Hypertension and hemodialysis: pathophysiology and outcomes in adult and pediatric populations

Abstract

Hypertension is prevalent in adult and pediatric end-stage renal disease patients on hemodialysis. Volume overload is a primary factor contributing to hypertension, and attaining true dry weight remains a priority for nephrologists. Other contributing factors to hypertension include activation of the sympathetic and renin–angiotensin–aldosterone systems, endothelial cell dysfunction, arterial stiffness, exposure to hypertensinogenic drugs, and electrolyte imbalances during hemodialysis. Epidemiologic studies in adults show that uncontrolled hypertension results in cardiovascular morbidity, but reveal increased mortality risk at low blood pressure, so that it remains unclear what the target blood pressure should be. Despite the lack of a definitive BP target, gradual dry weight reduction should be the first intervention for BP control. Renin–angiotensin–aldosterone system inhibitors have been shown to improve cardiovascular morbidity and mortality and are recommended as the initial pharmacologic therapy for hypertensive hemodialysis patients. Short-daily or nocturnal hemodialysis are also good therapeutic options for these patients. It is already established that hypertension in pediatric hemodialysis patients is associated with adverse cardiovascular outcomes, and there is emerging evidence that the mechanisms causing hypertension are similar to adults. Hypertension in adult and pediatric hemodialysis patients warrants aggressive management, although clinical trial evidence of a target BP that improves mortality does not currently exist.

Excess fluid volume: sociodemographic and clinical analysis in haemodialysis patients

“…Cardiovascular manifestations are commonly identified in chronic renal patients, and hypertension is related to the retention of sodium and fluid or the activation of the renin-angiotensin-aldosterone system in this population (24) . In addition to hypertension, jugular venous distension is an important sign of cardiovascular complications due to kidney failure (1) .…”

Pathogenesis and treatment of hypertension in haemodialysis patients with chronic kidney disease

“…The pathogenesis of hypertension in ESKD patients include increased extracellular volume, increased sympathetic and renin-angiotensin-aldosterone (RAA) systems activity, secondary hyperparathyroidism, endothelial cell dysfunction, increased oxidative stress and exposure to erythropoiesis-stimulating agents (ESAs) [19] (Table I).…”

“…The inadequate activity of RAA system has long been implicated in the etiology of hypertension in haemodialysis patients [19]. In a study of 51 haemodialysis patients, there were significant differences in the plasma renin activity (PRA) between normotensive subjects (n = 9), hypertensive subjects whose blood pressure was controlled by ultrafiltration and dietary sodium restriction (n = 24), and subjects with persistent hypertension (n = 18) [22].…”

“…Post-nephrectomy PRA was measured in 12 subjects, and was significantly lower, suggesting that elevated baseline PRA may have contributed to the poorly controlled hypertension. Angiotensin II and aldosterone which are primary mediators of RAA system, both contribute to left ventricular hypertrophy (LVH) and endothelial cell dysfunction independently of blood pressure [19].…”

“…The proposed mechanisms specific to haemodialysis patients include increase of ET-1 release and increased sensitivity to angiotensin II and adrenergic stimuli. The effect of blood pressure is dependent on the dose, but not necessary the pre-treatment blood pressure as both previously normotensive and hypertensive patients can have ESAs related blood pressure increase [19].…”