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)

The investigation of elderly patients presenting with raised PCV values has been described. Suitable clinical and laboratory investigation enables the separation of those with a raised red cell mass (RCM) into three groups: primary proliferative polycythaemia (PPP), secondary polycythaemia and idiopathic erythrocytosis. Those patients with a raised PCV but normal RCM either have apparent polycythaemia (normal plasma volume) or relative polycythaemia (low plasma volume). PPP is a clonal disorder with a peak incidence in the elderly. It commonly presents with vascular occlusive symptoms/signs involving larger vessels, both arterial and venous. The microvasculature may also be involved, particularly when there is associated thrombocythaemia. Effective treatment is required to minimize the future vascular occlusive incidence and diminish the complication rate of surgery if it is ever required. Both the PCV and the platelet count, if elevated, should be adequately controlled. 32P is probably the simplest treatment and is very effective, but venesection and intermittent low-dose busulphan is equally satisfactory in the co-operative patient with good peripheral veins. Secondary polycythaemia may arise from a variety of causes, particularly from arterial hypoxaemia and renal lesions. Occasionally, more than one pathology is identified in the elderly patient. Lung disease is the most common cause of hypoxaemia. Venesection may be indicated in those patients with excessively raised PCV values. The term idiopathic erythrocytosis should only be used for patients who have been adequately investigated. These patients most commonly present with ischaemic or vascular occlusive symptoms/signs. Relative polycythaemia may be caused by fluid loss, but generally the origin of the low plasma volume is not established. Apparent polycythaemia may represent a physiological variant or a stage before the development of a definitely raised RCM. The management of idiopathic erythrocytosis, and relative and apparent polycythaemia, should initially involved removal of known risk factors if present (e.g. hypertension) with the addition of venesection in selected patients. Reactive thrombocytosis in the elderly is most commonly due to malignant disease of chronic infection. The high platelet count is usually asymptomatic, and antiplatelet therapy is rarely required. Primary thrombocythaemia (PT) is a clonal myeloproliferative disorder similar to PPP. The finding of splenomegaly, abnormal platelet morphology or function helps to separate PT from reactive thrombosis. PT most commonly presents with digital or transient cerebral ischaemia or haemorrhage.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Polycythaemia and thrombocythaemia in the elderly. 332 42

An autosomal erythrocytosis, inherited as a dominant, occurred in seven members of a family. The propositus was first diagnosed as having erythrocytosis at 26 years of age. He had headaches and marked plethora. Polycythaemia vera and secondary erythrocytosis of known cause were excluded. Erythropoietin level was not elevated. Two of his three children were also found to have erythrocytosis. As in this family, the disease is characterized in middle age by hypertension, cardiovascular and thromboembolic phenomena, as well as abnormal bleeding. For over eight years the propositus has been successfully treated with repeated venous blood lettings.
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PMID:[Idiopathic familial erythrocytosis. Report on a family with autosomal dominant inheritance]. 337 Dec 13

For some unknown reason, the blood hematocrit will become elevated 50 percent or more in some cases of renal disease where hypertension is a factor. In the absence of other identifiable causes of erythrocytosis, this is believed to result from the formation of erythropoietin stimulating factor (ESF) by the kidney in response to some intrarenal hypoxic stimulus. In this study it could be demonstrated with the help of computer simulations, that the hypertension was caused by excess fluid being retained by the kidneys, whereas, the elevated hematocrit could only be attributed to primary increase in the resistance to blood flow. This suggests that the high hematocrit levels that have been reported probably could not have occurred, except for powerful excess vasoconstrictor activity affecting the whole circulation.
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PMID:Renal disease and hypertension: the erythrocytosis factor. 363 62

It is generally maintained that the variety of endocrine disorders which occur in uraemia and persist in dialysis (above all hormones whose production and/or metabolic clearance are pertinent functions of the kidney) usually abate after successful renal transplantation. However, a retrospective analysis of long-term results in 71 out of 275 cases serially studied by regular checks, indicates that this event occurs in no more than 2/3 of successfully transplanted patients. In the other patients various endocrine abnormalities may be documented: some seem apparently 'inherited' from uraemia (hyperparathyroidism, sexual dysfunction, growth retardation); some are mainly related to steroids (hyperinsulinism), and some have a de novo origin (erythrocytosis, reno-vascular hypertension). These endocrine abnormalities may occur with a normal or reduced graft function, have a baseline or stimulated expression, a clinical or subclinical course, and a reversible or irreversible outcome. A proper grasp of these events in renal transplantation is of clinical significance particularly for the long-term patient and graft prognosis.
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PMID:Hormonal abnormalities in renal transplantation. 391 11

Rats with spontaneous hypertension versus normotensive rats showed the development of erythrocytosis, an intensification of the erythropoietic properties of the blood plasma and an increase of the 2,3-DPG concentration in the red blood cells. An enhanced production of erythropoietin, a humoral stimulator of erythropoiesis, seems to be one of the causes of the erythrocytosis development in spontaneously hypertensive rats. An increase in the 2,3-DPG concentration in the erythrocytes is an important physiological mechanism ensuring the appropriate oxygen supply to tissues.
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PMID:[Mechanism of development of erythrocytosis in spontaneous arterial hypertension in rats]. 404 18

