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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.
Noninvasive laboratory testing is desirable to diagnose kidney diseases and reduce reliance on invasive renal biopsy. IgA nephropathy (IgAN) and diabetic nephropathy (DN) are the two major causes of hemodialysis initiation in Japan. Although corticosteroids are commonly used to treat IgAN, patients often develop steroid-induced diabetes mellitus (DM), and there are overlapping pathological mechanisms of IgAN and DN in which the primary cause of kidney injury cannot be distinguished. Therefore, differentiating IgAN from DN is crucial to guide treatment and prevent disease progression. Bioactive lipids are reportedly associated with kidney injury, and we previously showed that the urinary level of tetranor-prostaglandin E metabolite (tetranor-PGEM), a metabolite of PGE2, was elevated in patients with DM and increased with advancing DN stages. In the present study, we performed urinary lipidomics to evaluate the potential utility of urinary lipids and their metabolites for differentiating IgAN from DN.
18 subjects with IgAN and 13 subjects with DN, each diagnosed histologically by renal biopsy, were enrolled. Urine specimens collected closest to the biopsy date were analyzed. Urinary bioactive lipids were quantified by liquid chromatography-tandem mass spectrometry (LC-MS/MS), including diacyl-phospholipids (PLs—phosphatidylcholine, PC; phosphatidylserine, PS; phosphatidylethanolamine, PE; phosphatidylglycerol, PG; phosphatidylinositol, PI), lysophospholipids (LysoPLs—lysophosphatidylcholine, LPC; lysophosphatidic acid, LPA; lysophosphatidylserine, LPS; lysophosphatidylethanolamine, LPE; lysophosphatidylglycerol, LPG; lysophosphatidylinositol, LPI), eicosanoids and related mediators (e.g., prostaglandins [PGs], thromboxanes [TXs], leukotrienes [LTs], hydroxyeicosatetraenoic acids [HETEs]) and related metabolites (e.g., resolvins, protectins/maresins).
30 urinary bioactive lipid features differed significantly between IgAN and DN. Levels of 16:0 LPE (260.3 [Q1–Q3, 145.6–324.8] nmol/mgCr vs. 578.5 [393.3–799.4] nmol/mgCr) and 38:0 PE (14.6 [8.4–19.4] nmol/mgCr vs. 25.3 [22.9–29.7] nmol/mgCr) were significantly higher, whereas 18-carboxy-LTB4 (0.00 [0.00–0.00] vs. 1.86 [0.73–3.14] µg/gCr) was lower in DN than in IgAN. A quadrant analysis integrating P values, area under the receiver-operating characteristic curves (AUROCs), and Cliff’s delta identified 16:0 LPE as the most discriminative feature (P = 0.002, AUROC 0.838 [95%CI, 0.696–0.979], Cliff’s delta 0.68). An orthogonal partial least squares discriminant analysis (OPLS-DA) model with one predictive and three orthogonal components showed that top variable importance for prediction (VIP) scores included 34:1 PI (1.92), 36:6 PC (1.91), and 38:0 PE (1.89), which are significantly higher in DN than IgAN.
18-carboxy-LTB4 is a urinary metabolite produced during ω- and β-oxidation-mediated inactivation of LTB4, a potent neutrophil chemoattractant and activator, and has been implicated in the pathophysiology of IgAN. The elevation of urinary 16:0 LPE in DN may reflect enhanced phospholipid remodeling under metabolic and oxidative stress, together with impaired proximal tubular reabsorption.
Urinary lipidomics shows potential utility for differentiating IgAN from DN; however, validation in larger cohorts, including evaluation of its applicability to other kidney diseases, is warranted.
