7.6.3. No monoclonal proteins detectable by any routine laboratory method

Chapter 7

For a small proportion of AL amyloidosis patients, no monoclonal FLCs are detected by any routine laboratory methods. In a large screening study by Katzmann et al., 11 of 581 (2%) AL patients were normal by sFLC analysis, sIFE and uIFE (Chapter 23) [134]. Three possible explanations include: 1) some FLC molecules may have a high affinity for the amyloid deposits, resulting in circulating FLCs being rapidly removed; 2) in a similar manner, patients with extensive amyloid deposits might have a huge capacity for FLC removal. Any newly synthesised molecules would be cleared rapidly by a combination of binding to the amyloid mass and glomerular filtration, thereby preventing the accumulation of FLCs in serum; or 3) the amyloid is due to the deposition of a different protein [196].