseudohyponatremia) but the directly measured serum sodium will also be low – confirming the presence of true hyponatremia.