Kidney Week

Abstract: SA-PO0545

Effect of Sulforaphane and GSTM1 Genotype on Plasma 8-Isoprostane: A Phase 2, Randomized, Double-Blind, Placebo-Controlled Trial

Session Information

• CKD: Clinical - Therapies, CKM Health, Special Populations, and More
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

• 2202 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

• Le, Thu H., University of California Irvine, Irvine, California, United States

Thu H. Le, MD

• Sonawane, Sharvari A., University of Rochester Medical Center Department of Medicine, Rochester, New York, United States

Sharvari A. Sonawane, MS

• Ghimirey, Rita, University of California Irvine, Irvine, California, United States

Rita Ghimirey

• Stewart, Allison J., University of Rochester Medical Center Department of Medicine, Rochester, New York, United States

Allison J. Stewart

• Wang, Yves T., University of Rochester Medical Center Department of Medicine, Rochester, New York, United States

Yves T. Wang, PhD

• Ma, Jennie Z., UVA Health, Charlottesville, Virginia, United States

Jennie Z. Ma

Group or Team Name

• Health Effects (Renal) Of Extra Strength Avmacol (HEROES) Study Group

Background

Progression of chronic kidney disease (CKD) is associated with increased oxidative stress (OS). The common null allele of the glutathione S-transferase μ-1 (GSTM1) gene, which encodes an antioxidant enzyme and is a downstream target of nuclear factor erythroid 2-related factor 2 (NRF2), is associated with elevated OS and increased risk of CKD progression. In a Phase 2 randomized double-blind placebo-controlled safety and feasibility trial, we examined whether upregulating antioxidant enzymes by activating the NRF2 pathway via supplementation with sulforaphane (SFN) in the form of Avmacol Extra Strength (ES) would reduce plasma and urine 8-isoprostane, a marker of OS, in a GSTM1 genotype dependent manner.

Methods

Adults with CKD Stages 3-4 and ≥ 3 mL/min/1.73m² decline in eGFR in the preceding 12 months were recruited from a single center and randomized to 4 tablets once daily of Avmacol ES or placebo for 6 months. GSTM1 was genotyped, and blood and urine samples were collected at baseline, and at 1, 3, and 6 months, in addition to standard of care clinical labs. A minimum of 88 participants completing the study was needed to detect a 25% reduction in plasma 8-isoprostane at 6 months, the primary outcome.

Results

96 out of 100 targeted subjects were enrolled and 79 completed the study. Baseline characteristics were similar between groups, except GSTM1 null (0/0) (higher CKD progression risk) genotype was more prevalent in Avmacol ES group (61% vs 49%). Side effects were primarily gastrointestinal and were similar between groups. Compared to baseline, there were no significant differences in change in plasma or urine 8-isoprostane between groups at 6 months. However, when stratified by GSTM1 genotype, those with GSTM1 active genotype (1/1, or 1/0) showed a trend toward reduced plasma and urine 8-isoprostane levels at 6 months (see Figure).

Conclusion

Non-significant results may have been due to insufficient power. A larger and longer trial is needed to determine whether reduction in plasma and urine 8-isoprostane by SFN can delay CKD progression in GSTM1 null and active patients.

Blue - Avmacol ES Group, Red - Placebo Group

Funding

• NIDDK Support