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Abstract: SA-PO897

eGFR Changes in Uncontrolled Gout Patients Undergoing Pegloticase Plus Methotrexate Co-Therapy

Session Information

Category: CKD (Non-Dialysis)

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

Authors

  • Marder, Brad Allan, Horizon Therapeutics plc, Deerfield, Illinois, United States
  • Albert, John A., Rheumatic Disease Center, Milwaukee, Wisconsin, United States
  • Broadwell, Aaron, Rheumatology and Osteoporosis Specialists, Shreveport, Louisiana, United States
  • Padnick-Silver, Lissa, Horizon Therapeutics plc, Deerfield, Illinois, United States
  • LaMoreaux, Brian, Horizon Therapeutics plc, Deerfield, Illinois, United States
Background

Renal function decline is associated with hyperuricemia and gout. Pegloticase can lower serum uric acid (sUA) in uncontrolled gout (UG) patients (pts), independent of CKD status. Recent trial/case data support immunomodulator (IMM) use with pegloticase to limit anti-drug antibody formation, increasing urate-lowering response rate and decreasing infusion reaction (IR) risk. CKD can limit IMM use, particularly methotrexate (MTX), and pegloticase+IMM clinical trials excluded pts with eGFR <40. However, CKD is common in gout pts and pegloticase+IMM use in CKD pts has been reported. Here we analyse case data to examine eGFR changes during pegloticase+MTX co-therapy in CKD and non-CKD pts.

Methods

Deidentified case data of pegloticase+MTX co-therapy were pooled and retrospectively analyzed. Pts were labeled as CKD (baseline [BL] eGFR <60 ml/min/1.73m2) or non-CKD (BL eGFR ≥60 ml/min/1.73m2). sUA, eGFR, blood cell counts, and liver function tests were monitored. Pt characteristics, treatment parameters, response rate (≥12 infusions [inf], pre-inf 12 sUA <6 mg/dL), eGFR, and AEs were examined. Pts on therapy at data collection with <12 inf were excluded from response analyses.

Results

42 UG pts were included; 15 CKD (13 stage3, 2 stage4; eGFR=43±11 ml/min/1.73m2; sUA=9±2 mg/dL), 27 non-CKD (eGFR=83±19 ml/min/1.73m2; sUA=10±2 mg/dL). Comorbidity profiles were similar, but more CKD pts were female (33% vs 7%) and ≥65 yrs (60% vs 19%). MTX was started ~4 wks before pegloticase in both groups, but CKD pts had lower dose (15±6 vs 19±5 mg/wk). Pegloticase response rate (CKD: 92% vs non-CKD: 86%) and treatment (14.7±8.1 vs 14.1±7.1 inf) were similar. In non-CKD pts, 44% had an eGFR increase (mean[±SD]: +4.2±15.0 ml/min/1.73m2). In CKD pts, 60% had an eGFR increase (+11.5±20.9 ml/min/1.73m2), with CKD stage stability/improvement in 13 (87%, both stage4→3a; 2 stage3a→3b). No new safety signals were identified. 7 (47%) CKD and 13 (48%) non-CKD pts had ≥1 AE; most-commonly gout flare (47%, 41%). Pancytopenia (n=1) and mild IR (n=1) were reported (both non-CKD pts).

Conclusion

These limited data show similar pegloticase+MTX urate-lowering efficacy in CKD and non-CKD pts. Most CKD pts had renal stability/improvement during therapy, but further study is needed.

Funding

  • Commercial Support –