<p>The incremental value of 24-hour central systolic blood pressure in identifying target organ damage based on blood pressure phenotypes remains unclear. This multicenter, cross-sectional study enrolled 2589 non-dialysis patients with chronic kidney disease. Clinic and ambulatory brachial blood pressure were used to define blood pressure phenotypes. The net reclassification index and logistic regression analyses were performed. 24-h central systolic blood pressure gradually elevated across four blood pressure phenotypes with a linear trend (<i>P</i>-trend &lt;0.001). Incorporating 24-h central systolic blood pressure into blood pressure phenotypes significantly improved target organ damage discrimination, particularly 24-h central systolic blood pressure with c2 calibration (mean arterial pressure and diastolic blood pressure calibration method) for left ventricular hypertrophy (NRI = 0.192, 95% CI [0.085–0.298], <i>P</i> &lt; 0.001). Multivariable logistic regression revealed that, compared with normotension without central systolic hypertension (c2 calibration), only masked hypertension and sustained hypertension with central systolic hypertension (c2 calibration) had significantly increased odds of both left ventricular hypertrophy (ORs: 3.220 [95% CI, 1.861–5.537; <i>P</i> &lt; 0.001] and 4.054 [95% CI, 2.772–5.996; <i>P</i> &lt; 0.001]) and carotid hypertrophy (ORs: 2.059 [95% CI, 1.240–3.461; <i>P</i> = 0.006] and 1.368 [95% CI, 1.001–1.860; <i>P</i> = 0.049]). Moreover, the prevalence of kidney injury was higher in the masked hypertension and sustained hypertension groups with central systolic hypertension (c2 calibration) than in the group without central systolic hypertension (c2 calibration). 24-h central systolic blood pressure may provide additional value for target organ damage risk stratification based on blood pressure phenotypes in non-dialysis patients with chronic kidney disease.</p><p></p>

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Incremental value of 24-hour central systolic blood pressure based on blood pressure phenotypes for target organ damage in non-dialysis patients with chronic kidney disease

  • Cheng Chen,
  • Ruoyan Deng,
  • Menglei Ju,
  • Shengnan Ge,
  • Wenjuan Yu,
  • Qirong Song,
  • Ying Tang,
  • Qiong Li,
  • Man Li,
  • Cheng Wang

摘要

The incremental value of 24-hour central systolic blood pressure in identifying target organ damage based on blood pressure phenotypes remains unclear. This multicenter, cross-sectional study enrolled 2589 non-dialysis patients with chronic kidney disease. Clinic and ambulatory brachial blood pressure were used to define blood pressure phenotypes. The net reclassification index and logistic regression analyses were performed. 24-h central systolic blood pressure gradually elevated across four blood pressure phenotypes with a linear trend (P-trend <0.001). Incorporating 24-h central systolic blood pressure into blood pressure phenotypes significantly improved target organ damage discrimination, particularly 24-h central systolic blood pressure with c2 calibration (mean arterial pressure and diastolic blood pressure calibration method) for left ventricular hypertrophy (NRI = 0.192, 95% CI [0.085–0.298], P < 0.001). Multivariable logistic regression revealed that, compared with normotension without central systolic hypertension (c2 calibration), only masked hypertension and sustained hypertension with central systolic hypertension (c2 calibration) had significantly increased odds of both left ventricular hypertrophy (ORs: 3.220 [95% CI, 1.861–5.537; P < 0.001] and 4.054 [95% CI, 2.772–5.996; P < 0.001]) and carotid hypertrophy (ORs: 2.059 [95% CI, 1.240–3.461; P = 0.006] and 1.368 [95% CI, 1.001–1.860; P = 0.049]). Moreover, the prevalence of kidney injury was higher in the masked hypertension and sustained hypertension groups with central systolic hypertension (c2 calibration) than in the group without central systolic hypertension (c2 calibration). 24-h central systolic blood pressure may provide additional value for target organ damage risk stratification based on blood pressure phenotypes in non-dialysis patients with chronic kidney disease.