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      Dialysis Hypotension: A Role for Inadequate Increase in Arginine Vasopressin Levels? A Systematic Literature Review and Meta-Analysis

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          Background: Intradialytic hypotension is a common complication of hemodialysis (HD). Some studies have suggested that inadequate arginine vasopressin (AVP) increase could play a role in the pathogenesis of intradialytic hypotension. However, AVP levels during HD and its relation to hypotension has never been systematically studied. Summary: PubMed and Embase were searched (1970-2013, search terms ‘vasopressin' and ‘hemodialysis') for studies reporting on AVP levels during standard HD or other dialysis techniques. Observational studies reporting on AVP levels pre- and postdialysis were additionally included in a meta-analysis. Thirty-seven studies were included in the systematic literature review, of which 26 studies were eligible for meta-analysis. The main findings were that pretreatment AVP levels were higher in dialysis patients compared with healthy controls (6.4 ± 3.5 vs. 2.5 ± 1.3 pg/ml, p = 0.003) and that plasma AVP levels showed little or no increase during HD (from 7.0 ± 4.9 to 8.8 ± 9.3, p = 0.433) . Significant heterogeneity was found between studies. Meta-regression analysis revealed no significant associations between AVP and patient or study characteristics. Studies on other dialysis techniques showed mixed results regarding the AVP course. The eight studies that addressed the relation between intradialytic hypotension and AVP also showed inconsistent results. Key Messages: Plasma AVP levels are higher in dialysis patients compared with healthy controls, but show little or no increase during HD. The lack of a rise in AVP levels during HD may be pathophysiologically involved in the onset of intradialytic hypotension, but firm conclusions are not possible from our review of the literature.

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          Most cited references 49

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          Hemodialysis-associated hypotension as an independent risk factor for two-year mortality in hemodialysis patients.

          The relationship between blood pressure (BP) and mortality in hemodialysis patients has remained controversial. Some studies suggested that a lower pre- or postdialysis BP was associated with excess mortality, while others showed poorer outcome in patients with uncontrolled hypertension. We conducted a multicenter prospective cohort study to evaluate the impact of hemodialysis-associated hypotension on mortality. We recruited 1244 patients (685 males; mean age, 60 +/- 13 years) who underwent hemodialysis in 28 units during the two-year study period beginning in December 1999. Pre-, intra-, and postdialysis BP, and BP upon standing soon after hemodialysis, were measured in all patients at entry. Logistic regression analysis was used to assess the effect on mortality of pre-, intra-, and postdialysis BP, a fall in BP during hemodialysis, and a fall in BP upon standing soon after hemodialysis. During the study period, 149 patients died. Logistic models identified the lowest intradialysis systolic blood pressure (SBP) and degree of fall in SBP upon standing soon after hemodialysis as significant factors affecting mortality, but not pre- or postdialysis SBP and diastolic BP. The adjusted odds ratio for death was 0.79 (95% CI 0.64-0.98) when the lowest intradialysis SBP was analyzed in increments of 20 mm Hg, and was 0.82 (95% CI 0.67-0.98) when the fall in SBP upon standing soon after hemodialysis was analyzed in increments of 10 mm Hg. These results suggest that intradialysis hypotension and orthostatic hypotension after hemodialysis are significant and independent factors affecting mortality in hemodialysis patients.
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            Physiology of vasopressin relevant to management of septic shock.

            Vasopressin is emerging as a rational therapy for the hemodynamic support of septic shock and vasodilatory shock due to systemic inflammatory response syndrome. The goal of this review is to understand the physiology of vasopressin relevant to septic shock in order to maximize its safety and efficacy in clinical trials and in subsequent therapeutic use. Vasopressin is both a vasopressor and an antidiuretic hormone. It also has hemostatic, GI, and thermoregulatory effects, and is an adrenocorticotropic hormone secretagogue. Vasopressin is released from the axonal terminals of magnocellular neurons in the hypothalamus. Vasopressin mediates vasoconstriction via V1-receptor activation on vascular smooth muscle and mediates its antidiuretic effect via V2-receptor activation in the renal collecting duct system. In addition, vasopressin, at low plasma concentrations, mediates vasodilation in coronary, cerebral, and pulmonary arterial circulations. Septic shock causes first a transient early increase in blood vasopressin concentrations that decrease later in septic shock to very low levels compared to other causes of hypotension. Vasopressin infusion of 0.01 to 0.04 U/min in patients with septic shock increases plasma vasopressin levels to those observed in patients with hypotension from other causes, such as cardiogenic shock. Increased vasopressin levels are associated with a lesser need for other vasopressors. Urinary output may increase, and pulmonary vascular resistance may decrease. Infusions of > 0.04 U/min may lead to adverse, likely vasoconstriction-mediated events. Because clinical studies have been relatively small, focused on physiologic end points, and because of potential adverse effects of vasopressin, clinical use of vasopressin should await a randomized controlled trial of its effects on clinical outcomes such as organ failure and mortality.
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              Pathophysiology of dialysis hypotension: an update.

               J Daugirdas (2001)
              Dialysis hypotension occurs because a large volume of blood water and solutes are removed over a short period of time, overwhelming normal compensatory mechanisms, including plasma refilling and reduction of venous capacity, due to reduction of pressure transmission to veins. In some patients, seemingly paradoxical and inappropriate reduction of sympathetic tone may occur, causing reduction of arteriolar resistance, increased transmission of pressure to veins, and corresponding increase in venous capacity. Increased sequestration of blood in veins under conditions of hypovolemia reduces cardiac filling, cardiac output, and, ultimately, blood pressure. Adenosine release due to tissue ischemia may participate in reducing norepinephrine release locally, and activation of the Bezold-Jarisch reflex, perhaps in patients with certain but as yet undefined cardiac pathology, may be responsible for sudden dialysis hypotension. Patients with diastolic dysfunction may be more sensitive to the effects of reduced cardiac filling. The ultimate solution is reducing the ultrafiltration rate by use of longer dialysis sessions, more frequent dialysis, or reduction in salt intake. Increasing dialysis solution sodium chloride levels helps maintain blood volume and refilling but ultimately increases thirst and interdialytic weight gain, with a possible adverse effect on hypertension. Blood volume monitoring with ultrafiltration or dialysis solution sodium feedback loops are promising new strategies. Maintaining tissue oxygenation via an adequate blood hemoglobin level seems to be important. Use of adenosine antagonists remains experimental. Given the importance of sympathetic withdrawal, the use of pharmacologic sympathetic agonists is theoretically an attractive therapeutic strategy.

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                March 2014
                06 February 2014
                : 39
                : 2
                : 100-109
                aDivision of Nephrology, Department of Internal Medicine, bDialysis Center Groningen, and cDepartment of Health Sciences, University Medical Center Groningen, Groningen, The Netherlands
                Author notes
                *Casper F.M. Franssen, MD, PhD, Department of Internal Medicine, Division of Nephrology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, NL-9713 GZ Groningen (The Netherlands), E-Mail
                358203 Am J Nephrol 2014;39:100-109
                © 2014 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 1, Pages: 10
                In-Depth Topic Review

                Cardiovascular Medicine, Nephrology

                Hemodialysis, Arginine vasopressin, Intradialytic hypotension


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