What Causes Intradialytic Hypertension
Intradialytic hypertension is primarily caused by volume and sodium overload, with additional contributions from sympathetic nervous system overactivity, renin-angiotensin-aldosterone system activation, endothelial dysfunction, and arterial stiffness. 1
Primary Pathophysiologic Mechanism
Volume overload is the cornerstone mechanism underlying intradialytic hypertension, representing the most critical and modifiable factor. 1, 2 This explains why aggressive dry weight reduction remains the first-line therapeutic approach and why the blood pressure rise during dialysis paradoxically occurs despite fluid removal. 1
Multiple Overlapping Mechanisms
The blood pressure elevation during hemodialysis involves several interconnected pathways:
Volume-Related Factors
- Subclinical volume overload is the dominant mechanism, where patients appear clinically euvolemic but remain volume-expanded, leading to paradoxical blood pressure increases during ultrafiltration. 3
- Sodium overload works synergistically with volume excess, as interdialytic sodium accumulation drives fluid retention and perpetuates the hypertensive pattern. 1, 4
Neurohumoral Activation
- Sympathetic nervous system overactivity contributes significantly to the blood pressure rise, with excessive catecholamine release during dialysis causing vasoconstriction despite volume removal. 1, 4, 5
- Renin-angiotensin-aldosterone system activation occurs during ultrafiltration, triggering vasoconstriction and further blood pressure elevation, though this mechanism appears secondary to volume factors. 1, 5, 3
Vascular Dysfunction
- Endothelial dysfunction impairs normal vasodilatory responses during dialysis, with increased endothelin-1 levels promoting vasoconstriction. 1, 4, 5, 3
- Arterial stiffness reduces vascular compliance, preventing appropriate blood pressure buffering during volume shifts. 1, 2, 4
Hemodynamic Considerations
- Volume shifts during ultrafiltration create complex hemodynamic changes that unmask underlying volume overload rather than causing true hypovolemia. 2
- Vascular refilling capacity may be impaired, leading to paradoxical vasoconstriction as a compensatory mechanism. 2
Clinical Context
The relative importance of these mechanisms varies by patient, but volume control addresses the primary driver in the vast majority of cases, which is why guidelines universally recommend aggressive dry weight reduction as first-line management. 1 The other mechanisms—sympathetic overactivity, RAAS activation, and endothelial dysfunction—typically become clinically relevant only after volume status is optimized or in refractory cases requiring pharmacologic intervention. 1, 4
Key Clinical Pitfall
Do not assume intradialytic hypertension represents inadequate antihypertensive medication; this misinterpretation leads to polypharmacy while ignoring the underlying volume excess that drives the condition. 1 The blood pressure rise during dialysis is a marker of persistent volume overload requiring mechanical removal through ultrafiltration, not pharmacologic suppression. 1, 3