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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.
Several clinical and genetic factors influence mycophenolic acid (MPA) response and are associated with the development of adverse drug events (ADEs). However, studies investigating predictors of MPA outcomes in lupus nephritis (LN) patients are still limited.
To optimise MPA outcomes, an observational cohort study have been conducted to investigate clinical and pharmacogenetic predictors in 156 patients with proliferative lupus nephritis (PLN) classified as Class III or IV ± V. Clinical characteristics including comorbidities, co-medications and laboratory data, were collected to assess MPA outcomes at 12 months according to the KDIGO criteria, classifying patients as complete responders (CR), partial responders (PR), or non-responders (NR). Genotyping was performed for candidate genetic polymorphisms in CES2, SLCOB, ABCC2, UGT, CYP3A5, and IMDPH. Associations of these variants with treatment response and ADEs were tested using chi-square and logistic regression analysis.
The majority of the study cohort were female, with a mean age of 33.6 ± 10.2 years. Overall, 82.7 % of the participants were classified as responders, and 17.3 % as non-responders, with ADEs reported in 34.6 %. Based on initial screening with the Chi-Square test, variables including higher MPA dose (p < 0.01), hyperlipidaemia (p < 0.05), newly diagnosed LN (p = 0.001), and steroid pulse (p = 0.046) were subsequently identified as predictors of good response in the regression model. Conversely, elevated baseline proteinuria (p = 0.031) and hypertension (p = 0.019) were associated with delayed response. Multivariate analysis confirmed that higher MPA dose (P=0.006) with hyperlipidaemia (p = 0.004), and absence of liver disease (p = 0.037) as strong predictors of renal response. Hypertension remained a predictor of delayed response (OR = 0.19, p = 0.024).
Regarding ADEs, hypertension increased infection risk (OR = 4.57, p = 0.025). Statin use was significantly associated with increased gastrointestinal toxicity (p = 0.024) but reduced infection (p = 0.043) and bone marrow suppression (p = 0.024). ACEI or ARB therapy was protective against GI toxicity (p = 0.031).
Genetic analysis demonstrated that IMPDH1 rs2278293 (p = 0.007–0.03) and UGT2B7 rs7439366 (p = 0.007) were predictors of good response, whereas SLCO1B1 rs4149056 (p < 0.001) and SLCO1B3 rs7311358 (p = 0.018–0.029) were associated with delayed response. Additionally, SLCO1B3 rs7311358 (p = 0.022), SLCO2B1 rs2851069 (p = 0.018), and ABCC2 rs717620 (p < 0.001) were linked to increased infection risk. CYP3A5*3 rs776746 (p = 0.048) correlated with bone marrow suppression, while UGT2B7-900G>A rs7438135 was associated with gastrointestinal toxicity and infection.
Clinical and genetic factors play a significant role in modulating MPA treatment outcomes in LN. The observed associations between MPA outcomes and certain variants (rs2278293, rs7438135, rs4149056, rs2851069, and rs776746) are novel findings that warrant further validation. Notably, the associations involving rs7439366, rs7311358, and rs717620 are consistent with prior evidence, reinforcing their potential relevance in MPA pharmacogenomics. Integrating the clinical and genetic predictors into clinical practice may support precision medicine and improve therapeutic outcomes in LN management.
