Clinical and prognostic significance of glomerulonephritis in clinically indicated kidney allograft biopsies

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Abstract
Background/aim: Posttransplant glomerulonephritis (GN) is an underrecognized but clinically important cause of allograft dysfunction. It remains uncertain whether GN detected in a clinically indicated kidney allograft biopsy provides prognostic information beyond graft function and chronic histological injury. The present study evaluates the association between biopsy-detected GN and death-censored graft loss. Materials and methods: Included in this retrospective single-center study were kidney transplant recipients (KTRs) who underwent clinically indicated allograft biopsy between May 2012 and October 2025. The primary outcome was death-censored graft loss, defined as a return to kidney replacement therapy. Postbiopsy graft survival was assessed using Kaplan–Meier analysis and sequential parsimonious Cox models. Results: Of the 120 KTRs in the study, 35 (29.2%) had biopsy-detected GN. Median death-censored graft survival was 2.19 years in the GN group and 7.71 years in the non-GN group (log-rank p = 0.005). GN was associated with graft loss in univariable analysis (HR, 2.04; 95% CI, 1.22–3.40; p = 0.006). In the main multivariable model adjusted for age, sex, biopsy estimated glomerular filtration rate, and interstitial fibrosis/tubular atrophy grade I–III, GN remained associated with graft loss (HR, 1.84; 95% CI, 1.06–3.18; p = 0.030). A multiple-imputation sensitivity analysis of the full cohort showed that additional adjustment for proteinuria attenuated the GN estimate (HR, 1.46; 95% CI, 0.84–2.54). The proportional hazards assumption was not satisfied for GN, and exploratory time-varying analysis suggested that the association may have varied over follow-up; however, later estimates were imprecise as few recipients with GN remained at risk. Conclusion: In this indication-biopsy cohort, biopsy-detected GN was associated with poorer death-censored graft survival after adjustment for graft function and chronic histological injury; however, this association was attenuated after additional adjustment for proteinuria. The magnitude and temporal pattern of the association require confirmation in larger cohorts.

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