Evidence map›Paper›PMID 40700030›Full record

ArticleJournal of cachexia, sarcopenia and muscle2025

Association of Difference Between eGFR From Cystatin C and Creatinine and Serum GDF-15 With Adverse Outcomes in Diabetes Mellitus.

Tomohito Gohda, Nozomu Kamei, Marenao Tanaka, Masato Furuhashi, Tatsuya Sato, Mitsunobu Kubota, Michiyoshi Sanuki, Takeo Koshida, Shinji Hagiwara, Yusuke Suzuki and 1 more

Abstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Tomohito GohdaDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.ORCID 0000-0002-0513-4433
Nozomu KameiDepartment of Endocrinology and Metabolism, Hiroshima Red Cross Hospital & Atomic-Bomb Survivors Hospital, Hiroshima, Japan.
Marenao TanakaDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Masato FuruhashiDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Tatsuya SatoDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Mitsunobu KubotaDepartment of Endocrinology and Diabetology, NHO Kure Medical Center and Chugoku Cancer Center, Hiroshima, Japan.
Michiyoshi SanukiInstitute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Hiroshima, Japan.
Takeo KoshidaDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Shinji HagiwaraDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Yusuke SuzukiDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Maki MurakoshiDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProtein catabolism and chronic inflammation drive sarcopenia and frailty in individuals with diabetes mellitus and chronic kidney disease (CKD). The difference between estimated glomerular filtration rates derived from cystatin C and creatinine (eGFRcys and eGFRcr, respectively), termed eGFRdiff, along with growth differentiation factor-15 (GDF-15) levels, have emerged as markers of metabolic and inflammatory dysregulation. Lower eGFRdiff and elevated GDF-15 levels are associated with sarcopenia, frailty, CKD progression and mortality. However, their interplay and respective impacts on CKD progression and mortality remain unclear.

methodsA total of 638 Japanese individuals with diabetes mellitus were stratified into tertiles based on eGFRdiff. Serum GDF-15 levels were measured using enzyme-linked immunosorbent assays. The relationships between eGFRdiff and GDF-15 were assessed using Spearman's correlation coefficients. Multivariate ordered logistic regression was used to evaluate the association between eGFRdiff and GDF-15 tertiles, with GDF-15 as the dependent variable and eGFRdiff as the independent variable, adjusting for covariates including age, sex, urinary albumin-to-creatinine ratio (UACR) and eGFRcr or eGFRcys. Cox proportional hazards models with restricted cubic splines were used to examine associations between eGFRdiff and GDF-15 (independent variables) with CKD progression (≥ 30% decline in eGFRcr from baseline) and mortality (dependent variables). These models were adjusted for age, sex, glycated haemoglobin, UACR and eGFRcr.

resultsThe median age was 65 years (interquartile range: 58-73), and 53.9% of participants were male. Over median follow-up periods of 5.3 years for CKD progression and 5.4 years for mortality, 75 participants (11.8%) experienced CKD progression and 44 (6.9%) died. GDF-15 levels inversely correlated with eGFRdiff (r = -0.35, p < 0.001). Higher eGFRdiff values were associated with lower odds of being in a higher GDF-15 tertile (odds ratio 0.86; 95% confidence interval [CI]: 0.76-0.97; p = 0.01). Both lower eGFRdiff and higher GDF-15 levels were independently associated with adverse outcomes: CKD progression (GDF-15, hazard ratio [HR] 1.36, 95% CI: 1.02-1.81, p < 0.05; eGFRdiff, HR 0.67, 95% CI: 0.58-0.78, p < 0.0001) and mortality (GDF-15, HR 2.35, 95% CI: 1.63-3.41, p < 0.0001; eGFRdiff: 0.80, 95% CI: 0.65-0.99, p < 0.05).

conclusionsBoth eGFRdiff and GDF-15 were independently associated with adverse outcomes in individuals with diabetes mellitus. GDF-15 showed a stronger association with mortality, whereas eGFRdiff was more strongly linked to CKD progression. These findings underscore the potential utility of these markers in risk stratification for diabetes-related complications and may guide individualized interventions in clinical practice.

Indexed as

CreatinineCystatin CDiabetes MellitusGlomerular Filtration RateGrowth Differentiation Factor 15AgedBiomarkersDisease ProgressionFemaleHumansMaleMiddle AgedRenal Insufficiency, ChronicBiomarkersCreatinineCystatin CGDF15 protein, humanGrowth Differentiation Factor 15chronic kidney diseasediabetes mellitusdifference between estimated glomerular filtration rates derived from cystatin C and creatinine (eGFRdiff)growth differentiation factor‐15mortalitysarcopenia

Identifiers

PMID40700030
PMCPMC12285683

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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.