Hypertension in Hemodialysis. An Overview on Physiopathology and Therapeutic Approach in Adults and Children
Abstract
Chronic Kidney disease (CKD) patients, particularly those with end stage renal disease (ESRD), are at much higher risk of cardiovascular disease than the general population. Cardiovascular disease is by far the leading cause of morbidity and mortality in dyalisis patients, accounting for almost 40% of hospitalizations and almost 50% of deaths.
Hypertension is the single most important factor for the development of cardio and cerebrovascular complications. The etio-pathogenesis of hypertension in dialysis patients is multifactorial, sodium excess and extracellular volume expansion is the major factor in the development of hypertension, however there are other pathogenetic factors that should be considered, such as renin-angiotensin system hyperactivity, increased sympatic activity, altered endothelial cell function, hyperparathiroidism, and oxidative stress. The most important risk factors are anemia, hypoalbuminemia, chronic inflammation, prothrombotic factors, hyperomocisteinemia, vascular calcification and the traditional factors for cardiovascular risk (age, male gender, diabetes mellitus, dyslipidemia, smoke, physical inactivity, alcohol abuse).
Elevated blood pressure is frequent also in children on long term dialysis therapy. Data suggest that uremic factors or factors related to renal replacement therapy may be implicated in the pathogenesis of heart disease in adults and pediatric patients, because cardiovascular survival improves after transplantation.
The management of hypertension requires lifestyle modifications and control of volume status, with dietary salt and fluid restriction in combination with reduction of dialysate sodium concentration or with programmed “variable–sodium” dialysis.
The relationship between interdialytic weight and blood pressure is incompletely characterized; the dry weight (DW) method relies on the progressive reduction of the postdialysis body weight until blood pressure is normalized. There are several non clinical methods for evaluation DW such as measure the inferior vena cava diameter whit ultrasound, measure blood volume (BV) whit radiolabeled albumin and calculating post-hemodialysis BV from the change in hematocrit.
It may exist a lag time of several weeks between the normalization of the extracellular volume and blood pressure. It is related to the correction of the hemodinamic consequences of the extracellular volume overload.
The other problems to limit the possibility of correcting adequately volume expansion with dialysis are the use of antihypertensive drugs and the aggressive ultrafiltration required by short dialysis times. A possible treatment option for these patients may be increase time hemodialysis with slow, long hemodialysis; short, daily hemodialysis or nocturnal hemodialysis.
All classes of antihypertensive drugs can be used in dialysis patients, except the diuretics because inefficacy. Angiotensin-converting enzyme (ACE) and Angiotensin T1 receptor antagonist (AT1RA) appear to have the greatest ability to reduce left ventricular mass.