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Light Chain-Associated Renal Disorders Medication

  • Author: Malvinder S Parmar, MB, MS; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Nov 21, 2015
 

Medication Summary

No standard treatment has been established for light-chain nephropathy, and the mainstay remains treatment of the underlying disease process and monitoring for complications and early recognition and management of complications.

In patients with myeloma, prevention of cast nephropathy is the mainstay by reducing the production of light chains by dexamethasone-based chemotherapy and promoting light chain filtration by optimizing volume status and intravenous fluid therapy to maintain urine volume of approximately 3 L/day, unless contraindicated, and alkalization of urine.

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Antineoplastic agents

Class Summary

The mainstay of treatment is effective control of the underlying (primary) disease. A combination of an alkylating agent (eg, melphalan) and prednisolone, administered for 4-7 d q4-6wk, is the standard first-line approach and induces remission in approximately 40% of patients. This combination does not act rapidly, and the dose of melphalan often must be modified because the drug is excreted via the kidney.

Bortezomib (Velcade)

 

First drug approved of anticancer agents known as proteasome inhibitors. The proteasome pathway is an enzyme complex existing in all cells. This complex degrades ubiquitinated proteins that control the cell cycle and cellular processes and maintains cellular homeostasis. Reversible proteasome inhibition disrupts pathways supporting cell growth, thus decreases cancer cell survival.

Bortezomib-based chemotherapy, in addition to early plasmapheresis, in patients with multiple myeloma and kidney failure secondary to myeloma cast nephropathy has shown to achieve complete renal recovery in 40% of patients and is preferred therapy in this subset of patients.[18]

Melphalan (Alkeran)

 

Inhibits mitosis by cross-linking DNA strands. Effective against both resting and rapidly dividing tumor cells.

Vincristine (Vincasar PFS, Oncovin)

 

Inhibits cellular mitosis by inhibiting intracellular tubulin function and binding to microtubules and spindle proteins in the S phase.

Doxorubicin (Adriamycin, Rubex)

 

Inhibits topoisomerase II and produces free radicals, which may cause the destruction of DNA. The combination of these events can, in turn, inhibit the growth of neoplastic cells.

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Corticosteroids

Class Summary

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Meticorten, Orasone)

 

Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and also suppresses lymphocytes and antibody production. Reduced to its pharmacologically active form, prednisolone.

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Contributor Information and Disclosures
Author

Malvinder S Parmar, MB, MS FRCP(C), FACP, FASN, Associate Professor, Department of Internal Medicine, Northern Ontario School of Medicine; Assistant Professor, Department of Medicine, University of Ottawa Faculty of Medicine; Consulting Physician, Timmins and District Hospital, Ontario, Canada

Malvinder S Parmar, MB, MS is a member of the following medical societies: American College of Physicians, American Society of Nephrology, Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Departments of Pediatrics and Obstetrics and Gynecology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, Royal College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

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Light chain–associated renal disorders. Light microscopy (hematoxylin and eosin stain at 25X power) showing nodular glomerulosclerosis (arrow) and thickening of the basement membrane. Courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Light chain–associated renal disorders. Immunofluorescence (25X power) showing deposits of monotypic light chain along the basement membrane. Courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Light chain–associated renal disorders. Ultrastructure (electron microscopy at 29,000X power) showing deposition of nonfibrillar electron-dense material in the mesangial nodule (arrow). Courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Light chain–associated renal disorders. Ultrastructure (electron microscopy at 29,000X power) showing deposition of nonfibrillar electron-dense material along the basement membrane (arrows). Courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
Light chain–associated renal disorders. Immunoelectron microscopy (immunogold at 29,000X power) showing kappa light-chain deposition. Courtesy of Madeleine Moussa, MD, FRCPC, Department of Pathology, London Health Sciences Centre, London, Ontario, Canada.
 
 
 
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