Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is not known whether recombinant human erythropoietin has a direct, clinically apparent pressor effect in hemodialysis patients or whether hypertension developing or aggravated in these patients merely reflects increased hematocrit. We compared blood pressure after three different methods of partial correction of anemia in hemodialysis patients with similar baseline hematocrits (erythropoietin n = 12, intravenous iron alone n = 10, androgens n = 9). Shortly after the start of treatment and with a minimally increased hematocrit, the need for antihypertensive medication increased in the erythropoietin group. No such pressor effect was observed with iron or androgens. These data suggest a direct hypertensive effect of erythropoietin in some patients on hemodialysis.
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PMID:Blood pressure after three different forms of correction of anemia in hemodialysis. 151 88

The role of the rate of increase in hematocrit (Hct) and changes in vasoactive substances as a cause of hypertension induced by the administration of recombinant erythropoietin (r-EPO) were examined in 20 stable hemodialysis (HD) patients. Measurements were made twice at the start of treatment and when the Hct reached 30%. Patients were divided into 2 groups: Group I: 14 patients received r-EPO, 3000 units intravenously three times a week. Group II: 6 patients, needing repeated blood transfusion, were given 2 to 4 units of washed red blood cells during a HD session. The Hct increased by 0.65%/week in Group I and by 6.7%/2 days in Group II. An elevation in blood pressure was not seen in any patient. There was no difference in the levels of renin, angiotensin II, epinephrine, norepinephrine, dopamine, atrial natiuretic peptide (ANP), BUN, creatinine, cardiac thoracic ratio and body weight in any of the groups. In conclusion, elevation of the Hct in HD patients whatever the rate of increase within the 30% Hct range, does not cause an increase in blood pressure. In addition, the levels of vasoactive substances do not change in partially corrected anemic HD patients. As a result blood pressure control can be helped by aiming at the lower target Hct level of around 30%.
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PMID:The rate of increase in hematocrit, humoral vasoactive substances and blood pressure changes in hemodialysis patients treated with recombinant human erythropoietin or blood transfusion. 153 89

Long-term myocardial effects of recombinant human erythropoietin (rhEPO) therapy were investigated in nine hemodialysis (HD) patients greater than 60 years of age. Echocardiographic studies were performed before the administration of rhEPO with a hematocrit of 20.8% +/- 1.9% and repeated after 6 (period I) and 24 months (period II) of treatment, when the hematocrit was increased to 34.1% +/- 2.3% and 32.3% +/- 2.8%, respectively. Left ventricular diameters were not significantly changed by rhEPO, although they tended to decrease at the end of the study (30.6 +/- 5.3 v 27.7 +/- 3.6 mm systole, and 50.3 +/- 3 v 46.5 +/- 3.7 mm diastole). Thickness of the interventricular septum and left ventricular posterior wall remained unaltered, although there was a downward trend (14.5 +/- 5.2 to 12.8 +/- 2.8 mm and 11.7 +/- 1.9 to 10.6 +/- 1.4 mm, respectively). Left ventricular mass index (LVM) progressively decreased from 181.5 +/- 61 to 153.8 +/- 38.3 (period I) and 135.7 +/- 45.6 g/m2 (period II, P less than 0.05). Stroke volume remained unaltered in period I, but it decreased from 93.7 +/- 10 to 65.2 +/- 12.8 mL (P less than 0.001) in period II, resulting in a decrease of cardiac index (CI) from 3.93 +/- 0.86 to 2.54 +/- 0.68 L/min/m2 (P less than 0.001) at the end of the study. Heart rate did not change during the study period. Blood pressure was kept constant, although antihypertensive therapy needed to be adjusted to prevent occurrence or aggravation of hypertension in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term myocardial effects of correction of anemia with recombinant human erythropoietin in aged patients on hemodialysis. 153 83

Eleven anemic children and adolescents with a median age of 14 years (range six months-20 years) on chronic hemodialysis were treated with recombinant human erythropoietin (rHuEPO) intravenously three times a week for an average of 9.2 months. After eight weeks of therapy, hematocrit rose from 20.3 +/- 1.4% to 31.7 +/- 0.7% (0.20 +/- 0.01 to 0.31 +/- 0.007, p less than 0.001, mean +/- SEM). After reaching the target hematocrit of 30% to 33% (0.30 to 0.33), doses were adjusted individually. Blood transfusions were eliminated in all but one patient. All patients experienced an increase in appetite and energy level. Serum ferritin concentrations decreased in all patients who reached target hematocrit and seven required iron supplementation. Hypertension worsened in two patients and developed in two others. One patient's vascular access clotted. Dialysis efficiency and heparin requirements during dialysis did not change significantly. We conclude that rHuEPO is safe, effective, and should be recommended as treatment for anemia in children and adolescents on hemodialysis, but close monitoring for the development of hypertension and/or iron deficiency is necessary.
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PMID:Therapy of renal anemia in children and adolescents with recombinant human erythropoietin (rHuEPO). 154 82

