Kidney Week

Abstract: PUB199

Dialysis-Dependent Light-Chain Cast Nephropathy as the Presenting Renal Lesion of Waldenström Macroglobulinemia

Session Information

• Publication Only

Category: Onconephrology

• 1600 Onconephrology

Authors

• Ngwe, Herve Nonga, University of South Florida, Tampa, Florida, United States

Herve Nonga Ngwe, MD

• Ruiz Vera, Angel J., University of South Florida, Tampa, Florida, United States

Angel J. Ruiz Vera, MD, MPH

• Jayakumar, Vaishnavi, University of South Florida, Tampa, Florida, United States

Vaishnavi Jayakumar

• Trinh, Anhthu, University of South Florida, Tampa, Florida, United States

Anhthu Trinh, MD

• Nadayil, Jasmine, University of South Florida, Tampa, Florida, United States

Jasmine Nadayil, MD

• Audi, Akram, University of South Florida, Tampa, Florida, United States

Akram Audi, MD

• Bassil, Claude, University of South Florida, Tampa, Florida, United States

Claude Bassil, MD, FASN

Introduction

Light chain cast nephropathy (LCCN) is the prototypical renal lesion of multiple myeloma and is uncommon in Waldenström macroglobulinemia (WM)/lymphoplasmacytic lymphoma (LPL), where amyloidosis, cryoglobulinemic GN, monoclonal Ig deposition disease, and lymphomatous infiltration predominate. We report biopsy-proven LCCN as the inaugural renal manifestation of WM, severe enough to require ongoing hemodialysis (HD).

Case Description

A 64-year-old man with recently diagnosed low-grade B-cell lymphoma and IgM-kappa monoclonal gammopathy presented with AKI needing emergent HD. Baseline serum creatinine was normal in November 2025 and rose subtly into the 3 mg/dL range before presentation. CT showed diffuse adenopathy and mild bilateral hydronephrosis from pelvic nodal compression. Workup confirmed an IgM-kappa M-spike, elevated free kappa light chains (kappa/lambda ratio 192), and 3.6 g/day Bence Jones proteinuria. Bone marrow biopsy revealed findings consistent with LPL/WM. Despite Bendamustine, plasmapheresis, and Rituximab therapy, renal function did not recover, prompting kidney biopsy. The biopsy revealed LCCN with kappa-restricted, fractured tubular casts and giant cell reaction; one glomerulus showed an MPGN pattern with weak IgM/kappa capillary-wall staining and rare subepithelial electron-dense deposits, suggesting concurrent monoclonal Ig-mediated glomerular injury. Severe IFTA (50-60%) was present. The patient remains dialysis-dependent.

Discussion

LCCN is the renal hallmark of multiple myeloma, driven by precipitation of free light chains with Tamm-Horsfall protein in the distal nephron. In WM/LPL the paraprotein is overwhelmingly intact IgM and the kidney is usually injured by other mechanisms; LCCN is reported in only 4 to 14% of WM renal biopsy series. This case shows that sufficient free light chains, even from a B-cell lymphoproliferative disorder rather than overt myeloma, can reproduce the full myeloma kidney phenotype with dialysis-dependent AKI. Concurrent MPGN-pattern glomerular changes with monoclonal IgM/kappa deposits further place this case on the monoclonal gammopathy of renal significance spectrum. This underscores the value of early kidney biopsy in WM/LPL patients with unexplained acute renal failure.