Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
Metabolic acidosis was defined by low serum bicarbonate or total carbon dioxide concentration. However, as defended by many mechanisms, level of serum bicarbonate was always stable until advanced stages of chronic kidney disease (CKD) and thus cannot reflect acid-base status. By comparison, urinary citrate excretion, constituting defense mechanisms for acid load, was a more sensitive biomarker for metabolic acidosis. However, its effect on risk of CKD progression was not well studied. Here, we prospectively investigated kidney failure events in relation to 24-hour urinary citrate excretion among patients with CKD stages 2-4.
Study participants came from a prospective CKD cohort recruited in out-patients at a single tertiary hospital. Hypocitraturia was defined by urinary citrate excretion < 320 mg/24h. Outcomes included incidence of kidney failure with replacement therapy, estimated glomerular filtration rate (eGFR) declining for ≥40 % or composite of the two. Cox proportional hazards regression model was used to estimate the association between baseline urinary citrate excretion and outcomes. Change of area under receiver operating characteristic curve was used to evaluate discriminative ability of the biomarker.
Totally, 284 patients were included, with mean age of 46±14 years, 62.32% of male, average eGFR of 53.77±21.33 ml/min/1.73m2 and average urinary citrate excretion of 193.55±152.15 mg/24h. The majority of patients had the etiology of glomerular disease (89.44%). Two hundred and thirty-six patients (83.10%) had hypocitraturia. During a median follow-up of 3.17 years, 44 events of kidney failure with replacement therapy, 59 eGFR decreasing > 40% and 63 composite events occurred. Hypocitraturia was not associated with kidney failure with replacement therapy after adjusting for covariates including serum bicarbonate, but it was related to incidence of eGFR decreasing > 40% and the composite event with hazard ratios of 3.13 (95% confidence interval: 1.06, 9.27) and 3.02 (1.02, 8.90), respectively. Adding level of urinary citrate excretion into the model consisting of age, sex, mean blood pressure, hypertension, diabetes, eGFR, log-transformed 24h urine protein and serum bicarbonate increased area under receiver operating characteristic curve from 0.8347 to 0.8416 with a difference of 0.0068 (P=0.44).
Hypocitraturia was associated with increased risk of CKD progression among patients with CKD stages 2 and 4, but showed no capacity to improve discrimination of the event.
