A body shape index (ABSI) is an abdominal obesity index developed based on epidemiological statistics and designed to correlate minimally with body mass index (BMI). We examined the approximation between ABSI and other abdominal obesity indices based on biophysical concepts. The cross-sectional data from 62,514 Japanese urban residents were analyzed. Body adiposity indices comprising BMI, waist circumference (WC), ABSI, conicity index (CI), waist-to-height ratio (WHtR), and WC/BMI ratio were examined. ABSI and CI more strongly correlated with age and arterial stiffness assessed by cardio-ankle vascular index (CAVI) compared to the other indices. The discriminative power for high CAVI (≥9.0) was the strongest for ABSI followed by CI and other indices, in that order. The range and distribution of WC corresponding to the cutoff of ABSI (0.0801), or CI (1.23) seemed reasonable. The correlation between ABSI and CI was the strongest compared to any other combination of indices. CI correlated moderately with BMI, whereas ABSI correlated minimally with BMI. ABSI correlates strongly and approximates closely with CI. Hence, ABSI may be considered to reflect the degree of body shape change from cylindricity to conicity and is currently the only abdominal obesity index not affected by the obesity paradox.

Hyperuricemia is associated with kidney function decline (KFD), although whether hyperuricemia directly causes nephrotoxicity or is indirectly mediated by systemic arterial stiffening remains unclear. We examined the detailed relationship of serum uric acid (SUA) with KFD and potential mediation by arterial stiffness. Study population was 27,648 urban residents with an estimated glomerular filtration rate (eGFR) of ≥60 mL/min/1.73 m² at baseline, and they participated in a median of three consecutive annual health examinations. Arterial stiffness was assessed using cardio-ankle vascular index (CAVI). KFD was defined as a decrease in eGFR to below 60. Multivariate analysis showed an association between baseline SUA and CAVI independent of eGFR. During the study period, 6.6% of participants developed KFD. Stratified analysis revealed a linear relationship between the contribution of CAVI or SUA and KFD. ROC analysis determined a cutoff CAVI of 8.0 (males) or 7.9 (females) and a cutoff SUA of 6.3 (males) or 4.5 mg/dL (females) for predicting KFD. The linkage between SUA and CAVI was associated with a greater increase in the hazard ratio for KFD with an increase in SUA. CAVI showed the mediating effect on the relationship of SUA with KFD after an adjustment for confounders. SUA was associated positively with CAVI-mediated KFD. Further studies should verify whether intensive SUA-lowering treatment prevents KFD via improving vascular function.