This presentation focussed on J-shaped relationships between time-averaged blood pressure (BP) and outcomes in advanced chronic kidney disease (CKD) patients, who are usually excluded in clinical trials. Several observational studies demonstrate that low BP levels seem to be related to higher risk of cardiovascular (CV) events, end-stage renal disease (ESRD), or mortality in patients with CKD. The latest results from the SPRINT trial show that targeting a systolic BP (SBP) <120 mmHg among 2,646 patients with CKD was not as beneficial as for those without CKD.1,2 These studies raise concern that J-shaped relationships may exist in patients with CKD. This prospective observational study enrolled 2,340 CKD Stage 3–5 patients between November 2002 and May 2009 and followed them until July 2010 or death. Standardised BP measurements were obtained by a standard mercury sphygmomanometer or a validated automated device in seated patients after a 10-minute rest. The average of the first two BP readings was recorded at each visit. The BP records of each patient were averaged during the study period. Demographic, clinical, laboratory, and disease variables were measured. Three outcomes were assessed: ESRD, cardiovascular events, and all-cause mortality. The definitions of each outcome were the same as our previous study.3
The results of this study showed that, in fully-adjusted Cox regression, a J-shaped relationship existed between time-averaged SBP and ESRD: the hazard ratio (HR) of time-averaged SBP <110 mmHg was 2.01 (95% confidence interval [CI]: 1.14–3.57), and the HR of time-averaged SBP ≥160 mmHg was 2.82 (95% CI: 2.07–3.84), compared with the reference group (time-averaged SBP 120–129 mmHg). A J-shaped relationship also existed between time-averaged SBP and cardiovascular events or all-cause mortality. The association between time-averaged SBP and malnutrition-inflammation, defined as albumin <3.5 g/dL and C-reactive protein (CRP) >10 mg/dL, was also J-shaped. The odds ratio of time-averaged SBP <110 mmHg was 2.63 (95% CI: 1.31–5.27), and the odds ratio of SBP ≥160 mmHg was 1.63 (95% CI: 1.10–2.41), compared with the reference group. As for diastolic blood pressure (DBP), a J-shaped relationship also existed between time-averaged DBP and CV events and all-cause mortality. For CV events, the HR of time-averaged DBP <60 mmHg was 1.59 (95% CI: 1.14–2.22), compared with the reference group (time-averaged DBP 70–79 mmHg). For all-cause mortality, the HR of time-averaged DBP <60 mmHg was 1.50 (95% CI: 1.03–2.17), compared with the reference group (time-averaged DBP 70–79 mmHg). However, there were no J-shaped relationships between time-averaged pulse pressure and clinical outcomes. Malnutrition-inflammation complex syndrome could be a possible factor associated with the impact of low BP in advanced CKD patients. A schematic representation of protein-energy wasting and its complex inter-relationships in CKD patients has been proposed by Fouque et al.4 These factors include chronic inflammation, malnutrition, uraemic toxin, acidosis, ageing, oxidative stress, diabetes, cardiovascular disease, and atherosclerosis. Our findings may add another factor, low BP, to this complicated puzzle. Low BP may lead to hypoperfusion and end-organ damage. At the same time, it may be a result of inflammation. Therefore, low BP may be a cause, an effect, or both, of malnutrition-inflammation complex syndrome. Further analysis is warranted.