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Published on: October 2, 2020
Control of blood pressure in long slow hemodialysis
1Centre de Rein Artificiel, Tassin, France.
Insights
Long, slow hemodialysis effectively controlled blood pressure in patients, reducing cardiovascular risks. This method improved patient outcomes by managing fluid volume and potentially enhancing nitric oxide function.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Clinical Hypertension
Background:
- Hypertension is a significant contributor to mortality and morbidity in patients undergoing hemodialysis.
- Effective blood pressure management is crucial for improving outcomes in this patient population.
Purpose of the Study:
- To evaluate the impact of long, slow hemodialysis on blood pressure control and cardiovascular outcomes in hemodialysis patients.
- To explore potential mechanisms behind the observed effects.
Main Methods:
- A cohort of 692 unselected patients undergoing 8-hour dialysis sessions was studied.
- Blood pressure control, intradialytic hypotensive episodes, and cardiovascular events were monitored.
Main Results:
- Long, slow dialysis achieved excellent blood pressure control without antihypertensive medications.
- Lower cardiovascular morbidity and mortality were observed in patients with lower predialysis mean arterial pressure.
- Effective extracellular volume management and a low rate of hypotensive episodes were identified as probable explanations.
Conclusions:
- Long, slow hemodialysis is an effective strategy for managing hypertension in hemodialysis patients.
- This approach may improve cardiovascular outcomes by optimizing fluid balance and potentially restoring nitric oxide bioavailability.
Abstract:
Hypertension is a major cause of mortality and morbidity in hemodialysis patients. A long slow dialysis (8 h/session) was used in 692 unselected patients. It allowed for an excellent control of blood pressure without the need of antihypertensive medications. Cardiovascular morbidity and mortality were lower in the subgroups of patients presenting with a lower predialysis mean arterial pressure. The control of the extracellular volume with a low rate of intradialytic hypotensive episodes is the most probable explanation of this result. Another possible mechanism is the restoration by the large dose of dialysis of the nitric oxide vasodilator action inhibited by the accumulation of dimethylarginine in the serum of uremic patients.
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