We studied the therapeutic benefit of recombinant human erythropoietin (rHuEPO) in dialysis patients with thalassemia minor. Four of the 40 randomly selected patients (22 on hemodialysis [HD], 18 on continuous ambulatory peritoneal dialysis [CAPD]) were identified to be thalassemic prior to a trial of rHuEPO (alpha-thalassemia trait in three and beta-thalassemia minor in one). All patients were initially treated with rHuEPO at a dose of 100 +/- 25 U/kg/wk subcutaneously depending on the hemoglobin level. EPO injections were continued for 16 weeks with further adjustments of the doses according to the hemoglobin level increases attained. All nonthalassemic patients reached a target hemoglobin of 10 g/dL at week 16, with an average maintenance dose of 120 +/- 7.8 U/kg/wk, but the hemoglobin was increased by only 1 g/dL in the thalassemic patients receiving 175 U/kg/wk. Following cessation of rHuEPO therapy for 6 weeks, all four thalassemic patients and 18 randomly selected nonthalassemic patients received a fixed dose of rHuEPO 4,000 U/wk (equivalent to 80 U/kg/wk) for 16 weeks. The hemoglobin remained unchanged in the thalassemic patients, but a progressive and significant increase of hemoglobin was observed in the nonthalassemic patients. At the last phase of the study, the thalassemic patients received rHuEPO at a dose of 100 or 125 U/kg/wk with 4-weekly increments of 25 U/kg/wk until their hemoglobin reached 10 g/dL. One patient developed uncontrolled hypertension with a dose of 150 U/kg/wk, and one reached the target hemoglobin at a dose of 200 U/kg/wk.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of recombinant erythropoietin in thalassemic patients on dialysis. 155 68

Chronic renal failure is almost invariably accompanied by symptomatic anemia. It has been demonstrated that the primary cause of this anemia is inadequate production of erythropoietin by the diseased kidneys. The isolation of erythropoietin, followed by the cloning and expression of the human erythropoietin gene, made possible clinical trials of rHuEPO in uremic patients. rHuEPO produced dramatic increases in the hematocrit in almost all patients treated and also ameliorated many symptoms, such as lethargy, dizziness, and poor appetite, that had long been attributed to the effect of uremic toxins. Adverse effects of treatment with rHuEPO noted in the early clinical trials included hypertension, seizures, arteriovenous fistula or shunt thrombosis, and hyperkalemia. Further study of rHuEPO has shown that many of these side effects may be no more frequent in patients receiving rHuEPO than in other uremic patients not receiving rHuEPO. Reduction of the rHuEPO dosage and subcutaneous administration produce less rapid increases in the hematocrit and may lessen the incidence and severity of these side effects. rHuEPO therapy places great demands on both the body's iron stores and the capacity to rapidly transfer iron from storage sites to the erythroid progenitor cells. Thus, almost all patients treated with rHuEPO become iron deficient and require oral or parenteral iron replacement. Response to rHuEPO in uremic patients is diminished if the anemia is complicated by iron deficiency, inflammatory disorders, aluminum overload, or deficiency of folate or vitamin B12. rHuEPO therapy is safe and effective in the treatment of the anemia of chronic renal failure. The use of rHuEPO leads to enhanced quality of life and eliminates the need for red cell transfusions. In addition to hemodialysis patients, predialysis patients and those on CAPD benefit from and are candidates for rHuEPO therapy.
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PMID:Anemia of renal failure. Use of erythropoietin. 157 66

Two renal transplant patients developed anemia during treatment of hypertension with enalapril medication. Hemoglobin levels normalized after administration of enalapril was stopped. In one patient, it was demonstrated that the discontinuation of enalapril was followed by a decrease in renal blood flow and a significant increase in the plasma erythropoietin levels that preceded the rise in hemoglobin. These observations are consistent with the hypothesis that angiotensin-converting enzyme inhibition may cause anemia by increasing renal blood flow and consequently decreasing erythropoietin levels.
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PMID:Enalapril-induced anemia in two kidney transplant recipients. 158 Sep 86

