Jeffrey Zonder, hematologist at Karmanos Cancer Institute in Detroit Michigan and author of the Amyloid Planet Blog breaks down amyloid versus myeloma in the onconephrology region. He is a Duke graduate so it is okay to hate him.

As you consider this year’s NephMadness brackets, a potential bracket-busting sleeper might be “amyloidosis,” squaring off against “myeloma kidney.” The last year did not bring with it any major changes in our understanding of the pathophysiology or overall management strategy of myeloma kidney (aka, cast nephropathy), despite the fact that it is the most common renal injury seen amongst patients with plasma cell dyscrasias. No new information regarding the benefit (or lack thereof) of plasma exchange, and the status of the EuLITE trial (evaluating the role of high cut-off hemodialysis) hasn’t changed much since the topic was reviewed by the Renal Fellow Network back in the summer of 2013.

This has been a potentially pivotal year for management of amyloid-related kidney injury however. First, researchers from Pavia, Italy, have defined the risk of ESRD and the need for hemodialysis based on initial clinical factors (namely the GFR and the degree of albuminuria) in the journal Blood. This work provides for the first time hard data upon which clinical trials aimed at improving renal outcomes might be designed. The second major development in the last year is an ongoing Phase 1/2 trial evaluating an anti-amyloid fibril monoclonal antibody called NEOD001. Using the current therapy paradigm, serum light chains are reduced using anti-plasma cell therapy (i.e., chemotherapy) with the hope that organ function will eventually improve. In fact, renal function improvement occurs in a minority of patients – generally the ones who have the deepest and most sustained light chain suppression – often after a period of months or even years. NEOD001 may shake this up. By binding to toxic soluble oligomers and also to fibrillar amyloid deposits in tissues, NEOD001 may promote immune clearance of amyloid, thereby enhancing the rate of organ improvement. Other fibril-directed antibodies (11-1F4, and Pentraxin’s anti-SAP mAb GSK2398852) are also in development, though it is unclear whether each targets renal amyloid deposits to the same extent.

So fellow bracketologists: will the rapidly evolving therapies for amyloidosis help turn it into this year’s NephMadness Cinderella?

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