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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anaemia is a frequent complication of many diseases but the mechanisms that link reduced blood oxygen content to the long-term consequences of anaemia are incompletely understood. The maintenance of oxygen supply to the tissues during anaemia involves complex cardiovascular adaptations, including an increase in cardiac output, reduced peripheral resistance and increased oxygen extraction from haemoglobin (Hb). In addition, hypoxia-inducible factors are associated with the transcriptional activation of genes involved in adaptive mechanisms that increase oxygen delivery and provide alternative metabolic pathways. The complex pathophysiology of chronic kidney disease alters the adaptations to anaemia in uraemic patients. The increased cardiac output induced by anaemia is associated with left ventricular hypertrophy and cardiac disease in renal patients. Alterations in endothelial cell function, common in renal disease, may diminish endothelium-induced vasodilatation, increase the risk of atherosclerosis and impair angiogenesis. Many potential reasons for erythropoietin-induced hypertension in uraemic patients have been postulated, including increased blood viscosity as haematocrit rises, a reversal of hypoxic vasodilatation, increased blood volume that is not compensated by haemodialysis, ultrafiltration and impaired nitric oxide synthesis, preventing vascular relaxation in response to increased blood viscosity. In view of this impaired vascular reactivity, rapid increases in haematocrit should be avoided during epoetin treatment. As the interaction between anaemia and uraemia is very complex, it is not possible to derive the optimal Hb concentration for individual patients by using simple physiological or pathophysiological models and there is a need for good randomized controlled clinical trials to address this issue.
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PMID:Anaemia in end-stage renal disease: pathophysiological considerations. 1159 Feb 49

Several strategies are available to delay progression of renal disease and the development of associated co-morbidities. Hypertension is a strong independent risk factor for end-stage renal disease (ESRD) and there is consensus that blood pressure (BP) management is an important aspect of care in patients with chronic renal insufficiency (CRI). Clinical studies have shown that angiotensin-converting enzyme (ACE) inhibitors have renoprotective properties, independent of their antihypertensive effects, which can delay the onset of ESRD. Studies have also shown that intensive therapy of both type 1 and type 2 diabetes patients, to give near normal blood glucose concentrations, can reduce the incidence of progressive clinical proteinuria and may, therefore, protect against ESRD. Additionally, data are emerging that treatment of renal anaemia with epoetin can reduce mortality and delay the onset of dialysis in CRI patients, but these encouraging results need to be confirmed in large prospective studies. In conclusion, control of BP and hyperglycaemia, as well as use of ACE inhibitors and anaemia treatment, all have potential in delaying the progression of CRI or improving patient outcomes. If benefit is proven in future studies, these strategies will be most effective if implemented early in the course of CRI.
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PMID:The rationale for early management of chronic renal insufficiency. 1159 Feb 58

Three strategies can help delay chronic kidney disease (CKD) progression: early identification of patients, modification of risk factors, and implementation of the best interventions. Early identification of patients requires accurate screening tools. As serum creatinine is an unreliable marker of kidney dysfunction, clinicians should focus on the glomerular filtration rate or other markers of true kidney function. Clinicians should also be aware of other indicators of abnormal kidney function, such as anaemia, acidosis, and increases in parathyroid hormone level. Additionally, both clinicians and patients should be aware of the "non-modifiable" and "modifiable" risk factors for CKD. Non-modifiable risk factors include age, gender, race, diabetes, and genetic make-up, while modifiable risk factors include elevated blood pressure and blood glucose, proteinuria, anaemia, metabolic disturbances, and dyslipidaemia. Patients should be particularly aware of the risk factors common to both cardiac and kidney disease, such as hypertension, proteinuria, anaemia, and (possibly) dyslipidaemia and diabetes. A single centre study demonstrated that inclusion in a multidisciplinary CKD clinic programme produced the greatest increases in time to renal replacement therapy, haemoglobin levels, and epoetin treatment usage at initiation of dialysis in comparison with standard nephrology care or no care. Two years after starting dialysis, the number of deaths was lowest, and the number of patients who had received a transplant or were still on dialysis was highest, in the CKD clinic-treated group. These results confirm those of previous studies, which showed that timely referral to a multidisciplinary team for management prior to dialysis decreases the risk of adverse patient outcomes. This suggests that a multidisciplinary, collaborative, proactive approach increases the likelihood of early identification of CKD patients and risk factor modification. However, further evidence-based demonstrations of success are required, showing benefit to both patients and health care systems.
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PMID:Identification of patients and risk factors in chronic kidney disease--evaluating risk factors and therapeutic strategies. 1159 Feb 59

