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Review: Blood pressure in haemodialysis patients: The importance of the relationship between the renin-angiotensin-aldosterone system, salt intake and extracellular volume

Blood Pressure Unit, St George's Hospital Medical School, London, SW17 0RE, UK

Graham A MacGregor

Blood Pressure Unit, St George's Hospital Medical School, London, SW17 0RE, UK, g.macgregor@ sghms.ac.uk

This review outlines the major mechanisms for control of blood pressure (BP) in individuals with renal failure on haemodialysis. Dietary salt stimulates thirst and, thereby, greater fluid intake with excessive fluid gain between dialysis sessions and chronic expansion of extracellular volume. At the same time, this volume expansion often fails to suppress the renin-angiotensin system (RAS) appropriately and this inevitably leads to high BP in the majority of individuals on haemodialysis.

A greater understanding of the mechanisms involved leads to more rational treatment and better BP control. This can be achieved by careful measurement of BP before and after dialysis, allowing time for the equilibration of extracellular fluid shifts that occur after dialysis, combined with measurements of plasma renin activity. It is relatively easy to then decide how the high BP should be treated either by removal of excess volume by gradual ultrafiltration combined with restriction of salt intake to help prevent thirst and excessive fluid gain between dialyses, or by inhibition of the RAS, or by a combination of both.

In those individuals who are unable to adequately reduce their dietary salt intake and still continue to gain large amounts of weight between dialysis, and are resistant to reducing their pre-dialysis weight, calcium antagonists may help to lower BP, either alone or in combination with RAS blockade. However, the BP often remains resistant to treatment unless they can be persuaded to reduce their salt intake.

Key Words: haemodialysis • blood pressure • extracellular fluid volume • salt intake • renin-angiotensin system

Journal of Renin-Angiotensin-Aldosterone System, Vol. 5, No. 1, 14-22 (2004)
DOI: 10.3317/jraas.2004.001


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