Contributed by Michael Torbenson, MD and Robert Kelly, PhD
Published on line in May 1999
The patient is a 47 year old man working in the paint industry with a complicated past medical history that includes the following diseases:
The patient was hospitalized and treated in August of 1998 for bilateral transudative pleural effusions and a pericardial effusion of unknown etiology. As part of the workup, a serum protein electrophoresis (SPEP) was performed on 9/1/98, which showed a paraprotein.
At a clinic visit on 9/14, the patient was noted to have mild hepatomegaly and possible macroglossia. A fat-pad biopsy was negative for amyloid. The patient's blood showed a normochromic normocytic anemia. A bone marrow biopsy performed that day showed normocellular marrow with trilineage hematopoiesis and 1% plasma cells. A Congo-red stain (for amyloidosis) was negative. A repeat SPEP with immunofixation demonstrated a monoclonal IgG kappa of less than 100 mg/dl. A urine protein electrophoresis was negative for light chains (Bence Jones protein).
The patient continued to have a left sided pleural effusion that waxed and waned over the next several months. A follow-up SPEP on 4/26/99 was done (Figure 1). A UPEP (Figure 2a) with immunofixation (Figure 2b) was performed on 5/6/99 .
Figure 1. SPEP shows a probable paraprotein, approximately 340 mg/dL, but insufficient serum was available to characterize the protein further.
Figure 2. UPEP (Figure 2a) and immunofixation (Figure 2b) showed a monoclonal IgG/kappa (approximately 3.3 mg/dl) and two free lambda light chain bands, one approximately 1.9 mg/dl and one approximately 0.5 mg/dl. Note the glomerular pattern of proteinuria. The control (Figure 2a) shows a patient with a large amount of Bence Jones protein but with otherwise a relatively normal protein pattern.