Association between extracellular-to-total body water ratio and eGFR decline in diabetic kidney disease: a longitudinal cohort study.

Authors

Shotaro Miyamoto, Nao Imaishi, Machiko Morita, Hiroki Uchida, Yuko Yamazaki, Miyoko Osue, Yuko Hirota, Mitsuhiro Okamoto, Satoshi Nagai, Kentaro Sada, Naoki Matsuda, Takaaki Noguchi, Yoshinori Ozeki, Takeshi Nakata, Yuichi Yoshida, Akihiro Fukuda, Koro Gotoh, Takayuki Masaki, Hirotaka Shibata

Published in

Clinical and experimental nephrology. Jun 19, 2026. Epub Jun 19, 2026.

Abstract

Diabetic kidney disease (DKD) can progress even in the absence of overt albuminuria, highlighting the need for markers for evaluating nonglomerular pathways. The extracellular-to-total body water ratio (ECW/TBW), measured via bioelectrical impedance analysis (BIA), reflects systemic fluid status; however, its longitudinal relevance to DKD progression remains unclear to date.
We conducted a retrospective observational cohort study using longitudinal outpatient data from October 2020 to April 2025 at the Diabetic Kidney Disease Prevention Clinic, Oita University Hospital. A total of 40 adults with type 2 diabetes and clinically diagnosed DKD contributed 355 outpatient visits. The primary outcome was the annual rate of decline in estimated glomerular filtration rate (eGFR slope, mL/min/1.73 m²/year).
Both baseline and time-averaged ECW/TBW values were negatively correlated with eGFR slope in the univariate analysis (p = 0.014 and 0.025, respectively) and remained significant in the multivariate models. Log-transformed urinary albumin-to-creatinine ratio (UACR) was also significantly associated with faster eGFR decline. Treatment with sodium-glucose cotransporter 2 inhibitors (SGLT2is) was associated with lower ECW/TBW values, whereas other renoprotective medications exerted more modest individual effects, with greater reductions observed with the concurrent use of multiple agents.
Higher ECW/TBW values were associated with faster eGFR decline in DKD, suggesting that subclinical volume overload may represent a potential nonglomerular mechanism of disease progression. This volume-related burden may be attenuated by SGLT2is therapy.

PMID:
42319648
Bibliographic data and abstract were imported from PubMed on 19 Jun 2026.

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