Development of IgA nephropathy following risankizumab therapy for psoriatic arthritis: a case report.

IgA nephropathy (IgAN) has been reported in association with several biologic agents; however, renal events related to selective interleukin (IL)-23p19 inhibition remain poorly characterized. We report a case of biopsy-proven IgAN that became clinically apparent after initiation of risankizumab for psoriatic arthritis. A 37-year-old man with psoriatic arthritis achieved marked improvement in joint and skin manifestations after starting risankizumab in October 2022. Thereafter, kidney function gradually declined, with the estimated glomerular filtration rate decreasing from approximately 90-100 to 69.9 mL/min/1.73 m2 by August 2023, accompanied by proteinuria and microscopic hematuria. Despite supportive therapy with azilsartan and dapagliflozin, kidney function continued to worsen and proteinuria persisted, prompting a percutaneous kidney biopsy in February 2025. Light microscopy showed mesangial and focal endocapillary hypercellularity without crescents. Immunofluorescence demonstrated granular mesangial deposits of IgA and C3, and KM-55 staining was positive, indicating glomerular deposition of galactose-deficient IgA1; electron microscopy revealed para-mesangial electron-dense deposits. The biopsy was consistent with primary IgAN (Oxford classification M0E1S0T0C0). We administered steroid pulse therapy according to the Pozzi protocol (methylprednisolone 500 mg/day for 3 consecutive days), achieving remission of urinary abnormalities with modest improvement in kidney function, while risankizumab was continued. This case highlights the need for periodic urinalysis and kidney function monitoring during IL-23-targeted therapy and suggests that IgAN-directed treatment may be effective even when continuation of the biologic agent is clinically necessary.