ArticleScientific reports2025
Association of albumin-corrected anion gap with all-cause and cardiovascular mortality in overactive bladder patients.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overactive bladder (OAB) is a symptom syndrome characterized by urgency, often accompanied by frequency and nocturia. It significantly impacts patients' quality of life and imposes a substantial economic burden. The albumin-corrected anion gap (ACAG), an important indicator reflecting the body's acid-base balance and electrolyte disturbances, has predictive value in various chronic diseases. However, its association with the prognosis of OAB patients has not been adequately studied. This study aims to explore the relationship between ACAG levels and all-cause mortality and cardiovascular mortality in OAB patients. A total of 6592 OAB patients (representing 31,072,714 individuals in the U.S. population) from the 2005-2018 NHANES database were included based on strict inclusion criteria. The relationship between ACAG and mortality risk was analyzed using a multivariable-adjusted Cox proportional hazards regression model, with non-linear associations assessed using restricted cubic splines (RCS). Additionally, Kaplan-Meier survival analysis and subgroup analyses were conducted to evaluate the association between ACAG and mortality risk. During an average follow-up of 79.5 months, 1332 all-cause deaths and 352 cardiovascular deaths occurred. In the fully adjusted model, each 1-unit increase in ACAG was associated with an 11% higher risk of all-cause mortality (HR = 1.11, 95% CI 1.06-1.15) and an 8% higher risk of cardiovascular mortality (HR = 1.08, 95% CI 1.01-1.16). Analysis based on ACAG tertiles revealed that, compared to the lowest tertile, the highest tertile was associated with an 65% increased risk of all-cause mortality (HR = 1.65, 95% CI 1.33-2.04) and a 43% increased risk of cardiovascular mortality (HR = 1.43, 95% CI 1.22-1.63), showing a significant dose-response relationship (all-cause mortality P for trend < 0.001; cardiovascular mortality P for trend = 0.028). RCS analysis indicated a linear positive correlation between ACAG and mortality risk. Elevated ACAG levels are significantly associated with both all-cause and cardiovascular mortality in OAB patients, with this association being consistent across various subgroups. This study provides the first evidence of the potential value of ACAG as a prognostic biomarker for OAB patients, offering new insights for clinical risk stratification and personalized treatment strategies.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.