Hypertension due to chronic volume expansion is common in end-stage renal disease (ESRD) and a major contributor to the 30-fold higher annual cardiovascular mortality rate in these patients. Dialysis removes volume but adequate volume control is often difficult to achieve because episodes of intradialytic hypotension are common. In response to this hypotension, volume removal is limited and patients are frequently left volume expanded. This, in turn, leads to chronic interdialytic hypertension and its sequellae. Though the normal response to volume depletion is an increase in vascular tone, studies suggest that dialysis patients do not vasoconstdct appropriately during hemodialysis. We suspect a defect in the baroreceptor mediated release of vasopressin likely contributes to this lack of vasoconstriction. Though low-dose vasopressin does not increase blood pressure in normal subjects, recent studies have shown that in states where blood pressure is compromised and there is a deficiency in vasopressin, there is increased pressor sensitivity to vasopressin. In preliminary studies vasopressin was administered to dialysis patients. Vasopressin caused a statistically significant increase in blood pressure of approximately 10 mmHg in patients with ESRD. We hypothesize that low-dose exogenous vasopressin will support blood pressure during dialysis, leading to a lower incidence of intradialytic hypotension, greater fluid removal and ultimately improved long term blood pressure control.
|Thompson, Aliza M; Oliver, Juan A (2009) Endogenous and exogenous vasopressin during hemodialysis. Semin Dial 22:472-5|
|Thompson, Aliza M; Eguchi, Kazuo; Reznik, Michael E et al. (2007) Validation of an oscillometric home blood pressure monitor in an end-stage renal disease population and the effect of arterial stiffness on its accuracy. Blood Press Monit 12:227-32|
|Thompson, A M; Pickering, T G (2006) The role of ambulatory blood pressure monitoring in chronic and end-stage renal disease. Kidney Int 70:1000-7|