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Abstract: SA-PO253

Chronic Myelomonocytic Leukemia (CMML)-Related Glomerulopathy Without Lysozyme Nephropathy

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Koirala, Priscilla, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Chowdhury, Raad Bin Zakir, Mayo Clinic Minnesota, Rochester, Minnesota, United States
  • Leung, Nelson, Mayo Clinic Minnesota, Rochester, Minnesota, United States

Myeloproliferative neoplasms (MPN) are clonal hematopoietic cell disorders characterized by expansion of the myeloid lineages. We are increasingly recognizing myeloid disorders causing glomerular disease. Chronic Myelomonocytic Leukemia (CMML) is a unique MPN overlap which has a few glomerular presentations. We present a rare case of myeloproliferative glomerulopathy secondary to CMML and review the renal course as the neoplasm progressed.

Case Description

A 85-year-old male with past medical history of heart failure and CMML was admitted for acute kidney injury and proteinuria. Initial labs were significant for creatinine of 2.18 (baseline function of 1.1-1.3) mg/dl, 2.6g/day of total proteinuria and 1.8g/day albuminuria. Urinary sediment showed less than 3 red cells, 1-3 white cells, with occasional granular casts and free fat. Serological evaluation and infectious workup were unrevealing. Kidney biopsy was consistent with MPN associated with glomerulopathy. There was no evidence of lysozyme nephropathy even though serum lysozyme levels were elevated >10.8 mcg/ml. Post hospital, he was seen in clinic and was started on a course prednisone with improvement of pr/cr to 0.30 mg/mg and creatinine improved to 1.4 mg/dl. After completing steroids, his renal function and proteinuria began to worsen to >3 mg/dl and 1.48 mg/g, respectively. Additionally, he continued to have worsening leukocytosis (126x103/μl) and monocytosis. There were increasing peripheral blasts and serum lysozyme levels worsened to >19.3 mcg/ml. It was apparent that the patient’s CMML progressed to AML with coinciding worsening renal parameters.


Renal manifestations secondary to MPNs are rare. When it is present, those with elevated lysozyme are presumed to have lysozyme nephropathy, a sign of advanced hematological disease. In this case, the patient’s proteinuria and renal function improved with steroids. Once stopped, his hematological parameters worsened, with laboratory evidence of peripheral blasts, indicative of progression to AML. This coincided with worsening lysozyme levels and precipitous decline in renal function. In conclusion, renal disorders in the context of myeloid neoplasms warrant thorough investigation as it may be a sign of worsening hematological disease and the potential role of steroids for nephroprotection should be explored.