*Purpose: Kidney transplant (KT) recipients have high gout incidence due to reduced eGFR and medication use associated with hyperuricemia.¹ Oral urate-lowering therapies in KT patients are further limited by residual chronic kidney disease and potential drug-drug interactions. Pegloticase rapidly lowers serum urate in uncontrolled gout patients,^2-3 but efficacy is limited in ≥50% of treated patients by anti-drug antibodies that cause loss of urate-lowering effect and can lead to infusion reactions in some patients.^4-5 Commonly used anti-rejection medications have been known to reduce the development of anti-drug antibodies,⁶ but published data of pegloticase use in KT patients is limited. This claims-based analysis examined real-world pegloticase use in KT patients to determine the number of tolerated infusions compared to non-transplanted patients.

*Methods: Patients in the IQVIA database (2015-2020) who had ≥1 CPT or ICD9/10 code for KT and ≥1 pegloticase claim following KT were identified. Patients who returned to dialysis due to graft failure/rejection prior to pegloticase use were excluded. Patient characteristics and pegloticase therapy parameters were examined.

*Results: 91 KT recipients with pegloticase use were identified. Of 85 patients with demographics, 81% were male, mean(±SD) age at first transplant was 55.0±10.7 years, and 67% had tophaceous gout. The most common comorbidities were hypertension (84%), hyperlipidemia (48%), anemia (46%), type 2 diabetes (40%), and heart failure (34%). First transplant and gout codes occurred 2.6±1.7 and 2.1±1.7 years, respectively, before first pegloticase claim. Immunosuppressive medications used <3 months before and/or during pegloticase included tacrolimus (51%), mycophenolate mofetil (49%), and/or cyclosporine (37%; n=67 with medication codes). Patients received 13±16 pegloticase infusions (median: 8 [Q1, Q3: 4, 15]), with 38% receiving ≥12 and 20% receiving ≥20 infusions.

*Conclusions: This study showed a higher median number of pegloticase infusions than reported in prior claims-based studies of non-KT patients.⁷ Real world data from KT patients support the hypothesis that transplant immunosuppression can prevent the development of anti-drug antibodies to improve the rate of complete response to pegloticase in this vulnerable patient group that has a high risk for uncontrolled gout. References: 1. Clive DM, et al. J Am Soc Nephrol 2000; 11: 974. 2. Keenan RT, et al. Sem Arth Rheum 2021; 51: 347-52. 3. Botson JK and Peterson J. J Clin Rheum 2020 [Epub]. 4. Sundy JS, et al. JAMA 2011; 306(7): 711-20. 5. Lipsky PE, et al. Arthritis Res Ther 2014; 16(2): R60. 6. Hershfield MS, et al. Arthritis Res Ther 2014; 16: R63. 7. Chen SK, et al. BMJ Open 2020; 10(12): e041167.

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