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Research Article | DOI: https://doi.org/10.5281/zenodo.22796302

Focal Segmental Glomerulosclerosis and Primary Polycythemia: Report of Two Cases

G. Khellaf 1,2*, A. Benziane1,2 1,2

¹University of Health Sciences Dr. Youcef El Khatib, Faculty of Medicine, Algiers, Algeria

²Department of Nephrology, Bab El Oued University Hospital, Algiers, Algeria

*Corresponding Author: G. Khellaf, University of Health Sciences Dr. Youcef El Khatib, Faculty of Medicine, Algiers, Algeria

Citation: G. Khellaf, A. Benziane. (2026). Focal Segmental Glomerulosclerosis and Primary Polycythemia: Report of Two Cases, J International Journal of Public Health Research and Epidemiology; 2 (5) 24,Doi:https://doi.org/10.5281/zenodo.22796302

Copyright: G. Khellaf, et al © (2026). This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Received: 20 August 2026 | Accepted: 28 August 2026 | Published: 09 September 2026

Keywords: focal segmental glomerulosclerosis; polycythemia vera; vaquez disease; jak2 mutation; nephrotic syndrome

Abstract

Primary polycythemia, also known as polycythemia vera or Vaquez disease, is a myeloproliferative disorder characterized by excessive red blood cell production due to a mutation in the JAK2 protein, leading to uncontrolled proliferation of erythroid progenitor cells . Renal involvement in polycythemia vera is uncommon but can manifest as various glomerular diseases, including focal segmental glomerulosclerosis (FSGS) . We report two cases of patients with primary polycythemia and FSGS, highlighting the potential association between these two conditions and the importance of treating the underlying myeloproliferative disorder.

Case 1: A 19-year-old female patient, followed since the age of 15 years for primary FSGS diagnosed on renal biopsy performed for impure nephrotic syndrome with hematuria. Four years after complete remission, the patient presented with a relapse associated with polycythemia and thrombocytosis on complete blood count. Secondary causes of polycythemia were excluded. Bone marrow biopsy revealed findings consistent with polycythemia vera, despite negative JAK2 mutation testing. The hematology team proposed phlebotomy and myelosuppressive oral therapy. One month later, proteinuria regressed from 15 g/24h to 4.7 g/24h.

Case 2: A 45-year-old male patient, with a history of polycythemia vera diagnosed two years earlier, presented with nephrotic syndrome. Renal biopsy revealed focal segmental glomerulosclerosis. The patient was treated with phlebotomy and myelosuppressive therapy, with improvement in proteinuria.

Discussion: The association between FSGS and polycythemia vera is rare but has been reported in the literature. The pathophysiology is thought to involve hyperviscosity, increased glomerular capillary pressure, and possible direct effects of JAK2 mutations on podocytes. Treatment of the underlying myeloproliferative disorder can lead to improvement of proteinuria, as observed in our patients.

Conclusion: Primary polycythemia should be considered in patients with FSGS and unexplained polycythemia. While polycythemia vera is not curable, early detection and appropriate treatment can reduce the risk of vascular complications and may improve renal outcomes.

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