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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Membranous nephropathy (MN) exhibits relatively uniform glomerular pathology, whereas clinical courses are heterogeneous. Anti-PLA2R antibody positivity and clinical features such as male sex, older age, and heavy proteinuria at diagnosis have been linked to prognosis, and electron microscopy (EM) stage is also considered in risk assessment. Structural determinants, particularly nephron number, remain understudied. We evaluated whether the estimated nephron number at diagnosis predicts subsequent kidney outcomes in MN.
We conducted a retrospective, longitudinal cohort study of biopsy-proven primary MN. Nephron number per kidney was estimated by combining non-sclerotic glomerular density from histomorphometry with cortical volume measured on non-contrast computed tomography. The primary endpoint was the annualized slope of eGFR decline. The secondary endpoint was a 40% reduction from baseline eGFR during follow-up. For the primary endpoint, we used linear mixed-effects models with patient-level random intercepts and a time-by-nephron-number interaction term, adjusting for age, sex, baseline eGFR, proteinuria, EM stage, and anti-PLA2R status. For the secondary endpoint, group differences over time were visualized with Kaplan–Meier curves and compared using log-rank tests.
Among 93 patients (mean age 64 years, 73% male, mean eGFR 65 mL/min/1.73 m², mean proteinuria 4.2 g/day), the median nephron number was 730,000 per kidney, and 36% were anti-PLA2R positive. EM stage at diagnosis was Stage I in 17 patients (18.3%), Stage II in 47 (50.5%), Stage III in 24 (25.8%), and Stage IV in 5 (5.4%). Median follow-up was 7.8 years, and 29 patients (31%) met the endpoint of a 40% reduction from baseline eGFR. Lower nephron number was independently associated with a faster eGFR decline (−0.031 mL/min/1.73 m² per 100,000 nephrons per year, P=0.006). In tertile analyses, fewer nephrons were associated with a significantly steeper annual eGFR decline (P for trend <0.001). The low-nephron-number group experienced a 0.69 mL/min/1.73 m² per year faster eGFR decline than the high-nephron-number group (−1.486 vs −0.799 mL/min/1.73 m² per year, P<0.001) (Figure A). Kaplan–Meier curves showed lower renal event-free survival in patients with lower nephron number (log-rank P=0.025) (Figure B).
Lower nephron number at diagnosis was independently associated with a faster loss of kidney function and a higher incidence of a 40% eGFR decline in MN, beyond EM stage, anti-PLA2R status, and clinical covariates including age, sex, and proteinuria. Incorporating nephron number into prognostic assessment may improve risk stratification at diagnosis by capturing structural reserve that is not fully reflected by serologic findings or routine clinical measures.
