ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: TH-PO947

SGLT2i-Induced Erythrocytosis Unveiling Heterozygous Hereditary Hemochromatosis (HH) Gene Mutation in an Individual with CKD

Session Information

Category: Anemia and Iron Metabolism

  • 200 Anemia and Iron Metabolism


  • Schumacher, Kamilya, Albany Medical College, Albany, New York, United States
  • Gosmanova, Elvira O., Albany Stratton VA Medical Center Albany, Albany, New York, United States

SGLT2i were shown to increase hemoglobin (Hb) levels in clinical trials. We report a case of symptomatic erythrocytosis in an individual treated with SGLT2i empagliflozin who was later found to have a HH gene mutation.

Case Description

This was a 72-yo male with CKD and baseline serum creatinine (SCr) of 2.1mg/dL (eGFR 33mL/min/1.73m2), controlled type 2 diabetes (A1C 6.9%) and hypertension. Empagliflozin 12.5mg daily was initiated due to persistent grade A3 proteinuria (uACR ~1.5g/g) despite daily combination of losartan 100mg and spironolactone 25mg. Hb and hematocrit (Hct) were 16.8g/dL (normal 13.5-17) and 49.5% (normal 38-50) at the time of SGLT2i start. The patient had no history of obstructive sleep apnea. There was a remote history (>30 years ago) of smoking. Over the years, he had intermittent mild Hb elevation in 17-17.5g/dL range. At that time, erythropoietin level was normal and polycythemia vera was excluded. Within 6 months of empagliflozin initiation, Hb (Hct) gradually rose to 20g/dL (59.3%) despite advice to maintain adequate hydration. The patient reported worsening fatigue and diffuse myalgias. Physical examination and vital signs were normal. Transferrin saturation (Tsat) was 30%. Ferritin was 145ng/mL. SCr rose to 2.6mg/dL (eGFR 25 ml/min/1.73m2). Screening for HH in the nephrology clinic revealed H63D heterozygosity in the HFE (Hemostatic Iron regulator) gene and negative C282Y gene mutation. Two serial phlebotomies were performed and lead to the normalization of Hb (Hct) to 16.5g/dL (48%), resolution of symptoms, and an improvement in SCr to 2.0mg/dL (eGFR 35 ml/min/1.73m2). Tsat and ferritin remained stable. Empagliflozin was continued for renoprotection. Monthly phlebotomy was continued to maintain adequate Hb.


SGLT2i reduce risk of anemia in patients with CKD. Their use may also be associated with erythrocytosis. The presence of underlying heterozygous HH gene mutation was likely predisposing risk factor of SGLT2i-induced erythrocytosis. This case suggests that periodic monitoring of Hb level should be considered. Additionally, screening for HH could be offered to patients with SGLT2i-induced erythrocytosis to implement phlebotomy if a HFE gene mutation is detected. Stopping SGLT2i will likely lower Hb to baseline, but it will also remove their cardiorenal benefits.