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Kidney Week

Abstract: TH-PO564

Semaglutide (Ozempic), a Possible Cause of Focal Segmental Glomerulosclerosis (FSGS)

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: From Inflammation to Fibrosis

Authors

  • Khan, Jahanzeb, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Juncos, Luis A., University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Ali, Umair, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Bukhari, Sehrish W., Kidney Care Center, Little Rock, Arkansas, United States
  • Khalid, Mariam, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
  • Khan, Nasir, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States
Introduction

Semaglutide use has been increasing rapidly because of its beneficial effects on diabetes control, cardiovascular protection, and weight loss. Adverse renal events are rare. We present a case of semaglutide-associated FSGS.

Case Description

A 55-year-old nondiabetic female with history of end stage kidney disease secondary to IgA nephropathy treated by kidney transplantation 3 years earlier. Her baseline serum creatinine was 1.2 mg/dL and she had no proteinuria. She was initiated on Semglutide for weight loss. Soon after starting. 0.5 mg weekly, she developed proteinuria; UPC (urine protein to creatinine ratio) =400 mg/mg. The association was not suspected and so her dose was increased to 1.0 and then 2.0 mg weekly. The increases in Semaglutide dose coincided with worsening UPC 3300 mg at 2 months and 9 g/g at 4 months. She was subsequently admitted due to progressive edema and dyspnea; her 24 hour urine protein was 16 g/g now. Her serum creatinine remained at 1.2-1.5 mg/dL while her albumin and LDL levels were 1.7 and 303 mg/dL, respectively. She remained on Tacrolimus, Mycophenolate and Prednisone throughout. Blood tests for HIV, hepatitis, drug use and APOL1 gene were negative. A kidney biopsy showed FSGS on light microscopy (figure A), moderate to marked segmental foot process effacement by electron microscopy (figure B).

Discussion

To the best of our knowledge, this is the first case of FSGS that appears to be associated with the Semaglutide use. While we did not establish causality, the time course and progression of proteinuria raise the possibility that Semaglutide was the trigger. The mechanism is unknown but Semaglutide therapy is known to induce formation of anti-Semaglutide antibodies in up to 1% of patients. The clinical significance of this immune response is unknown but raises the possibility that it could have led to the formation of a circulating glomerular permeability factor that caused the FSGS. Identification of more cases may allow for further investigations into the potential causality and mechanisms of Semaglutide-associated FSGS.