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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.
Introduction. The prevalence of chronic kidney disease (CKD) has a steady upward trend. Diagnosis is still based on the determination of indicators that determine the condition of the glomeruli - albuminuria and glomerular filtration rate. There are no clear criteria for damage to the tubular apparatus in the clinical recommendations, which leads to an underestimation of the prevalence of CKD. One of the recognized risk factors is a violation of the diet regarding the consumption of table salt. It is believed that excessive consumption of table salt contributes to an increase in blood pressure, the development of intraglomerular hypertension, glomerular hypertrophy and damage to the glomerular filter.
The aim of the study was to evaluate the relationship between salt intake and granular tubular dystrophy in CKD of various etiologies.
518 patients with glomerulopathy, 267 men and 251 women, were examined. The average age is 45,1±15,6 years. All of them were hospitalized during 2016-2019 years. A traditional nephrological clinical and laboratory examination was performed. Additionally, the indicators of electrolyte transport, osmotically active substances and salt intake were calculated.
It examined 132 patients with nonproliferative glomerulopathy, 226 patients with proliferative glomerulopathy, 54 patients with al-amyloidosis, 31 patients with chronic tubulointerstitial nephritis, 30 patients with diabetes mellitus type and 45 patients with arterial hypertension. All patients underwent nephrobiopsy. All of them consumed more than 5 g of salt per day.
Etiology of CKD
Salt, g per day
Area under the ROC curve
Associated criterion
Sensitivity
Specificity
Positive predictive value
Nonproliferative glomerulopathy
12,1±3,6
0,965
8,10
92,5
92,9
13,0
Proliferative glomerulopathy
11,7±3,5
0,936
9,85
72,6
100,0
AL-amyloidosis
10,1±2,9
0,952
9,12
88,5
94,7
16,7
Chronic tubulointerstitial nephritis
11,1±3,4
0,954
7,30
Diabetes mellitus type 2
11,5±3,1
0,947
9,61
77,9
98,2
43,3
Arterial hypertension
12,0±3,6
0,985
6,10
99,9
The table shows the results of statistical analysis after correction for the estimated glomerular filtration rate and the level of proteinuria. Regardless of the etiology of CKD, the relationship between salt intake and granular tubular dystrophy is beyond doubt.
Our study shows that excessive salt intake can cause damage to the tubular apparatus. In this regard, we propose to include the definition of salt intake in the algorithm for examining patients at risk of developing CKD. The positive nephroprotective effects of glyphlozines may have a mechanism other than their effect on glomeruli.
We have no potential conflict of interest to disclose.
We did not use generative AI and AI-assisted technologies in the writing process.
