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Abstract: PO1905

Secondary Polycythemia Associated with Membranous Nephropathy

Session Information

Category: Glomerular Diseases

  • 1203 Glomerular Diseases: Clinical, Outcomes, and Trials

Authors

  • Thotakura, Ramakrishna, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Siddamreddy, Suman, Baptist Health, Little Rock, Arkansas, United States
  • Kanuru, Sruthi, Central Arkansas Veterans Healthcare System John L McClellan Memorial Veterans Hospital, Little Rock, Arkansas, United States
  • Kadiyala, Aditya, University of Maryland Medical System Corporation, Baltimore, Maryland, United States
Introduction

Polycythemia has been recognized as a common occurrence in certain renal diseases such as cystic diseases of the kidney, renal cancer, tuberous sclerosis and hydronephrosis. However, polycythemia in association with membranous nephropathy has rarely been reported. Here we report a case of secondary polycythemia from membranous nephropathy. Although the mechanism of this phenomenon is unclear, decreased effective circulating volume leading to hypoxemia and thereby polycythemia seems to be the most likely explanation

Case Description

37-year old white male with Hypertension, OSA using CPAP, tobacco use was admitted with 40-lb weight gain and anasarca. 24-hour urine collection revealed 17-gram protein excretion with serum albumin of 1.1 and marked hyperlipidemia. Kidney biopsy revealed membranous nephropathy. Staining for PLA2R and THSD7a were negative within the glomerular deposits. Evaluation for secondary causes of membranous nephropathy was negative for ANA, RPR/syphilis antibodies, Hepatitis, HIV, ANCA, Anti-GBM Ab and normal C3,C4 levels. CT of torso was negative for overt malignancy or hepatosplenomegaly. Patient’s hemoglobin ranged between 16.5– 18.5 G/dl (hct 52-60%). Serum erythropoietin level was 12.3 IU/L (Normal 5-30IU/L) with corresponding hemoglobin of 18.2 G/dl. JAK2 exon12, V617F mutations were negative. Hematology evaluation concluded that primary polycythemia is unlikely. Patient received 2 doses of 1 Gm Rituximab given 2 weeks apart. Patient was placed on Apixaban for prophylactic anticoagulation. Follow up labs to evaluate response to therapy are currently pending. It is yet to be seen if polycythemia resolves with remission of membranous nephropathy.

Discussion

Polycythemia is seldom seen in patients with membranous nephropathy. We postulated that hypoxia induced by decreased renal perfusion is the main trigger for polycythemia. However, it is puzzling as to why more patients with membranous nephropathy are not polycythemic. This leads us to believe that there might be some unique processes leading to polycythemia in membranous nephropathy, as in this patient, which might need further investigation. Polycythemia would further enhance the risk of thromboembolism in such patients whose risk of hypercoagulability is already high in setting of severe hypoalbuminemia. Hence, prophylactic anticoagulation should strongly be considered in these patients.