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Effect of Dose-Intensive Intravenous Melphalan and Autologous Blood Stem-Cell Transplantation on AL Amyloidosis–Associated Renal Disease

Laura M. Dember, MD; Vaishali Sanchorawala, MD; David C. Seldin, MD, PhD; Daniel G. Wright, MD; Michael LaValley, PhD; John L. Berk, MD; Rodney H. Falk, MD; and Martha Skinner, MD
[+] Article and Author Information

From Boston University School of Medicine, Boston, Massachusetts.


Acknowledgments: The authors thank Raymond Comenzo, MD, for helpful review of the manuscript and Kathleen Finn, RN, Karen Donovan, and Akira Murakami for assistance with data collection.

Grant Support: By the U.S. Food and Drug Administration (Fd-R-001346), the Young Family Amyloid Research Fund, the Sue Sellors Finley Cardiac Amyloid Research Fund, and the Amyloid Research Fund.

Requests for Single Reprints: Laura M. Dember, MD, Renal Section, EBRC 504, Boston University Medical Center, 650 Albany Street, Boston, MA 02118; e-mail, ldember@bu.edu.

Current Author Addresses: Dr. Dember: Renal Section, EBRC 504, Boston University Medical Center, 650 Albany Street, Boston, MA 02118.

Dr. Sanchorawala: Hematology Oncology, F3, Boston University Medical Center, 88 East Newton Street, Boston, MA 02118.

Drs. Seldin and Wright: Hematology–Oncology Section, EBRC 4, Boston University Medical Center, 650 Albany Street, Boston, MA 02118.

Dr. LaValley: Arthritis Center, A203, Boston University Medical Center, 88 East Newton Street, Boston, MA 02118.

Dr. Berk: Pulmonary Section, R3, Boston University Medical Center, 88 East Newton Street, Boston, MA 02118.

Dr. Falk: Cardiology Section, D822, Boston University Medical Center, 88 East Newton Street, Boston, MA 02118.

Dr. Skinner: Amyloid Program, EB33, Boston University Medical Center, 15 Albany Street, Boston, MA 02118.

Author Contributions: Conception and design: L.M. Dember, V. Sanchorawala, D.C. Seldin, D.G. Wright, R.H. Falk, M. Skinner.

Analysis and interpretation of the data: L.M. Dember, M. LaValley.

Drafting of the article: L.M. Dember, J.L. Berk.

Critical revision of the article for important intellectual content: V. Sanchorawala, D.C. Seldin, D.G. Wright, M. LaValley, J.L. Berk, R.H. Falk, M. Skinner.

Final approval of the article: L.M. Dember, V. Sanchorawala, D.C. Seldin, D.G. Wright, M. LaValley, J.L. Berk, R.H. Falk, M. Skinner.

Provision of study materials or patients: L.M. Dember, V. Sanchorawala, D.C. Seldin, D.G. Wright, R.H. Falk, M. Skinner.

Statistical expertise: M. LaValley.

Obtaining of funding: M. Skinner.

Administrative, technical, or logistic support: D.G. Wright, M. Skinner.

Collection and assembly of data: L.M. Dember, V. Sanchorawala, M. Skinner.


Ann Intern Med. 2001;134(9_Part_1):746-753. doi:10.7326/0003-4819-134-9_Part_1-200105010-00011
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Primary (AL) amyloidosis is a plasma cell dyscrasia in which clonal plasma cells in the bone marrow produce a monoclonal immunoglobulin protein (M protein). The M protein light chains or light-chain fragments form insoluble fibrils with β-pleated sheet configurations, rendering them avid for Congo red dye. The deposition of amyloid fibrils into the extracellular matrix of a variety of tissues results in severe organ dysfunction and poor patient survival.

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Figure. . Patients with complete hematologic response at 12-month follow-up ( = 21). . Patients with persistence of the plasma cell dyscrasia at 12-month follow-up ( = 28). One patient with persistence of the plasma cell dyscrasia is not represented because data for 24-hour urinary protein collection were not available at 12 months.
Change in 24-hour urinary protein excretion in individual patients surviving at least 12 months.LeftnRightn
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