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Abstract: SA-PO227

Cryoglobulinemic Glomerulonephritis in the Setting of Chronic Lymphocytic Leukemia

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Valdesuso, Alejandro, Landmark Medical Center, Woonsocket, Rhode Island, United States
  • Shah, Ankur, Rhode Island Hospital, Providence, Rhode Island, United States
  • Chang, Anthony, The University of Chicago Medicine, Chicago, Illinois, United States
  • Hu, Susie L., Rhode Island Hospital, Providence, Rhode Island, United States

Cryoglobulinemia is characterized by the presence of immunoglobulins that precipitate in vitro at temperatures below body temperature. End organ damage can occur due to hyperviscosity syndrome, more specifically in the kidney due to the formation of intracapillary (known as cryo-plugs), capillary wall and mesangial cryoglobulin deposits. This is referred to as cryoglobulinemic glomerulonephritis.

Case Description

A 76-year-old female with a history of biopsy proven chronic lymphocytic leukemia presented with dyspnea, edema, and weight gain. Evaluation was notable for hematuria and proteinuria, quantified at 5.8g/g. Serologies revealed an elevated C3 and undetectable C4. Serum cryocrit was 50 UL cryo/ml serum and serum viscosity was 1.4. Cryoglobulin isotyping showed monoclonal IgM-kappa (gamma), faint monoclonal IgM-kappa (beta) and faint monoclonal IgA-lambda (gamma) most consistent with type I cryoglobulinemia in view of her chronic lymphocytic leukemia. Kidney biopsy was obtained demonstrating prominent immune complex deposition in the form of numerous hyaline pseudothrombi with frequent duplication of the glomerular basement membrane most consistent with membranoproliferative glomerular injury. Patient met criteria for plasmapheresis due to the significantly elevated cryocrit and underwent one session. Afterwards, additional plasmapheresis was held and she was started on cyclophosphamide and rituximab. Patient continued to deteriorate and died due to respiratory failure.


Type I cryoglobulinemia typically causes end organ damage through hyperviscosity with type II and III cryoglobulinemia doing so through vasculitis. Atypical to our case was a serum viscosity at the lower limit of normal. We hypothesize that the degree of cryo-plugging was so high it resulted in hyperviscosity at the level of the glomerular capillary that was not detectable in the blood. The possibility of this constellation is important for clinicians to be aware of.

Cryo-plugging on light microscopy H&E stain