Background Endothelial dysfunction and impairment of endothelium-dependent vasodilatation is implicated as the underlying abnormality in hypertension; this effect may be mediated by cytokines. As cytokines have been shown to be temperature sensitive both in vivo and in vitro, we tested the effect of decreasing dialysate temperature on blood pressure and cytokines.
Methods The sample included 24 stable HD subjects randomized to either a control (n = 13) or experimental (n = 11) group. Each individual patient was followed in the study for 9 months, divided into three 3-month phases. During Phase 1 and Phase 3, both groups of subjects received standard treatment (warm dialysate). During Phase 2, the patients were randomized to treatment with either warm dialysate (378C) or cool dialysate (18C lower than the mean pre-HD oral body temperature during the baseline 3 months). Serum samples for IL-1 beta, IL-2, IL-6, IL-10, and TNF-alpha were collected for 9 subjects at the end of each 3-month period and were measured in duplicate by using a multiplex assay (R&D).
Results There was a significant improvement in prehemodialysis systolic blood pressures in Phase 2 in the experimental group (150.99 6 20.5 vs145.17 6 16.3, p = .04 by repeated measures ANOVA) as compared to the control group. The prehemodialysis diastolic blood pressures (85.09 6 14.1 vs 81.64 6 10.8, p = .06) also showed a similar direction of change. The mean pre-HD IL-1 beta (3.02 6 1.6 vs 1.24 6 0.26, p = .06) and TNF-alpha (21.11 6 30.21 vs 7.39 6 3.62, p = .06) were also lower in the experimental group after 3 months in the cool condition. Our hypothesis was further supported by the observation that there was a decrease in serum ferritin, an acute-phase reactant (709.2 6 299.6 vs 579.7 6 212.9) in the experimental group, which is also regulated by these same cytokines (IL-1 beta and TNF-alpha) and could possibly be related to improvement in inflammatory changes.
Conclusions These data suggest that using cool dialysate during HD decreases pre-HD systolic and diastolic blood pressure. This effect may be mediated by an improvement in endothelial function, as measured by a decrease in selected markers of inflammation. Further study is warranted to explore the long-term beneficial effects of these changes on outcomes related to cardiovascular morbidity and mortality.