After the synthesis of epoetins alpha and -beta, a third molecule of recombinant human erythropoietin (rHuEPO) was synthesized and was named epoetin-omega. The molecule of epoetin-omega is a sialoglycoprotein with smaller amounts of O-bound sugars, less acidic and with different hydrophylity than the other 2 epoetins. The purpose of the study was to assess the efficacy, safety and clinical tolerance of epoetin-omega for treatment of renal anemia. In an open-label, uncontrolled prospective clinical study, 22 end-stage renal disease patients (9 male and 13 female) were followed for 6 months. They all had a hemoglobin (Hb) value below 85 g/l, and were on regular hemodialysis therapy 3 times a week, 4 hours per session. The initial weekly dose of epoetin-omega was 90 units per kg of body weight (b.w.) divided in 3 equal portions and administered subcutaneously after each dialysis session. After correction of the hemoglobin, the dose of rHuEPO was individualized to keep Hb within target limits of 100-120 g/l. To follow efficacy and safety, a number of clinical and laboratory parameters were monitored. All patients responded well to the therapy with corrected hemoglobin after the 10th week of the study. The mean dose of epoetin-omega during the correction period never exceeded 100 U/kg b.w. per week. The average maintenance dose of rHuEPO was 50-60 U/kg b.w. per week. Iron was, where needed, supplied intravenously. We noted no change in serum urea. creatinine, phosphorus, and heparin dose per dialysis session. The prothrombin time improved during the study. Serum albumin increased. No change was observed in urea reduction ratio (URR), body weight and mean arterial pressure. One serious adverse event was noted: worsening of hypertension in 1 patient, with the development of hypertensive encephalopathy and severe headache. rHuEPO treatment was stopped. The blood pressure was effectively controlled by reducting her body weight by 5%. Thereafter, rHuEPO therapy was resumed with good blood pressure control. We could conclude that recombinant human erythropoietin-omega was an efficient and safe therapeutic agent for the treatment of renal anemia.
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PMID:Epoetin omega for treatment of anemia in maintenance hemodialysis patients. 1192 56

The major function of the erythrocyte is to transport oxygen from the lungs to the other tissues, a function ensured by the glycoprotein hormone erythropoietin which couples red cell production to long term tissue oxygen requirements. Tissue hypoxia is the only physiological mechanism for increasing erythropoietin production but there are a variety of mechanisms for its down regulation including hyperoxia, increased catabolism by an expanded erythroid progenitor cell pool, blood hyperviscosity independently of its oxygen content, renal disease and the cytokines produced in inflammatory, infectious and neoplastic disorders. Erythropoietin lack results in severe and often transfusion-dependent anemia but if bone marrow function is otherwise normal, recombinant human erythropoietin therapy can restore the red cell mass and alleviate the transfusion need. However, elevation of the red cell mass by recombinant human erythropoietin is associated with a reduction in plasma volume and in some patients, hypertension is induced. Elevation of the red cell mass is also associated with a reduction in cerebral blood flow. When used to gradually elevate the hematocrit to 36% in anemic patients, recombinant human erythropoietin therapy is usually uneventful. However, when the normal hematocrit level is exceeded, the risk for thrombotic events increases since blood viscosity varies exponentially with the hematocrit. Increasing the hematocrit by autologous blood transfusions can enhance athletic performance in fit individuals and recombinant human erythropoietin administration is an obvious surrogate for autologous blood transfusions. However, paradoxically, its effects are the opposite of those of endurance training, namely a change in red cell mass without an increase in the total blood volume. Thus, the use of recombinant human erythropoietin as a performance-enhancing agent is dangerous, particularly in the less fit athlete, and probably of little benefit in the highly conditioned one. Differences in the carbohydrate content of native and recombinant human erythropoietin are identifiable by isoelectric focusing, providing a direct means for detecting erythropoietin abuse using urine specimens; a panel of surrogate blood markers of enhanced erythropoiesis such as soluble transferrin receptors, serum erythropoietin, reticulocyte hematocrit and percent macrocytes provide an indirect means for this purpose. Timing of surveillance is, of course, critical due to biological limitations on the physical presence of the hormone. However, education about its dangers may prove to be the most valuable solution to abuse of recombinant human erythropoietin for competitive advantage.
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PMID:Erythropoietin use and abuse: When physiology and pharmacology collide. 1195 Jan 39

(1) The standard treatment for symptomatic anaemia due to cytotoxic chemotherapy is blood transfusion. (2) The licensing terms for epoetin alfa have been extended to cover the treatment of anaemia induced by all cytotoxic drugs, no longer only by platinum salts. The licensing terms for epoetin beta have been extended to cover some haematological malignancies. (3) The clinical file on epoetin alfa contains data from 8 placebo-controlled double-blind trials in patients with anaemia. Four trials showed a significant reduction (of 12-35%) in the number of patients transfused during the second and third months of treatment with epoetin alfa. (4) Quality of life was mentioned in only two trial reports. In one, the score was significantly better on epoetin alfa than on placebo, but the practical repercussions of this difference are unclear. In the other trial there was no significant difference between the groups. (5) The clinical file on epoetin beta contains data only from unblended dose-finding studies showing a favourable impact on the haemoglobin level and transfusion requirements. (6) The preventive effect of the two epoetins has not been compared with that of alternative treatments. (7) The main known risks of epoetin are arterial hypertension and thrombosis. Stimulation of tumour growth cannot be ruled out. (8) Epoetin beta has a practical advantage, in that it can be stored for a few days at room temperature. (9) In practice, epoetin is the standard treatment of anaemia after chemotherapy, outside emergency situations.
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PMID:Epoetin alfa and epoetin beta: new indication. Treatment of anaemia due to cytotoxic chemotherapy. 1198 10

