We read the article by Shimizu et al1 examining the effect of hyperosmolality on vasopressin secretion in patients with intradialytic hypotension (IDH) with interest. The authors showed that administration of small volumes of hypertonic solution (saline or glucose) increased plasma vasopressin concentrations and blood pressure (BP) without significantly changing plasma volume. This contrasts with the increase in plasma volume and BP noted with larger volumes of isotonic saline (no effect on plasma vasopressin concentrations). This suggests the existence of a previously unrecognized mechanism by which hypertonic saline and glucose increase BP in patients administered these substances when hypotension develops during hemodialysis.
Of even more interest was the demonstration that plasma vasopressin concentrations did not increase (6.32 versus 6.28 pg/mL) despite significant decreases in mean arterial pressure (94.0 to 63.8 mm Hg) during hemodialysis (before infusion of hypertonic solutions) in 12 patients.1 Because pulse rate also did not change during IDH (76.0 versus 76.6 beats/min), one may speculate that autonomic/baroreceptor dysfunction was present. As the authors noted, insufficient or absent vasopressin release during hypotension may contribute to IDH in these patients. We agree and recently published similar results in 10 patients with IDH.2 Despite decreases in systolic (43.1 mm Hg) and diastolic BP (25.5 mm Hg) in these patients, vasopressin concentrations did not change (5.18 versus 5.25 pg/mL). Similar results documenting vasopressin insufficiency during episodes of IDH were published by Freiss et al.3
Thus, it appears that patients prone to IDH experience insufficient vasopressin release in response to volume-mediated (nonosmotic) stimuli. This may be related to underlying autonomic/baroreceptor dysfunction. This aberrant response importantly may contribute to IDH in hemodialysis patients. However, they maintain an intact response to osmotic stimuli, which may provide an avenue of intervention, as noted in the present study. Also, low-dose intravenous or intranasal vasopressin administration may offer an effective therapy.
Acknowledgements
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References
1. 1Shimizu K, Kurosawa T, Sanjo T. Effect of hyperosmolality on vasopressin secretion in intradialytic hypotension: A mechanistic study. Am J Kidney Dis. 2008;52:294–304. Abstract | Full Text |
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2. 2Rho M, Perazella MA, Parikh CR, Peixoto AJ, Brewster UC. Serum vasopressin response in patients with intradialytic hypotension: A pilot study. Clin J Am Soc Nephrol. 2008;3:729–735.
3. 3Freiss U, Rascher W, Ritz E, Gross P. Failure of arginine vasopressin and other pressor hormones to increase in severe recurrent dialysis hypotension. Nephrol Dial Transplant. 1995;10:1421–1427. MEDLINE
Yale University School of Medicine, New Haven, Connecticut