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

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO0764

Preeclampsia as a Trigger for Collapsing Glomerulopathy in a Young Female Patient with Systemic Lupus Erythematosus

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Siddiqi, Mahwash, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Tahir, Maria, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Raza, Muhammad, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Kaur, Gurwant, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Karasinski, Amanda A., Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Farooq, Umar, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Miller, Ronald P., Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Ghahramani, Nasrollah, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States
  • Verma, Navin, Penn State Health Milton S Hershey Medical Center, Hershey, Pennsylvania, United States

Group or Team Name

  • Division of Nephrology
Introduction

Preeclampsia is associated with glomerular endotheliosis, thrombotic microangiopathy, and anti-angiogenic dysregulation. Collapsing glomerulopathy, though rare in this context, can be triggered by the severe podocyte injury mediated by excess sFlt-1, which sequesters VEGF (vascular endothelial growth factor) and disrupts glomerular homeostasis. We report a case of preeclampsia-associated collapsing glomerulopathy in a young female with systemic lupus erythematosus, highlighting the critical importance of obstetric history in the evaluation of nephrotic syndrome

Case Description

A 21-year-old female with SLE controlled on prednisone, mycophenolate mofetil, and hydroxychloroquine, with a history of preeclampsia 8 months before presentation, was seen for bilateral lower extremity edema, fatigue, and acute kidney injury requiring dialysis. Labs revealed creatinine 6.0 mg/dL (baseline 0.9 one year prior), UPCR (Urine protein-to-creatinine ratio) 5.43 g/g, hypoalbuminemia, and hypertension. Serologies showed ANA titer 1:2560 with negative anti-dsDNA, normal complements, and negative hepatitis and HIV panels. Renal biopsy revealed focal collapsing glomerulopathy, with background class II lupus nephritis and with full-house immunofluorescence. She was treated with pulse steroids, and renal function improved in a few days without any need for dialysis.

Discussion

This case illustrates the dual pathological interplay between preeclampsia and glomerular disease. Preeclampsia can induce de novo glomerular injury, while underlying nephropathy independently increases preeclampsia risk. The anti-angiogenic milieu of preeclampsia, marked by excess sFlt-1 suppressing VEGF, can precipitate severe podocyte injury and collapsing lesions, analogous to mechanisms seen in HIV-associated nephropathy. In this patient, APOL1 high-risk genotypes prevalent in individuals of African descent may have further amplified susceptibility to collapsing glomerulopathy. This case underscores how an incomplete obstetric history can misdirect the diagnostic workup.