Children with end-stage renal disease (ESRD) often remain hypertensive despite bilateral nephrectomy and aggressive fluid removal on hemodialysis. We speculated that an extrarenal source of renin might contribute to the release of "tissular" angiotensin-II (AT-II) generating hypertension in anephric patients. At the same time, experimental evidence supports that peripheral AT-II vasoconstrictive effect is likely mediated by endothelin-1 (ET-1). Thus, it is conceivable that hypertension in ESRD patients may be due, in part, to a cascade involving vascular production and secretion of AT-II and ET-1. In order to establish the relationship between AT-II, ET-1, and blood pressure we performed a pilot study to measure predialysis systolic and diastolic blood pressures (SBP and DBP, respectively) and serum AT-II and ET-1 levels in 12 anephric children receiving hemodialysis. Predialysis AT-II and ET-1 levels were similar in all patients, and neither value correlated with their mean SBP or DBP. In patients with postdialysis hypertension, there was no correlation between predialysis AT-II and ET-1 plasma levels. We therefore find no evidence to suggest that vascular-mediated AT-II and/or ET-1 contributes significantly to hypertension in anephric patients.
|Original language||English (US)|
|Number of pages||4|
|State||Published - Jan 1 2001|
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health