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Abstract: SA-PO220

Renal Limited Thrombotic Microangiopathy (TMA) Secondary to Chronic Lymphocytic Leukemia (CLL): A Case Report

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Karam, Sabine, University of Minnesota Twin Cities School of Medicine, Minneapolis, Minnesota, United States
  • Klomjit, Nattawat, University of Minnesota Twin Cities School of Medicine, Minneapolis, Minnesota, United States

Chronic lymphocytic leukemia (CLL) is a monoclonal B cell lymphocytosis that produces a nephrotoxic monoclonal immunoglobulin (MIg). Complement-TMA and C3 Glomerulonephritis with systemic manifestations have been rarely reported associated to CLL. We report the first case of renal limited TMA secondary to CLL.

Case Description

70-year-old female with a history of type 2 diabetes exceeding10 years, hypertension (HTN), and CLL diagnosed nine years prior presented with massive proteinuria with a UPCR a 10g/g, increased from 1.9 g/g six months prior along with lower extremity edema. The creatinine level was 0.84 mg/dL (eGFR around 74 mL/min/m2) and at baseline. Her CLL had never been treated as she had been considered asymptomatic despite having a WBC count above 200000. Her UA showed pyuria and microscopic hematuria. The serological work-up was unrevealing except for trace cryoglobulin IgG lambda with a kappa lambda ratio at 0.34. A total body CT scan done 5 months prior to presentation had shown stable mild retroperitoneal lymphadenopathy and unchanged mild splenomegaly. A kidney biopsy showed early nodular sclerosis likely from diabetes along with endothelial injury with glomerular basement membrane duplication and endothelial swelling suggestive of TMA on electron microscopy. Pronase immunofluorescence studies were negative for immune deposits. There was no evidence of peripheral TMA with stable hemoglobin and platelet counts and normal LDH and reticulocyte count. Complement studies revealed unregulated activity at the C3 and C5 convertase level with depleted CH50 levels. The patient’s HTN and proteinuria were initially managed with losartan 50 mg daily, empagliflozin 10 mg daily and furosemide 40 mg daily, however as her UPCR increased to 17g/g, her nephrotic syndrome was deemed to be secondary to her CLL and she was initiated on ibrutinib. The proteinuria improved and is now 4.82 g/g three months later. In addition, her WBC count went down to 92.8k.


The significant improvement in proteinuria after initiation of ibrutinib and the unregulated activity at the C3 and C5 convertase level suggests renal endothelial injury secondary to activation of the complement pathway by the MIg. Clinicians need to be aware of this potential complication of CLL to initiate treatment promptly.