ArticleInternational urology and nephrology2026
Unraveling the causal link between inflammatory cytokines and hypertensive renal disease: a Mendelian randomization analysis.
Article in International urology and nephrology, 2026. 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeHypertensive renal disease is a primary contributor to morbidity and death, with inflammation serving a crucial role in its development. Elevated levels of inflammatory cytokines are frequently observed in hypertensive renal disease patients; however, their causal relationship with the disease remains unclear.
methodsA two-sample Mendelian randomization (MR) analysis was conducted using genetic variants associated with inflammatory cytokine levels obtained from genome-wide association studies (GWAS) of 14,824 healthy participants. Summary statistics for hypertensive renal disease were derived from the FinnGen R10 dataset. The inverse variance weighted (IVW) method was the primary approach for assessing causal effects, complemented by multiple sensitivity analyses to ensure robustness of the findings.
resultsIn the bidirectional MR analysis, the IVW analysis identified two inflammatory cytokines as risk factors for hypertensive renal disease: interferon-gamma levels (OR 1.500, 95% CI 1.130-1.992) and oncostatin-M levels (OR 1.414, 95% CI 1.086-1.841). Additionally, the study identified three cytokines as protective factors against hypertensive renal disease: CD40L receptor levels (OR 0.817, 95% CI 0.679-0.983), interleukin-10 receptor subunit beta levels (OR 0.829, 95% CI 0.703-0.976), and interleukin-20 receptor subunit alpha levels (OR 0.725, 95% CI 0.549-0.957). These results highlight the complex role of inflammatory cytokines in the progression of hypertensive renal disease. No evidence of horizontal pleiotropy, heterogeneity, or reverse causality was found in the above results.
conclusionThis Mendelian randomization analysis identified inflammatory cytokines associated with hypertensive renal disease, providing a foundation for future mechanistic research and potential therapeutic targets.
Indexed as
Identifiers
40699416What OpenQuestion 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 OpenQuestion graph.