Intradialytic hypertension is associated with adverse outcomes, yet the mechanism is uncertain. Patients with intradialytic hypertension exhibit imbalances in endothelial-derived vasoregulators nitric oxide and endothelin-1, indirectly suggesting endothelial cell dysfunction. We hypothesized that intradialytic hypertension is associated in vivo with endothelial cell dysfunction, a novel predictor of adverse cardiovascular outcomes.
We performed a case-control cohort study including 25 hemodialysis (HD) subjects without (controls) and 25 with intradialytic hypertension (an increase in systolic BP pre- to postdialysis ≥10 mmHg ≥4/6 consecutive HD sessions). The primary outcome was peripheral blood endothelial progenitor cells (EPCs) assessed by aldehyde dehydrogenase activity (ALDH(br)) and cell surface marker expression (CD34(+)CD133(+)). We also assessed endothelial function by ultrasonographic measurement of brachial artery flow-mediated vasodilation (FMD) normalized for shear stress. Parametric and nonparametric t tests were used to compare EPCs, FMD, and BP.
Baseline characteristics and comorbidities were similar between groups. Compared with controls, 2-week average predialysis systolic BP was lower among subjects with intradialytic hypertension (144.0 versus 155.5 mmHg), but postdialysis systolic BP was significantly higher (159.0 versus 128.1 mmHg). Endothelial cell function was impaired among subjects with intradialytic hypertension as measured by decreased median ALDH(br) cells and decreased CD34(+)CD133(+) cells (ALDH(br), 0.034% versus 0.053%; CD34(+)CD133(+), 0.033% versus 0.059%). FMD was lower among subjects with intradialytic hypertension (1.03% versus 1.67%).
Intradialytic hypertension is associated with endothelial cell dysfunction. We propose that endothelial cell dysfunction may partially explain the higher event rates observed in these patients.
[Show abstract][Hide abstract] ABSTRACT: Hypertension is common in hemodialysis patients and contributes to this population's high risk for cardiovascular morbidity and mortality. Patients with intradialytic hypertension, or increases in blood pressure during hemodialysis, have been shown to have the highest risk for these outcomes. The purpose of this review is to describe new findings that shed light on the epidemiology and pathophysiology of intradialytic hypertension and discuss how a better understanding of these mechanisms may lead to improved blood pressure management and outcomes in hemodialysis patients.
Our laboratory demonstrated that intradialytic hypertension occurs at least sporadically in most hemodialysis patients, but in 25% of patients it occurs in over 31% of their hemodialysis treatments. We also identified that, compared with hemodialysis patients without intradialytic hypertension, those with intradialytic hypertension have worse endothelial cell function and have higher interdialytic ambulatory blood pressure. Pilot study data show that carvedilol reduces the frequency of intradialytic hypertension and improves endothelial cell dysfunction.
Intradialytic hypertension is associated with increased morbidity and mortality, impaired endothelial cell function, and higher overall blood pressure burden. Further investigation is required to determine whether interventions aimed at preventing or treating intradialytic hypertension improve long-term outcomes.
Current opinion in nephrology and hypertension 01/2012; 21(1):15-23. DOI:10.1097/MNH.0b013e32834db3e4 · 3.96 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The blood pressure (BP) of a proportion of chronic hemodialysis (HD) patients rises after HD. We investigated the influence of postdialysis BP rise on long-term outcomes.
A total of 115 prevalent HD patients were enrolled. Because of the fluctuating nature of predialysis and postdialysis BP, systolic BP (SBP) and diastolic BP before and after HD were recorded from 25 consecutive HD sessions during a 2-month period. Patients were followed for 4 years or until death or withdrawal.
Kaplan-Meier estimates revealed that patients with average postdialysis SBP rise of more than 5 mmHg were at the highest risk of both cardiovascular and all-cause mortality as compared to those with an average postdialysis SBP change between -5 to 5 mmHg and those with an average postdialysis SBP drop of more than 5 mmHg. Furthermore, multivariate Cox regression analysis indicated that both postdialysis SBP rise of more than 5 mmHg (HR, 3.925 [95% CI, 1.410-10.846], p = 0.008) and high cardiothoracic (CT) ratio of more than 50% (HR, 7.560 [95% CI, 2.048-27.912], p = 0.002) independently predicted all-cause mortality. We also found that patients with an average postdialysis SBP rise were associated with subclinical volume overload, as evidenced by the significantly higher CT ratio (p = 0.008).
A postdialysis SBP rise in HD patients independently predicted 4-year cardiovascular and all-cause mortality. Considering postdialysis SBP rise was associated with higher CT ratio, intensive evaluation of cardiac and volume status should be performed in patients with postdialysis SBP rise.
[Show abstract][Hide abstract] ABSTRACT: Variations in intradialytic blood pressure (BP) are a common and predictable occurrence in ESRD patients. These are caused by a decrease in blood volume provoked by ultrafiltration, lack of normal compensatory responses to fluid removal, underlying cardiac disease, and electrolyte changes that may adversely affect cardiovascular function. Intradialytic hypotension is the most frequent complication of the hemodialysis (HD) procedure and is fundamentally a consequence of an ultrafiltration rate that surpasses mechanisms activated to avert a decline in BP. Intradialytic hypertension is a less well-understood problem that has been recently associated with increased mortality. Fundamental patient characteristics and components of the HD procedure are involved in the pathophysiology of intradialytic hypotension and intradialytic hypertension. Correction of patient factors, modulation of HD prescription, and management of pharmacologic agents are the strategies to deal with adverse intradialytic BP changes.
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