ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

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

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO1508

Guselkumab-Associated Severe AKI from Collapsing Glomerulopathy

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Madireddy, Varun, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, New York, United States
  • Malieckal, Deepa A., Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, New York, United States
  • Maturostrakul, Boonyanuth N., Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, New York, United States
  • Yune, Philip Sungho, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, New York, United States
  • Bijol, Vanesa, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, New York, United States
  • Shah, Hitesh H., Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Great Neck, New York, United States
Introduction

Collapsing glomerulopathy (CG) has been commonly associated with viral infections, mainly HIV. Several medications have also been associated with CG. We present the first case of Guselkumab-associated rapidly progressive AKI from CG and acute tubular injury.

Case Description

86-year-old African American female with history of HTN, RCC with left nephrectomy, CKD, CHF, and psoriasis (on Guselkemab treatment since 2018) presented to our hospital for worsening bilateral LE edema and AKI. On presentation, Scr was elevated at 3.75 and serum albumin was WNL (3.5). Three weeks prior to presentation, Scr was elevated but stable at 1.77 on outpatient labs. Of significance, pt. received Guselkemab injection one week prior to presentation. During hospital stay, UA was significant for proteinuria and hematuria. Spot urine total protein-to-creatinine ratio (TP/CR) was significantly elevated at 13.7. Of note, spot urine TP/CR was 1.6, four months prior to presentation. There was no right hydronephrosis or renal vein thrombosis seen on imaging. Serological tests including ANCAs, HBsAg, Hep C ab, HIV, RVP, COVID-19 PCR, Parvovirus B19 PCR, and CMV PCR were all negative. Patient initially received diuretic therapy for LE edema. Kidney biopsy performed during hospital stay showed CG and acute tubular injury. Electron microscopy examination of kidney biopsy specimen was significant for extensive effacement of podocyte foot processes and rare tubuloreticular inclusions in endothelial cell cytoplasm. Scr rapidly worsened to 7.98 and HD treatment was initiated. Our patient was also initiated on daily high dose oral corticosteroid therapy.

Discussion

Guselkumab, an IL-23 blocker is FDA approved for the treatment of plaque psoriasis and active psoriatic arthritis. A case of Ustekinumab (IL-23/IL-12 inhibitor) associated FSGS (after 2 years of treatment) has been reported in the literature. Our patient while on chronic Guselkumab treatment developed rapidly worsening AKI and CG, a week following the last dose of Guselkumab. We believe that in absence of any additional known risk factors, Guselkumab was responsible for AKI and CG in our patient. Our patient currently remains dialysis dependent. Clinicians should be aware of this very rare but potential association.