Secondary hypertension is elevated blood pressure that results from an underlying, identifiable, often correctable cause. Only about 5 to 10 percent of hypertension cases are thought to result from secondary causes. The ABCDE mnemonic can be used to help determine a secondary cause of hypertension: Accuracy of diagnosis, obstructive sleep Apnea, Aldosteronism, presence of renal artery Bruits (suggesting renal artery stenosis), renal parenchymal disease (Bad kidneys), excess Catecholamines, Coarctation of the aorta, Cushing's syndrome, Drugs, Diet, excess Erythropoietin, and Endocrine disorders. An algorithm showing the general strategy to help screen for factors involved in secondary hypertension is presented. Routine urinalysis, complete blood cell count, blood chemistry profile (potassium, sodium, creatinine, fasting glucose, fasting lipid levels), and a 12-lead electrocardiogram are recommended for all patients with hypertension.
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PMID:Diagnosing secondary hypertension. 1288 12

It was hypothesized that subjects with metabolic syndrome (hypertension, obesity, hyperlipidemia, diabetes mellitus): (1) develop measurable peripheral edema at moderate altitude and (2) might show differences on erythropoiesis, iron status and vascular endothelial growth factor (VEGF) in comparison to healthy subjects during and after a long-term stay (3-week exposure) at moderate altitude (congruent with 1700 m). Twenty-two male subjects with metabolic syndrome were selected. Baseline investigations (t1) were performed in Innsbruck (500 m). All participants were transferred by bus to 1700 m (Alps) and remained there for 3 weeks with examinations on day 1 (after the first night at altitude, t2), day 4 (t3), day 9 (t4) and day 19 (t5). After returning to Innsbruck, post-altitude examinations were conducted after 7-10 days (t6) and 6-7 weeks (t7), respectively. Body mass was decreased from t1 to t7 (P<0.01). Total body water was decreased at t2 (P<0.01), returned to control level (t3, t4), and was found elevated at t7 (P<0.01). Lean body mass did not change, but body fat decreased during the study (P<0.01). Tissue thickness at the forehead decreased during and after altitude exposure (P<0.01), whereas tissue thickness at the tibia did not alter. Erythropoietin (EPO) was elevated as early as t2 and remained increased until t5. Reticulocyte count was increased at t3 and remained above pre-altitude values. VEGF levels were unchanged. After a 3-week exposure to moderate altitude, patients with metabolic syndrome had reduced their body mass, mainly because of a reduction in body fat. The moderate altitude was found to stimulate erythropoiesis in these patients but this was not sufficient to increase serum VEGF concentration.
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PMID:Austrian Moderate Altitude Study (AMAS 2000) - fluid shifts, erythropoiesis, and angiogenesis in patients with metabolic syndrome at moderate altitude (congruent with 1700 m). 1256 Sep 47

Hypertension is a potentially dangerous side effect of erythropoietin treatment; however, extreme elevations in blood pressure are rare. A 75-year-old woman with chronic renal insufficiency was treated with subcutaneous erythropoietin. Three weeks before she started receiving erythropoietin, her hematocrit was 27.2%; after 5 weeks of treatment, it rose to 45.7%. The patient came to the emergency department and was admitted with hypertensive urgency. During her hospital stay she was treated with nitroglycerin and nitroprusside infusions, extended-release nifedipine, a variety of beta-blockers, clonidine, and furosemide. By day 3, her blood pressure was adequately controlled. Her renal insufficiency may have progressed as a result of the hypertensive episode, which probably was related to erythropoietin administration and the resultant rapid increase in her hematocrit. Erythropoietin dosing should be titrated to increase the hematocrit gradually, and blood pressure should be monitored closely to avoid serious side effects such as hypertensive emergencies.
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PMID:Erythropoietin-induced hypertensive urgency in a patient with chronic renal insufficiency: case report and review of the literature. 1258 17

Chronic kidney disease (CKD) affects over 6.2 million people in the U.S. and most commonly results from diabetes and/or hypertension. Patients with CKD have an increased risk of anemia and hypertension. Anemia occurs early in CKD and can be effectively treated with epoetin alfa. Hypertension can be managed with lifestyle modifications and medications. Nurses play a vital role in managing these patients by providing early CKD/anemia screening and intervention, education, patient monitoring, and support for patients and caregivers.
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PMID:Advancing chronic kidney disease care: new imperatives for recognition and intervention. 1259 4


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