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Abstract: PO1533

Collapsing FSGS in a Patient with Acute Myeloid Leukemia and Prior COVID-19 Infection

Session Information

Category: Glomerular Diseases

  • 1203 Glomerular Diseases: Clinical, Outcomes, and Trials

Authors

  • Manivannan, Surya, University of North Carolina System, Chapel Hill, North Carolina, United States
  • Pavlovich, Stephanie S., University of North Carolina System, Chapel Hill, North Carolina, United States
  • Malek, Irshadjahan, University of North Carolina System, Chapel Hill, North Carolina, United States
  • Jain, Koyal, University of North Carolina System, Chapel Hill, North Carolina, United States
Introduction

Collapsing focal segmental glomerulosclerosis (c-FSGS) has been independently associated with COVID-19 infection, acute myeloid leukemia (AML), and apolipoprotein L1 (APOL1) risk variants. We describe a patient with homozygous APOL1 G1 risk allele and AML who developed renal failure due to c-FSGS and acute tubular injury.

Case Description

A 25-year-old male with a history of mild asthma and COVID-19 infection 1 month prior presented with a 3-week history of severe fatigue, weight loss, persistent dyspnea, and fevers. He was found to have leukopenia, thrombocytopenia, an acute kidney injury, and nephrotic range proteinuria. The patient was diagnosed with AML by bone marrow biopsy (BMBx). At presentation, his serum creatine was 2.8 mg/dL, which rapidly increased to 6.9 mg/dL over 2 weeks. Urine protein:creatinine ratio (UPCR) was 3.4g/g on admission. Renal biopsy demonstrated c-FSGS (Figure) and diffuse acute tubular injury. He was treated with standard remission induction therapy for AML with 7+3 therapy (7-day continuous infusion of cytarabine, daunorubicin on days 1-3, and high dose steroids). High dose steroids were continued for c-FSGS treatment with plan for a slow taper over several months. Within a few days of starting 7+3 treatment, his renal function began to improve. His 14-day BMBx demonstrated a hypocellular marrow consistent with complete remission. After 1 month, his creatine improved to 1 mg/dL, along with improvement in his serum albumin. Repeat UPCR is pending.

Discussion

COVID-19 is associated with immunologic alterations precipitating c-FSGS, especially in patients with APOL1 high risk alleles. Additionally, FSGS has been reported in AML, but the etiology behind glomerular pathologies in AML is unclear and likely multifactorial. Studies have indicated immunologic dysregulation related to leukemia, as well as viral-related etiologies. The trigger for c-FSGS in our patient is uncertain.

Light microscopy demonstrated focal and segmental glomerulosclerosis with global and segmental collapse.