Hypertension In Hemodialysis Patients Research Articles

Association between sympathetic activity and the atherogenic serum cholesterol fraction

A possible modulating influence of noradrenergic activity on serum lipoproteins was assessed under placebo conditions and following 4 weeks of sympathetic neurone blockade with debrisoquine in 9 normal subjects, 11 patients with mild essential hypertension, 9 normotensive, and 9 hypertensive hemodialysis patients. Plasma norepinephrine (NE) did not differ significantly among groups on placebo and was consistently reduced (P less than 0.05-0.001) by sympathetic blockade. The latter also decreased (P less than 0.05-0.001) plasma total cholesterol (C) as well as low and very low density lipoprotein cholesterol (LDL + VLDL-C) in the three patient groups. In the two dialysis groups, basal levels of plasma triglycerides (Tg) were increased and high density lipoprotein cholesterol (HDL-C) was diminished (P less than 0.01-0.001); sympathetic blockade lowered Tg and raised HDL-C (P less than 0.01-0.001). In normal subjects, sympathetic blockade did not significantly modify plasma lipoproteins. In the three patient groups, significant correlations (r = 0.62 - 0.88; P less than 0.05 - less than 0.001) existed between (a) basal plasma NE and total C or LDL + VLDL-C and (b) debrisoquine-induced changes in NE and changes in total LDL + VLDL-C. These findings suggest that in essential hypertension as well as in hemodialysis patients, the atherogenic C fraction, represented by LDL + VLDL-C, may be modulated by the noradrenergic activity.

Blood rheology and hypertension in hemodialysis patients treated with erythropoietin.

Fifteen hemodialysis patients suffering from stable anemia were treated with recombinant human erythropoietin (r-HuEPO). Within 16 weeks, hematocrit values increased from 23.7 +/- 1.2 to 35.7 +/- 0.2%. Simultaneously, mean predialytic blood pressure rose significantly from 131/79 to 139/85 mm Hg. Three out of 15 patients developed frank hypertension and had to be put on antihypertensive therapy. When the hematocrit was lowered again from 36.3 +/- 1.8 to 30.5 +/- 1.2% in these 3 patients, blood pressure was attenuated and the antihypertensive medication could be reduced or abolished. With rising hematocrit values, whole blood viscosity increased at both low (+42%) and high shear rates (+33%) without reaching the values seen in healthy subjects. By contrast, plasma viscosity was already elevated in hemodialysis patients prior to r-HuEPO treatment and showed only a slight, but insignificant increase during r-HuEPO treatment. Since whole blood viscosity is one factor that determines vascular resistance, it is conceivable that the development of hypertension during correction of the renal anemia is, at least partly, due to an increment of blood viscosity.

Pathophysiology and management of hypertension in hemodialysis patients.

Pathophysiology and management of hypertension in hemodialysis patients.

Neurologic Complications of Renal Failure

T HE ASSOCIATION between abnormal renal function and central nervous system disease was recognized nearly 40 years ago . Seizures and coma were frequent complications of acute uremia , whereas peripheral neuropathy and encephalopathy, observed in progressive uremia, were terminal events. Despite improvements in the medical management of end-stage renal failure, including dialysis and transplantation, patients manifest a variety of neurologic disorders . The acute cerebral changes associated with uremia may present as the dialysis disequilibrium syndrome or as subdural, intracerebral or intraspinal hemorrhage; these bleeding diatheses occur in up to 10% of hypertensive hemodialysis patients . Potential toxins accumulating in uremia are numerous (see article by Powell et aI, this issue). To be considered a uremic toxin , the concentration of any putative compound should correlate better with some measurement of nerve or cerebral function than with a reduction in glomerular filtration rate. To date , this has not been convincingly demonstrated. The neurologic complications of arterial hypertension in children include convulsions in over 90 % of children with severe hypertension and facial palsy, blindness, paraplegia, and alterations in the level of consciousness.' Children may present with seizures as the first sign of hypertension. The prognosis for children having had a single episode of hypertensive encephalopathy is good, with no demonstrative neurologic deficit or focal abnormality on brain scan by computerized tomography.'

Frequency dependency of causal factors for hypertension in hemodialysis patients.

Frequency dependency of causal factors for hypertension in hemodialysis patients.

Norepinephrine-related mechanism in hypertension accompanying renal failure

Various blood pressure (BP)-regulating factors were assessed before and after 4 weeks of selective norepinephrine (NE) inhibition with the sympathetic neurone blocker, debrisoquine, in nine hypertensive, nine normotensive hemodialysis patients (HDP), and 11 normal subjects. On placebo, hypertensive HDP had an increased total blood volume (P less than 0.05) and exchangeable sodium (P less than 0.001), while both HDP groups had increased (P less than 0.05) plasma clearances of NE and angiotensin II (AII), and tended to have higher basal plasma NE, renin, and AII levels, and lower BP responses to NE or AII than normal subjects. Plasma epinephrine and the chronotropic dose of isoproterenol (CDI) did not differ significantly among groups. Debrisoquine lowered supine BP markedly in hypertensive HDP (on average from 181/107 to 148/88 mm Hg) and slightly in normotensive HDP (143/78 to 131/76 mm Hg), but not in normal subjects (116/74 to 120/79 mm Hg). In all groups, plasma NE, CDI, and NE pressor dose were reduced in parallel (by 35 to 75%; P less than 0.05 to less than 0.001), and the relation between stepwise increasing plasma NE and BP changes during NE infusion was commensurably displaced to the left (P less than 0.01). The remaining parameters were not changed consistently. HDP, as normal subjects, respond to decreased sympathetic outflow with increased alpha- and beta-receptor sensitivity. Hypertension in HDP depends strongly on a NE-related mechanism. The latter seems to complement renin-angiotensin, sodium and fluid volume in the pathogenesis of high BP.

