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Abstract: PO2195

Diffuse Large B-Cell Lymphoma Presenting with Light Chain Cast Nephropathy: A Case Report

Session Information

  • Onco-Nephrology - 2
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Report

  • 1500 Onco-Nephrology

Authors

  • Cho, Sheng-Li, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
  • Wu, Hao-Yu, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
  • Huang, Tai-Chung, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
  • Chu, Tzong-Shinn, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
  • Huang, Taomin, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
Introduction

Light chain cast nephropathy is caused by filtration of excessive amounts of free light chains into the renal tubules, leading to acute kidney injury (AKI). The main associated malignancy is multiple myeloma (MM). No adult case of cast nephropathy associated with diffuse large B-cell lymphoma (DLBCL) was reported

Case Description

A 55-year-old previously healthy man presented with foamy urine for 3 months and exercise intolerance. Physical exam showed pale conjunctiva, multiple neck masses, and no edema. His serum creatine (SCr) was 7.6 and 15.2 mg/dL initially and on admission 4 weeks later, whereas baseline SCr had been normal one year ago. His hemoglobin level was 7.9 g/dL, and white blood cell count was 8750/μL without eosinophilia. No active urine sediments were found. A UPCR was 7250 mg/g, and a UACR 300 mg/g. Ultrasound showed decreased kidney sizes (R 9.0, L 9.7 cm). Immuno-electrophoresis detected monoclonal λ light chain in both his serum and urine, and a serum λ free light chain level was 8830 mg/L, with a κ-to-λ ratio of 0.0024. Following a diagnosis of DLBCL (Lugano stage IV) by neck mass biopsy, a renal biopsy disclosed diffuse aggregation of amorphous eosinophilic proteinaceous casts in the tubules, with a normal glomerular compartment and mild arteriosclerosis, findings consistent with IgG-λ light chain cast nephropathy. He was treated with 4 courses of R-CHOP, hemodialysis, and a short course of plasmapheresis. λ free light chain level decreased to 2830 mg/L after plasmapheresis. A complete response for DLBCL was achieved 6 months later but he remained on hemodialysis.

Discussion

This is, in the literature, the first adult DBLCL patient presenting with proteinuria and renal deterioration proven to be light chain cast nephropathy. Standard lymphoma treatments were given, and based on limited evidence, plasmapheresis was given to reduce the light chain load (Median serum free light chain level was 6590 mg/L in MM patients as reported by Bridoux in JAMA 2017). Decreasing plasma light chain concentration leading to improvement in AKI has been reported for MM. However, this case remained dialysis-dependent despite a decline in light chain levels. To conclude, we provide a unique case of DLBCL with cast nephropathy. Clinicians could take this entity into consideration and treatment may be tailored for better outcomes.