Polycythemia vera (PV) is one of the myeloproliferative diseases, and, as such, is an example of clonal hematopoiesis. The progeny of a single, abnormal, hematopoietic stem cell gain a growth advantage over their normal counterparts resulting in overproduction of red cells generally accompanied by overproduction of granulocytes and platelets as well. There are a variety of nonspecific symptoms at onset related to the increased red cell mass and hematocrit accompanied by the more specific manifestations of pruritus, erythromelalgia, and hepatic, portal, and mesenteric vein thrombosis. Splenomegaly and hypertension are common. The laboratory hallmark is an increased red cell mass. There is also often an increase in white cell count, platelet count, and leukocyte alkaline phosphatase along with other findings reflecting the increased rate of turnover of hematopoietic cells. The bone marrow biopsy generally displays hypercellularity involving all three cell lines and absent iron stores. The diagnosis of PV depends on excluding spurious polycythemia in which there is a high hematocrit but a normal red cell mass and secondary polycythemia in which there is an increased red cell mass in response to tissue hypoxia or the inappropriate production of erythropoietin, generally by a tumor. In addition, one should try to establish the diagnosis in a positive fashion by a combination of studies of the blood and bone marrow. Phlebotomy and occasionally plateletpheresis should be used as acute therapy. Chronic therapy is guided by the knowledge that patients treated with phlebotomy alone have an increased rate of thrombotic complications particularly in older patients and those with previous thrombotic disease. Myelosuppressive therapy can reduce the incidence of these complications, but is commonly associated with an increased incidence of second malignancies, particularly acute leukemia. At present, hydroxyurea is the myelosuppressive agent of choice. Antiplatelet agents have a limited role except in the palliation of the syndrome of erythromelalgia. Median survival is approximately 10 years. As implied above, the causes of morbidity and mortality vary with the mode of chronic therapy which has been employed, leukemia being more common after myelosuppressive therapy and thrombotic complications being more common after therapy with phlebotomy alone. Ten percent to 50% of patients move into a spent phase followed by postpolycythemic myeloid metaplasia, irrespective of previous therapy employed. Eventually, the major problems may be cytopenias and massive splenomegaly.
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PMID:Polycythemia vera. 158 7

Seventeen haemodialysis patients with renal anaemia were treated with recombinant human erythropoietin (rhEPO) and observed for 30 weeks. The viscosity of whole blood and plasma, the erythrocyte aggregation tendency, and the erythrocyte deformability, measured as fluidity, were analysed every second week. All patients responded with increasing haematocrit and whole-blood viscosity. The plasma viscosity and the erythrocyte aggregation tendency were already increased before the start of treatment, and remained unchanged during treatment. The basal erythrocyte fluidity tended to be impaired, although not significantly so. During treatment, significant impairment of fluidity was observed at the beginning of the treatment period. After 24 weeks the fluidity started to increase, and it later reached values observed before the start of treatment. Hence, the quality of the erythrocytes formed during the corrective phase of rhEPO treatment differs in some respects from that of cells formed at a normal production rate. The impaired fluidity might have important implications for the flow resistance in small vessels, and contribute to the development or aggravation of hypertension that is often seen during rhEPO treatment.
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PMID:Impaired erythrocyte fluidity during treatment of renal anaemia with erythropoietin. 161 83

The hemodynamic hallmark of hypertension complicating the treatment of renal anemia with recombinant human erythropoietin (rHu-EPO) is increased total peripheral vascular resistance, but the mechanisms underlying the arteriolar vasoconstriction are still an enigma. We studied body fluid volumes, plasma renin activity, plasma norepinephrine, and calcium metabolism in platelets in 40 previously normotensive hemodialysis patients before and after 12 weeks of rHu-EPO treatment. Partial correction of anemia caused a rise in arterial pressure (94 +/- 6 mmHg vs 124 +/- 7 mmHg, p less than 0.05) and in platelet cytosolic calcium concentration (113 +/- 5 nM vs 171 +/- 18 nM, p less than 0.05) in eight patients. Hypertensive patients had significantly higher plasma noradrenaline concentrations, but they did not differ significantly in body fluid volumes and plasma renin activities. There was a close correlation between free calcium concentration in platelets and mean arterial pressure in patients developing rHu-EPO-induced-hypertension (r = 0.95). Short-term antihypertensive treatment resulted in a reduction of free calcium concentrations in platelets and a concomitant fall in blood pressure. The main results of the present studies suggest that rHu-EPO-induced hypertension might be associated with altered cellular calcium homeostasis and hyperactivity of the sympathetic nervous system. If rHu-EPO therapy induces alterations of pressor factors or the hormone itself raises the cytosolic calcium not only in platelets but also in vascular smooth muscle cells, altered cellular calcium influx may contribute to the arteriolar vasoconstriction.
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PMID:Correlation of blood pressure in end-stage renal disease with platelet cytosolic free calcium concentration during treatment of renal anemia with recombinant human erythropoietin. 163 25


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