Abstract
Background
Fluid retention is a major complication of peritoneal dialysis (PD). Arginine vasopressin (AVP), an antidiuretic hormone, is known to be one of the important factors related to fluid management. However, the effect of the PD fluid (PDF) on AVP dynamics remains unclear.
Methods
Plasma AVP levels and osmolality (direct measurement/calculation) were tested upon arrival. Next, we studied the effects of icodextrin-based PDF (I-PDF) and glucose-based PDF (G-PDF) on hypothalamic AVP synthesis in transgenic rats expressing AVP-enhanced green fluorescent protein (eGFP) under the AVP promoter.
Results
The average plasma AVP levels in PD patients were higher than the normal range and patients with end-stage kidney disease (ESKD), however, the difference was not significant between PD and ESKD patients. In patients with PD, there is a significant correlation between plasma AVP levels and plasma osmolality (measured directly). In the G-PDF and I-PDF groups, eGFP fluorescence intensity increased in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus, which are the main AVP synthesis sites. Immunohistochemical analysis revealed the expression of Fos protein, a useful indicator of neuronal activity, in eGFP-positive neurons in the PVN and SON after G-PDF administration.
Conclusion
To the best of our knowledge, this is the first report demonstrating increased plasma AVP levels in patients with PD and upregulation of hypothalamic AVP after PDF administration in transgenic rats. This study revealed that osmotic changes during PD treatment strongly influence AVP dynamics. These findings provide new insights into fluid management in patients with PD.
Keywords
Get full access to this article
View all access options for this article.
References
Supplementary Material
Please find the following supplemental material available below.
For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.
For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.
