A Case of Pseudo-bisalbuminemia and Nephrotic Syndrome in an Adult

Abstract

Bisalbuminemia, whether hereditary or acquired, remains a rare electrophoretic abnormality of albumin; "pseudo-bisalbuminemia” is even rarer. It presents in several forms and is not a pathological condition in itself. In this paper, we report a rare case of "pseudo-bisalbuminemia” in an adult with nephrotic syndrome. In patients with nephrotic syndrome, significant quantitative and qualitative changes in serum proteins occur due to increased glomerular permeability and selective urinary protein loss. Hypoalbuminemia, increased hepatic synthesis of certain proteins, and alterations in albumin structure or binding properties may modify the electrophoretic profile. Rarely, nephrotic syndrome may be associated with pseudo-bisalbuminemia, potentially related to altered albumin metabolism, drug interactions, or post-transplantation modifications under conditions of heavy proteinuria and systemic inflammation. The detection of bisalbuminemia on the electrophoresis, even without inherent pathological significance, should nevertheless alert the clinician, especially when clearly associated with nephrotic syndrome in an adult. Outside of this context, the presence of interfering molecules should also prompt the prescriber to adopt an appropriate approach to this abnormality. The hyperlipidemia results from hypoalbuminemia, which reactively and nonspecifically stimulates hepatic synthesis of all proteins, including lipoproteins. It is also linked to increased LDL and VLDL production, associated with reduced catabolism. This case also presents the peculiarity of an impure nephrotic syndrome; nearly 90% of nephrotic syndromes are pure, generally responsive to corticosteroids, and have a good prognosis.