ArticleFrontiers in nutrition2026
Associations of metabolic dysfunction-associated steatotic liver disease and significant fibrosis phenotypes with glomerular hyperfiltration defined by indexed eGFR.
Article in Frontiers in nutrition, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: To examine associations of metabolic dysfunction-associated steatotic liver disease (MASLD) and significant fibrosis with glomerular hyperfiltration (GHF) defined from indexed estimated glomerular filtration rate (eGFR), accounting for body size. Methods: We analyzed 9,140 NHANES participants and 721 adults from a Chinese clinical study. Liver phenotypes were G1 (no steatosis/no significant fibrosis), G2 (MASLD without significant fibrosis), and G3 (MASLD with significant fibrosis). Primary GHF was indexed eGFR above the survey-weighted age- and sex-specific 95th percentile of a low-risk NHANES reference, applied unchanged to both studies. BMI-adjusted Model 3 was central; metabolic adjustment and alternative GHF definitions were sensitivity analyses. Results: In NHANES Model 3, G2 and G3 had higher odds of GHF than G1 (OR 2.19, 95% CI 1.57-3.07; OR 2.46, 1.51-4.00), whereas G3 did not differ from G2 (OR 1.12, 0.74-1.70). In the identical fasting subsample, further metabolic adjustment attenuated G2 and G3 versus G1 (OR 1.94 and 2.08), while G3 versus G2 remained near the null. In China, G2 versus G1 was null, whereas G3 had higher odds than G1 and G2; however, G3 included only 29 participants and 8 events. NHANES findings were generally robust to indexed P90, age/sex/BSA-residual, and de-indexed sensitivity definitions. Conclusion: In NHANES, MASLD phenotypes were associated with higher odds of GHF after accounting for body size, whereas significant fibrosis showed no clear incremental association beyond MASLD. The fibrosis-related association observed in the Chinese clinical study should be interpreted cautiously because of the small G3 subgroup and cross-population differences in GHF calibration. Prospective studies using measured GFR are needed to clarify the temporal and prognostic significance of GHF in MASLD.
Indexed as
Identifiers
What 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.