Treatment of hypertension in hemodialysis patients with nifedipine.

The hemodynamic effects of nifedipine were studied in nine patients with acute or chronic renal failure undergoing hemodialysis. Arterial blood pressure was lowered within 15 minutes of oral administration of nifedipine 10 mg. Mean arterial pressure and total systemic peripheral resistance were significantly decreased, whereas cardiac index and heart rate revealed slight but statistically insignificant changes. Changes in pulmonary artery diastolic pressure and mean right atrial pressure which were closely related to cardiac preload were not significant. However, the antihypertensive effect was enhanced in patients with lower pretreatment preload. Results show that oral nifedipine is effective in rapidly reducing blood pressure during or following hemodialysis.

Exercise training improves hypertension in hemodialysis patients.

6 patients with end-stage renal disease, hypertension and anemia were studied to determine the effect of endurance exercise training on their blood pressure. Initial exercise capacities were low (VO2 max = 18 +/- 2 ml/kg/min); however, their capacities increased (17 +/- 9%, p less than 0.05) after 14 +/- 5 months of training. This was associated with reductions in the antihypertensive medications in the 5 patients initially requiring them, and decreases in both predialysis systolic and diastolic blood pressures. There were significant increases in hemoglobin concentrations (7.3 +/- 0.4 to 9.8 +/- 0.9 g%) and hematocrit levels (23 +/- 2 to 30 +/- 3%) during training with no changes in body weights, interdialysis weight gains or serum albumin concentrations. 6 nonexercising dialysis patients had no changes in these same variables over the same period of time. These results suggest that endurance exercise training will reduce blood pressure and improve anemia in some hemodialysis patients.

Renin, blood volume and response to saralasin in patients on chronic haemodialysis: evidence against volume- and renin-'dependent' hypertension.

1. No significant relationship was found between blood pressure and blood volume, sulphate space or plasma angiotensin II concentration in 59 non-nephrectomized haemodialysis patients, of whom 42 were hypertensive. Supine mean blood pressure was only weakly correlated with plasma renin activity and the correlation was not improved when blood pressure was related to expressions combining renin and volume. 2. Changes in supine mean blood pressure during saralasin infusion were related to pre-infusion plasma renin activity (P < 0·001) or plasma angiotensin II (P < 0·02) but also to blood volume (P < 0·001) or sulphate space (P < 0·001). A fall of more than 10% in mean blood pressure during saralasin infusion was observed in only 12 patients (one normotensive), in five of whom there was evidence of volume depletion. 3. Thirteen patients (nine hypertensive) were studied at two levels of dietary sodium: 100 mmol/day and < 20 mmol/day. Supine mean blood pressure in hypertensive patients was lower during the period of higher salt intake despite increased volumes. 4. Hypertension in haemodialysis patients cannot be adequately explained by abnormalities either in volume homeostasis and/or in the renin—angiotensin system.

Hypertension in terminal renal failure

Inverse interrelations between plasma renin activity and exchangeable sodium or blood volume were found in both normotensive (N = 23) and hypertensive (N =29) hemodialysis patients (r= 0.47; P less than 0.005); however, mean plasma renin for any given sodium/volume state was at least two-fold higher in hypertensive than in normotensive hemodialysis patients or normal subjects (N =31). In the hemodialysis patients, blood pressure correlated weakly but significantly with the products of circulating renin and exchangeable sodium (r=0.37; P less than 0.005) or blood volume (r = 0.29; P less than 0.05). Multiple regression analysis including duration of previous hypertension as the second independent variable increased these correlation coefficients to 0.44 and 0.42, respectively. This suggests that hypertension in endstage kidney disease is often associated with resetting of the body sodium/fluid=renin feedback mechanism. Inappropriately increased plasma renine activity relative to the body sodium/volume state as well as high blood pressure-induced vascular changes may play important complementary roles, but it appears evident that additional mechanisms are also operative in maintaining end-stage renal hypertension.

Haemodynamic and blood volume studies in long-term haemodialysis patients, and in patients with successfully transplanted kidneys.

1. Stabilized hypertensive haemodialysis patients, as well as those with normotension, had a greatly elevated cardiac index (CI) that was not due to hypervolemia, but was most likely secondary to their anaemic condition. The hypertension itself was not accompanied by hypervolaemia, but was associated with a relatively very high total peripheral resistance. 2. In eight patients with successfully transplanted kidneys the following results were found. (a) Five were clearly hypertensive and had supine mean arterial pressure between 117 and 143 mmHg. It is noted that they were receiving prednisone at the time of the studies. (b) CI was normal in seven. (c) Total blood volume was normal in all. (d) The presence of wide-open arterio-venous fistulae was not associated with an increase in CI.