Abstract
Hypertension is a frequent problem in patients with renal failure, whether or not they are on renal replacement therapy. Little is known, however, about the pathophysiological mechanisms leading to an elevation of blood pressure. Although there is a relationship between body fluid volumes and blood pressure, it is unlikely that hypertension can be explained on the basis of volume expansion alone. Haemodynamically, hypertension in renal failure is characterized by an increased peripheral vascular resistance, but there is no convincing evidence that this is secondary to a high-output state. Among the pressor systems that have been implicated, the renin-angiotensin system and the adrenergic system are likely candidates, but overactivity of these systems or enhanced reactivity to the mediators still cannot explain all elements of renal failure associated hypertension. Therefore, other factors, such as intracellular electrolytes and the Na-K pump, are under scrutiny. However, given the heterogeneity of patient groups studied so far, it is virtually impossible to draw any meaningful conclusions about the pathogenesis of high blood pressure in patients on renal replacement therapy.
Published Version
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