Key result
Severe obesity linked to ~456% higher risk of ACR positivity versus normal weight.
Why the study?
Obesity is associated with elevated urinary albumin-creatinine ratio, but bidirectional relationships and hormone-mediated effects remained unclear.
Does obesity increase the risk of elevated urinary albumin-creatinine ratio in non-diabetic, non-hypertensive individuals?
Cross-Sectional (n=2,724)
Does obesity increase the risk of elevated urinary albumin-creatinine ratio in non-diabetic, non-hypertensive individuals?
Central obesity and elevated ACR have a bidirectional relationship mediated by cortisol, with visceral fat level being a key risk factor in males and body fat percentage in females.
Answers are grounded in this paper and cite their sources.
May warrant ACR screening in severe obesity; extends cross-sectional links but leaves causality and mediation open.
Introduction and Objective: Obesity is associated with elevated urinary albumin-creatinine ratio (ACR), but bidirectional relationships and hormone-mediated effects remain unclear. We examined obesity-ACR bidirectionality and cortisol’s role in non-diabetic/non-hypertensive individuals. Methods: We conducted a cross-sectional study of 2,724 participants without diabetes or hypertension. Obesity indices included body mass index (BMI), visceral fat level (VFL), body fat percentage (PBF), and waist-hip ratio (WHR). The primary outcome was ACR positivity (≥30 mg/g). Spearman correlation, multivariate logistic regression and stratified analysis were used to assess associations, adjusted for demographics and metabolic factors. Results: Compared with normal-weight participants, severely obese individuals had a 5.56-fold higher risk of ACR positivity (95% CI: 3.48-8.87, P<0.001). Conversely, ACR positivity was associated with a 23% increased risk of central obesity (P=0.002). VFL showed the strongest correlation with ACR (r=0.32, P<0.001), and cortisol mediated 31.3% of this association. Gender differences were observed: VFL was an independent risk factor in males (OR=1.14, 95% CI: 1.10-1.18, P<0.001), while PBF was critical in females (OR=1.07, 95% CI: 1.04-1.10, P<0.001). The VFL-ACR correlation was 1.78-fold stronger in the high-cortisol group (r=0.32) than in the low-cortisol group (r=0.18). The ACR positivity prediction model had an AUC of 0.836 (95% CI: 0.802-0.870). Conclusion: Central obesity and ACR have bidirectional links, with cortisol as key mediator and gender-specific effects. VFL and cortisol aid obesity-related renal injury risk stratification, supporting targeted visceral fat reduction.
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DING et al. (2026) conducted a cross-sectional in Obesity and elevated urinary albumin-creatinine ratio (n=2,724). Severe obesity vs. Normal weight was evaluated on ACR positivity (≥30 mg/g) (OR 5.56, 95% CI 3.48-8.87, p=<0.001). Severe obesity was associated with a 5.56-fold higher risk of urinary albumin-creatinine ratio positivity compared with normal weight (OR 5.56; 95% CI 3.48-8.87; P<0.001).
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