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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and a leading cause of end-stage kidney disease requiring dialysis or transplantation. Its clinical course is highly heterogeneous, and current risk stratification based on proteinuria, eGFR, and histological grading often fails to fully account for this variability. Nephron number, reflecting the structural reserve of the kidney, progressively declines with aging and is further reduced by disease-related injury. However, distinguishing between physiological loss due to aging and pathological depletion remains a challenge. To address this, we introduced a novel nephron deficit index (NNdiff), defined as the difference between observed nephron number and age-expected values derived from healthy kidney donors. We hypothesized that incorporating NNdiff would allow more accurate contextualization of structural kidney reserve and improve prognostic assessment in IgAN.
Nephron number was estimated using a combined approach based on cortical volume derived from unenhanced CT imaging and biopsy-based assessment of non-sclerotic glomerular density. A reference regression line of age-related nephron decline was generated from 49 living kidney donors. NNdiff was then calculated for each patient as the observed nephron number minus the age-expected reference value. Patients were stratified into two groups: NNdiff ≥0 (adequate or preserved reserve) and NNdiff <0 (structural deficit). The primary endpoint was a composite of ≥30% decline in eGFR or initiation of kidney replacement therapy. Multivariable Cox proportional hazards models adjusted for conventional prognostic factors (age, sex, baseline eGFR, proteinuria, and hypertension).
This study included 222 patients with biopsy-proven IgAN. At baseline, mean age was 42.7 years, eGFR 60.6 mL/min/1.73m², median proteinuria 1.4 g/day, and nephron number 68 × 10⁵ per kidney. Of the 222 patients, 137 patients (62%) exhibited NNdiff <0, indicating a pathological deficit relative to age, whereas the remaining 85 patients (38%) had NNdiff ≥0. Over a median follow-up period of 5.4 years, a total of 99 composite kidney outcome events were observed. Kaplan–Meier curves demonstrated significantly poorer kidney survival in the NNdiff <0 group (log-rank p<0.001). In adjusted analyses, NNdiff <0 independently associated with adverse kidney outcomes (HR 1.69, 95% CI 1.01–2.82, p = 0.046).
A nephron number lower than age-expected values strongly associates with poor kidney outcomes in IgAN, independent of established clinical and pathological markers. The NNdiff index allows structural kidney reserve to be interpreted relative to age-specific expectations, enhancing risk stratification and facilitating earlier intervention in patients with reduced structural kidney reserve. Beyond IgAN, this concept may extend to other chronic kidney diseases where structural reserve and nephron adaptation play a critical role in long-term prognosis. This study was presented at the 68th Annual Meeting of the Japanese Society of Nephrology.
