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: FR-PO286

Focal Segmental Glomerulosclerosis (FSGS) Associated with Chimeric Antigen Receptor T-Cell (CAR-T) Therapy

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Orozco Scott, Paloma Claire, Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Abramson, Matthew, Icahn School of Medicine at Mount Sinai, New York, New York, United States

CAR-T therapy was first used to treat pediatric leukemia, and has since expanded to other hematologic malignancies. The most common adverse reactions include cytokine release syndrome (CRS) and neurotoxicity. Acute kidney injury (AKI) has been reported in up to 30% of adult patients post CAR-T. Treatment for CRS is non-standardized but may include tocilizumab or steroids. The mechanism behind CAR-T associated AKI is not well elucidated, given small retrospective studies lacking biopsy data. With increasing popularity of CAR-T therapy, better understanding the etiology and character of CAR-T associated kidney injury may improve kidney outcomes.

Case Description

We present a case of a 47-year-old man with IgA Kappa multiple myeloma, hypertension, and diabetes, with normal proteinuria at baseline. As part of a clinical trial, he received CAR-T therapy (ciltacabtagene autoleucel). He developed CRS on day 6, and was treated with tocilizumab and anakinra. Four days after infusion there was a gradual increase in serum creatinine (SCr) from baseline 0.9 to 1.35mg/dL, downtrending to 0.99mg/dL after one month. The patient also developed hypoalbuminemia, hyponatremia, and hypophosphatemia during his course, which improved by discharge.
24-hour urine protein one month post CAR-T was 2.6 grams, and subsequent UPCR peaked at 2.56 g/g three months post CAR-T. Kidney biopsy performed at that time showed FSGS, not otherwise specified (NOS) variant, without immune deposits or substantial interstitial scarring, and with preserved podocyte foot processes. The patient was treated conservatively with losartan, and subsequent UPCR improved to 0.17 g/g by 7 months post CAR-T.


This is the second case report of biopsy-proven FSGS after CAR-T in the literature. In contrast to the other case, our patient did not have interstitial inflammation or complete podocyte foot-process effacement, suggesting against primary FSGS, nor did he develop oliguria or edema. The presentation of new-onset proteinuria was temporally related to the CAR-T infusion, possibly representing either a CRS-related global or an off-target local inflammatory response. This case highlights the importance of understanding of CAR-T’s effects on the kidney. A limitation of our case is the lack of APOL-1 testing to investigate as a second-hit phenomenon.