Serum electrophoresis with a bifid albumin peak

A 51-year old female patient with newly diagnosed chronic kidney disease (CKD) presented to the hospital with an acute exacerbation of chronic obstructive pulmonary disease (COPD). On admission her serum creatinine was 247 µmol/L and urea was 15 mmol/L. The patient was a known hypertensive and was on irregular treatment. The CKD was probably a result of hypertensive nephropathy. As the liver function test showed a reversal of the albumin globulin ratio, a serum protein electrophoresis was requested. The overall electrophoresis was normal, except that the gamma globulin was elevated and a bifid peak was seen in the albumin region. The electrophoretic pattern of serum in Figure 1 shows that the albumin peak has a bifid mountain where albumin has two heads; this condition is commonly known as Bisalbuminemia. It is a result of two types of serum albumin that differ in their electrophoretic mobility as a result of splitting of the serum albumin into two components, of which one represents a variant on account of genetically inherited or acquired determinant [1]. Fig. 1. The top serum protein electrophoresis shows the presence of bisalbuminemia. Below is a normal serum protein electrophoresis. Bisalbuminemia is of two types, genetic and acquired. Genetic bisalbuminemia is quite rare and is inherited in autosomal dominant form. Bisalbuminemia is of little diagnostic or therapeutic significance, except that in some cases it might result in altered binding of steroid hormones and thyroxine. Familial dysalbuminemic hyperthyroxinemia (Arg 218 AEHis and Arg 218 AE Pro mutations) and hypertriiodothyroninemia (Leu 66 AEPro mutation) have been directly linked to the presence of inherited bisalbuminemia [2]. The acquired type may result from long-term, aggressive beta lactam antibiotic therapy or in acute pancreatitis. Physicians should be aware of this condition and interpret such findings with caution as well as in the context of the clinical scenario.