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Sympathetic overactivity in patients with chronic renal failure
R L Converse1, T N Jacobsen, R D Toto
1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235-9034.
The New England Journal of Medicine
|January 10, 1993
Summary
Sympathetic nerve activity is elevated in chronic kidney disease patients with native kidneys, contributing to hypertension. This activation is reversible and linked to signals from failing kidneys.
Area of Science:
- Nephrology
- Cardiovascular Physiology
- Hypertension Research
Background:
- Hypertension is a common complication of chronic renal failure (CRF), but its underlying mechanisms remain unclear.
- Increased sympathetic nervous system (SNS) activity is suspected in CRF-related hypertension, yet direct measurements are lacking.
- This study investigates direct sympathetic nerve activity in patients with CRF.
Purpose of the Study:
- To directly measure sympathetic nerve discharge in patients with chronic renal failure.
- To determine if elevated sympathetic activity contributes to hypertension in CRF.
- To explore the role of native kidneys in sympathetic activation in CRF.
Main Methods:
- Recorded postganglionic sympathetic nerve discharge using microelectrodes in the peroneal nerve.
- Studied three groups: hemodialysis patients with native kidneys (n=18), hemodialysis patients post-bilateral nephrectomy (n=5), and healthy controls (n=11).
- Measured vascular resistance and mean arterial pressure alongside nerve discharge rates.
Main Results:
- Sympathetic nerve discharge was 2.5 times higher in hemodialysis patients with native kidneys compared to controls (58 vs. 23 bursts/min).
- Patients without native kidneys showed normal sympathetic nerve discharge, similar to controls (21 vs. 23 bursts/min).
- Elevated sympathetic activity in patients with native kidneys correlated with higher vascular resistance and mean arterial pressure.
Conclusions:
- Chronic renal failure with native kidneys is associated with reversible sympathetic activation.
- This sympathetic activation appears to originate from signals generated by the failing kidneys.
- The findings suggest a kidney-brain-vascular axis in CRF-related hypertension.