ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: SA-PO751

Steroid-Resistant Minimal Change Disease Induced by Waldenstrom Macroglobulinemia

Session Information

Category: Glomerular Diseases

  • 1304 Glomerular Diseases: Podocyte Biology


  • Pham, Tin T., HCA Healthcare Graduate Medical Education, Orlando, Florida, United States
  • Carilli, Allison, Orlando VA Healthcare System, Orlando, Florida, United States
  • Vanbeek, Christine A., AmeriPath Inc, Oklahoma City, Oklahoma, United States
  • Martinez Osorio, Jorge Ivan, Orlando VA Healthcare System, Orlando, Florida, United States

Waldenstrom’s macroglobulinemia (WM) is an IgM-secreting B-cell lymphoproliferative disorder associated with a variety of renal manifestations. Glomerular pathology in WM most commonly occurs because of direct monoclonal protein deposition resulting in light chain amyloidosis, cryoglobulinemic glomerulonephritis, or non-cryoglobulinemic membranoproliferative glomerulonephritis. Minimal Change Disease (MCD) rarely develops in the setting of non-Hodgkin lymphomas (NHLs) including WM. We present a case of steroid resistant MCD induced by WM requiring the use of cytotoxic agents with successful remission achieved of nephrotic syndrome.

Case Description

67-year-old man, with history of hyperlipidemia was evaluated for acute onset of anasarca, asthenia, and weight gain of 40 lbs. He had heavy proteinuria (12 grams), hypoalbuminemia (1.0 grams/dL), and normal serum creatinine level (1.1 mg/dL). Serum protein electrophoresis showed 2 M spikes (one IgM kappa, one IgM lambda). Serum free light chain ratio was normal at (1.42). PCR for gene mutation was positive. Bone marrow biopsy revealed a mildly hypercellular bone marrow (60%) with involvement by a B-cell lymphoproliferative disorder. Renal biopsy showed MCD. He was started on prednisone 80 mg that was tapered to 60 mg over 4 months. However, he had persistent fatigue, lower extremity edema, and ongoing proteinuria (7 to 14 grams). On repeat renal biopsy, there was extensive podocyte foot process effacement, consistent with MCD. The treatment was transitioned to 6 cycles of rituximab, cyclophosphamide, and corticosteroids. The patient reported remarkable improvement in fatigue and lower extremity edema by the middle of his treatment. After finishing the full treatment course, he had complete resolution of proteinuria, stable serum creatinine (1.1 mg/dL), and normalization of serum albumin (3.8 g/dL).


MCD is a rare renal manifestation of WM. Although the lesion is not due to direct monoclonal protein deposition, it may be related to other factors secreted by the tumor. MCD in the setting of NHL is often steroid-sensitive. However, this case demonstrates that cytotoxic agents and monoclonal antibodies may be required to achieve complete remission.