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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.
Hypertension (HTN) is closely associated with glomerular diseases (GD). Elevated blood pressure (BP) significantly contributes to the progression of chronic kidney disease (CKD), impacts treatment outcomes and prognosis. Despite significant progress in reducing cardiovascular mortality, the risk of fatal outcome with a combination of kidney damage of any etiology and HTN increases. The combination of HTN with kidney damage in diabetes mellitus (DM) and with an estimated glomerular filtration rate (eGFR) of <60 ml/min has been extensively studied, while the combination of HTN with primary GD and kidney damage in systemic diseases remains insufficiently studied. Therefore, the aim of our study is to investigate the prevalence and clinical features of HTN phenotypes in patients with GD
A single-center, observational cohort study was conducted. The study included 93 patients (56% M , median age 46 years) with primary glomerulonephritis n=81 (87%, 66 (71%) patients with biopsy-proven) and kidney damage in systemic diseases n=12 (13%). Office BP was measured three times in both arms for all patients. Ambulatory blood pressure monitoring (ABPM) was performed in 66 (71%) patients according to the standard protocol. Clinical HTN was defined as office BP ≥140/90 mm Hg, while ambulatory HTN was defined as a 24-hour average BP ≥130/80 mm Hg. The BP phenotypes were identified: masked HTN - office BP ≤140/90 mm Hg with ambulatory BP >130/80 mm Hg; normotension - office BP <140/90 mm Hg with ambulatory BP <130/80 mm Hg; sustained HTN - office BP ≥140/90 mm Hg with ambulatory BP ≥130/80 mm Hg; nocturnal HTN - nighttime systolic BP ≥120 mm Hg and/or diastolic BP ≥70 mm Hg; isolated nocturnal HTN - daytime BP <135/85 mm Hg with nighttime BP ≥120/70 mm Hg.
Office blood BP ≥140/90 mm Hg was detected in 65 (60%) patients. ABPM was performed in 66 patients, including those with office BP ≤140/90 mm Hg. According to ABPM results, sustained HTN was identified in 26 (39.4%) patients, masked HTN in 13 (19.7%), and isolated nocturnal HTN in 4 (6.1%). All patients with newly diagnosed masked HTN had normal office BP readings. Normotension was confirmed in 23 patients (34.8%). (Figure 1) The most common nocturnal systolic BP profile was the non-dipper pattern (36.3%).
In ¼ of patients with GD ABPM reveals specific phenotypes: masked HTN (19.7%) and isolated nocturnal HTN (6.1%). As eGFR declines, the HTN phenotype changes, with sustained AH becoming predominant starting from CKD stage 3b. These findings highlight the inadequacy of single office BP measurements for assessing the true BP profile in patients with GD. Wider implementation of ABPM is necessary for the timely diagnosis of HTN in patients with early-stage CKD and for guiding appropriate antihypertensive treatment.
