Dialysis is a medical treatment that takes over the functions of failing kidneys by cleaning the blood and removing accumulated waste products and excess fluid. This process involves mechanically manipulating the body’s fluid volume and solute concentrations. Because blood pressure is directly linked to the volume of fluid circulating, dialysis alters a patient’s blood pressure, often leading to fluctuations that range from dangerously low to persistently high. Understanding this relationship between artificial fluid removal and circulatory stability is important for managing the health of individuals with kidney failure.
The Kidney’s Role in Blood Pressure Control
Healthy kidneys regulate blood pressure through control of fluid balance and hormonal signaling. They monitor the body’s volume status and electrolyte concentrations, adjusting the amount of water and sodium excreted in the urine. When blood pressure drops, the kidneys activate the Renin-Angiotensin-Aldosterone System (RAAS) to restore pressure.
This system begins with the release of the enzyme renin, leading to the production of angiotensin II, a compound that causes blood vessels to narrow. Angiotensin II also stimulates the adrenal glands to release aldosterone, prompting the renal tubules to increase the reabsorption of sodium and water back into the bloodstream. This combined action of vessel constriction and fluid retention increases circulating blood volume and systemic vascular resistance, thereby raising blood pressure. When the kidneys fail, this control is lost, resulting in the chronic retention of salt and water, which is the primary cause of hypertension in most patients awaiting dialysis.
Fluid Removal and the Mechanism of Blood Pressure Change
Dialysis replaces the kidney’s fluid-regulating function through ultrafiltration, the controlled removal of plasma water from the blood across a semipermeable membrane. This removal is driven by creating a pressure gradient, known as the transmembrane pressure, between the blood and dialysate compartments. The ultrafiltration rate is set to remove the fluid weight gained by the patient since their last treatment.
The rapid withdrawal of fluid causes an acute reduction in circulating volume. To prevent blood pressure from falling, the body attempts to replenish the volume by mobilizing fluid from surrounding tissues, a process called plasma refill. If the ultrafiltration rate exceeds the plasma refill rate, blood volume drops quickly, leading to a reduction in cardiac output and a sudden drop in blood pressure.
The composition and temperature of the dialysate fluid also influence the vascular response. Using a dialysate that is too warm can cause peripheral blood vessels to widen, reducing systemic vascular resistance and increasing the likelihood of a drop in blood pressure. Conversely, a higher sodium concentration can encourage faster fluid movement into the blood, assisting plasma refill, though this may lead to greater fluid retention between sessions. Furthermore, the removal of urea and other solutes can cause a rapid decline in plasma osmolality, which slows plasma refill and increases the risk of hemodynamic instability.
Understanding Dialysis-Related Blood Pressure Issues
The intense fluid dynamics of dialysis lead to two primary, yet opposing, blood pressure complications: intradialytic hypotension (IH) and interdialytic hypertension. IH is the most common acute complication, defined by a significant drop in blood pressure during the treatment session, often accompanied by symptoms like cramping, dizziness, or nausea. This event occurs when the programmed rate of fluid removal is too aggressive, depleting the intravascular volume faster than the body can compensate.
A high rate of fluid gain between sessions, often exceeding four kilograms, forces a high ultrafiltration rate, which increases the risk of IH. Autonomic nervous system dysfunction, common in kidney failure or diabetes, can also impair the body’s ability to constrict blood vessels to maintain pressure during volume loss. IH can lead to inadequate dialysis or tissue damage in organs such as the heart and brain due to temporary low blood flow.
In contrast, interdialytic hypertension refers to consistently high blood pressure that persists between dialysis sessions and is a marker of chronic fluid overload. This condition results from the retention of salt and water during the interval between treatments, which raises the baseline circulating volume. In some patients, a paradoxical increase in blood pressure can even occur during the dialysis session, known as intradialytic hypertension. This rebound may be triggered by the acute activation of the RAAS or an imbalance in hormones like endothelin, which cause blood vessels to constrict despite the ongoing fluid removal.
Strategies for Managing Blood Pressure During Dialysis
Blood pressure management focuses on achieving and maintaining a patient’s “dry weight,” the weight at which a patient is free of excess fluid (euvolemic) without becoming hypotensive. Physicians must reassess this target weight, as overestimation can cause chronic hypertension, while underestimation can lead to recurrent episodes of intradialytic hypotension. Gradual dry weight reduction, often over weeks or months, improves blood pressure control for patients with hypertension.
A primary strategy involves precisely controlling the ultrafiltration rate, aiming to keep it below a specific threshold, such as 13 milliliters per hour per kilogram of post-dialysis weight, to allow for adequate plasma refill. Adjusting the dialysate prescription, such as lowering the temperature, can help prevent vasodilation and improve tolerance to fluid removal.
Patients must adhere to strict dietary restrictions on sodium and fluid intake, minimizing weight gain between sessions and reducing the amount of fluid that must be removed. The timing of antihypertensive medications is also adjusted; some are withheld immediately before a session to prevent a severe drop in blood pressure, while others targeting the RAAS may be maintained to control associated hypertension.