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Dialysis and Renal Disease Management / Chronic Kidney Disease and Diabetes / Diabetes, Cardiovascular Risks, and Lipoproteins · Journal article
Scientific Reports · August 7, 2026
Encouraging direction, but not yet definitive.
This cross-sectional analysis of 4,674 community-managed type 2 diabetes patients found that central obesity (but not isolated generalized obesity) associates with diabetic kidney disease risk, with insulin resistance explaining approximately 22.5% of this association in the basic model and 9.7% after full adjustment. The association between central obesity and DKD was attenuated to non-significance after metabolic adjustment, suggesting insulin resistance and related metabolic disturbances are key intermediate factors.
Cross-sectional study. Community-managed type 2 diabetes mellitus patients from Kaihua County, Zhejiang Province, China. Intervention: Classification by obesity phenotype (central, generalized, combined, or neither based on BMI and waist circumference). Compared with: Insulin resistance status and obesity phenotype categories. n = 4,674. Kaihua County, Zhejiang Province, China.
DKD prevalence was 52.439% overall, significantly higher in the insulin-resistant group (60.046% vs. 48.001%, P < 0.001) Isolated central obesity associated with DKD (OR 1.214, 95% CI 1.053–1.399, P = 0.007) before metabolic adjustment Combined generalized and central obesity associated with DKD (OR 1.189, 95% CI 1.001–1.412, P = 0.048) before metabolic adjustment
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Clinicians should consider measuring waist circumference alongside BMI for DKD risk stratification in type 2 diabetes patients, as central obesity appears to carry greater risk than generalized obesity. The partial mediation by insulin resistance suggests that metabolic interventions targeting insulin resistance may be important for DKD prevention in centrally obese patients.
Cross-sectional study with a large community sample demonstrating that central obesity associates with DKD risk via insulin resistance as a partial mediator, but causality cannot be inferred and the effect is attenuated by metabolic adjustment.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians should consider measuring waist circumference alongside BMI for DKD risk stratification in type 2 diabetes patients, as central obesity appears to carry greater risk than generalized obesity. The partial mediation by insulin resistance suggests that metabolic interventions targeting insulin resistance may be important for DKD prevention in centrally obese patients.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Abstract Obesity is a key risk factor for diabetic kidney disease (DKD). However, BMI fails to capture body fat distribution. We hypothesized that central obesity, rather than generalized obesity, is associated with DKD risk in patients with type 2 diabetes mellitus (T2DM), and that this association is mediated by insulin resistance (IR). A cross-sectional study of 4674 community-managed T2DM patients in Kaihua County, Zhejiang Province. Participants were classified into four obesity phenotypes based on BMI and waist circumference (WC). DKD was defined as UACR ≥ 30 mg/g and/or eGFR < 60 mL/min/1.73 m 2. Multivariable logistic regression and mediation analysis were used to assess the associations and the mediating role of HOMA-IR. The overall prevalence of DKD in the study population was 52.439%, and the overall prevalence of obesity was 42.790%, with central obesity being predominant. DKD prevalence was significantly higher in the IR group compared to the non-IR group (60.046% vs. 48.001%, P < 0.001). Multivariable logistic regression showed that after adjustment for demographic and lifestyle factors, isolated central obesity (OR 1.214, 95% CI 1.053–1.399, P = 0.007) and combined generalized and central obesity (OR 1.189, 95% CI 1.001–1.412, P = 0.048) were significantly associated with DKD risk, while isolated generalized obesity showed no significant association ( P > 0.05). After further adjustment for metabolic factors including glycemic parameters, IR, and lipid profiles, these associations were attenuated and no longer statistically significant ( P > 0.05). Mediation analysis revealed that in the basic model, HOMA-IR explained 22.484% of the association between central obesity and DKD (indirect effect P < 0.001). After adjusting for BMI and multiple covariates, this explanatory proportion remained 9.715% ( P = 0.006). Central obesity is associated with DKD risk in community-managed T2DM patients, and this association was attenuated after metabolic adjustment. These findings suggest that metabolic disturbances including IR may contribute to the central obesity–DKD link. WC measurement could be considered alongside BMI for DKD risk stratification.
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