Objective  To investigate the association between cumulative systolic blood pressure (SBP) exposure and the risk of new-onset chronic kidney disease and all-cause mortality.

Methods  Data for this study were derived from the Kailuan Study database. Participants were Kailuan employees who completed health examinations in the 2006–2007 and 2010–2011 survey cycles, with complete SBP data. Average cumulative systolic blood pressure (ACSBP) was calculated, and participants were categorized into three groups according to ACSBP levels: ＜120, 120–＜140, and ≥140 mmHg. Incident CKD was defined as a new onset of estimated glomerular filtration rate (eGFR) ＜60 mL/(min·1.73 m²) and/or urinary protein ≥1+ (>30 mg/dL) during follow-up. Cox proportional hazards regression models were used to assess the associations of ACSBP with incident CKD and all-cause mortality. Stratified analyses were performed by age (＜65 vs. ≥65 years) and by glucose and lipid metabolism (normal vs. abnormal), to examine the interaction of these factors with ACSBP.

Results  A total of 48 074 participants were included. Over a median follow-up of 10.9 years, 7227 incident CKD cases and 4305 all-cause mortality occurred. Compared with the ACSBP＜120 mmHg group, the ACSBP 120–＜140 mmHg group had a 14.8% higher risk of CKD (HR = 1.148, 95%CI: 1.074–1.226) and a 28.8% higher risk of all-cause mortality (HR = 1.288, 95%CI: 1.166–1.422). The ACSBP ≥140 mmHg group had a 40.6% higher risk of CKD (HR = 1.406, 95%CI: 1.282–1.542) and a 64.3% higher risk of all-cause mortality (HR = 1.643, 95%CI: 1.453–1.858). Stratified analyses revealed significant interactions between age and ACSBP for both CKD and all-cause mortality (P for interaction ＜0.01 for both). In the ＜65 years subgroup, compared with ACSBP ＜120 mmHg, the 120–＜140 and ≥140 mmHg groups had 16.0% (HR = 1.160; 95%CI: 1.080–1.246) and 48.0% (HR = 1.480; 95%CI: 1.334–1.642) higher risks of CKD, and 23.0% (HR = 1.230; 95%CI: 1.085–1.393) and 76.5% (HR = 1.765; 95%CI: 1.498–2.080) higher risks of all-cause mortality, respectively. In the ≥65 years subgroup, compared with ACSBP＜120 mmHg group, in the ACSBP 120–＜140 mmHg and ≥140 mmHg groups, the CKD risk was not statistically significant (P = 0.660 and 0.263, respectively), but all-cause mortality remained significantly elevated, with increases of 25.9% (HR = 1.259, 95%CI: 1.062–1.493) and 40.0% (HR = 1.400, 95%CI: 1.154–1.697), respectively. When stratified by glucose and lipid metabolism status, among those with normal metabolism, compared with ACSBP＜120 mmHg group, the CKD risk was not no increased, but the all-cause mortality risk increased by 27.9% (HR = 1.279; 95%CI: 1.111–1.472) in the 120–＜140 mmHg group, and the CKD and all-cause mortality risk increased by 38.3% (HR = 1.383; 95%CI: 1.226–1.560) and 65.4% (HR = 1.654; 95%CI: 1.410–1.940) respectively in the ≥140 mmHg group. Among those with abnormal metabolism, compared with ACSBP＜120 mmHg group, the CKD and all-cause mortality risk increased by 24.2% (HR = 1.242, 95%CI: 1.132–1.363) and 20.6% (HR = 1.206, 95%CI: 1.047–1.389) respectively in the 120–＜140 mmHg group, and which increased by 48.7% (HR = 1.487; 95%CI: 1.325–1.669) and 52.5% (HR = 1.525; 95%CI: 1.300–1.789) respectively in the ≥140 mmHg group.

Conclusions  Cumulative SBP exposure is positively associated with the risk of incident CKD and all-cause mortality. Even below the diagnostic threshold for hypertension, high-normal SBP is associated with increased risks of both outcomes. The strength of these associations varied according to age and the presence of glucose and lipid metabolism abnormalities.