During the study of an inbred strain of Wistar rats which spontaneously develop hypertension when they reach a weight of approximately 150 g, it was found that these animals also develop an erythrocytosis. A significant increase in red cell count was observed in spontaneously hypertensive (SH) rats (8-11 x 10(6) RBC/mm(3)) when compared with normotensive rats (6-7 x 10(6) RBC/mm(3)) of the same strain. This increase in red cell count paralleled the increase in body weight and the rise in blood pressure. Since the plasma volume, as measured with labeled albumin was normal, there was an absolute increase in red cells. The hematocrit and hemoglobin content of the blood measured in SH rats were only slightly greater than those found in normotensive rats. However, the mean cell volume (MCV) of the red cells in the SH rats was 45-47 mu(3) as compared with 51-53 mu(3) in normotensive rats.A fourfold increase in 24 hr (59)Fe incorporation into the red cells was found in the SH rats when compared with normotensive controls. The bone marrow of the SH rats showed erythroid hyperplasia. When the SH rats were treated with alpha-methyldopa (Aldomet 200 mg/kg daily, i.p.) the red cell count fell in parallel with the drop in blood pressure. No change in red cell count or blood pressure was observed in normotensive rats treated in the same manner. The erythropoietin titer was high in SH rats, and was undetectable in normotensive rats. These observations suggest a direct relationship between the hypertension and the erythrocytosis mediated by erythropoietin; both are genetically controlled.
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PMID:Erythrocytosis in spontaneously hypertensive rats. 501 Nov 7

Widespread arteriosclerotic lesions were detected by histological examinations of rats killed at seven or nine weeks after an intrarenal (ir) injection of nickel subsulfide (Ni3S2, 5 mg per rat). Arteriosclerotic plaques were readily visualized by administering hematoporphyrin derivative (HPD) iv to rats at 24 hours before sacrifice. At necropsy, the major arteries were inspected under ultraviolet light, revealing patches of intense HPD-fluorescence in the arterial endothelium of Ni3S2-treated rats, but not in control rats. Consistent with previous reports, the Ni3S2-treated rats developed pronounced erythrocytosis; blood hematocrit values averaged 70 +/- 4 percent at seven weeks after ir injection of Ni3S2 (P less than 0.001 vs corresponding value of 49 +/- 2 percent in vehicle controls). At seven weeks, blood platelet counts averaged 17 percent lower and serum glucose concentrations averaged 23 percent lower in Ni3S2-treated rats than in controls; serum lipids, lipoproteins, non-protein nitrogen constituents, electrolytes, proteins, and enzymes were not significantly affected. Body weights and systolic blood pressures of rats at two, four, and six weeks after ir injection of Ni3S2 did not differ from corresponding values in controls. Addition of egg yolk to the diet caused mild hypercholesterolemia, but it did not enhance the incidence or severity of arterial lesions in Ni3S2-treated rats. These findings exclude hypertension and hyperlipidemia as pathogenic factors in Ni3S2-induced arteriosclerosis.
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PMID:Studies of the pathogenesis of arteriosclerosis induced in rats by intrarenal injection of a carcinogen, nickel subsulfide. 623 39

Review of a large renal transplant experience revealed a 17.3% incidence of posttransplant erythrocytosis. The influence of kidney source, pretransplant hematocrit, duration of pretransplant dialysis, renal transplant function, acute rejection, transplant renal artery stenosis, urinary tract obstruction, smoking, diabetes, retention of native kidneys, splenectomy, parathyroidectomy, immunosuppression, hypertension, and liver enzyme abnormalities on the development of erythrocytosis in 53 recipients was determined. Comparison was made with 49 control recipients matched for kidney function, time after grafting, age, and sex. Erythrocytosis occurred 3 to 90 months after transplantation and persisted for 1 to over 84 months. Risk factors for the development of erythrocytosis were smoking, diabetes, and a rejection free course. In contradistinction to previous smaller series, erythrocytosis occurred in patients with good renal function (serum creatinine 1.62 +/- 0.43 mg/dl) without prominence of graft rejection, transplant artery stenosis or obstruction. Despite therapeutic phlebotomy, 11 thromboembolic events occurred in 10 of the 53 patients with erythrocytosis, but in none of the controls (P less than 0.001). The high incidence of erythrocytosis following renal transplantation and the risk of associated thromboembolic events should encourage awareness and controlled evaluation of therapeutic modalities.
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PMID:Postrenal transplant erythrocytosis: a review of 53 patients. 634 69

Twenty-five patients underwent bilateral native nephrectomy one to 68 months (mean, 15.6 months) following renal transplantation. The indications were erythrocytosis in two patients, recurrent urinary tract infection in three, medically uncontrolled hypertension in 18, and hypertension and urinary tract infection in two. One patient died two months after the nephrectomy, and one allograft was lost because of acute tubular necrosis. Both patients with erythrocytosis had prompt return of the hematocrit level and RBC mass to normal. Native nephrectomy eradicated the infection in each of the five patients with recurrent urinary tract infections. Results of nephrectomy for hypertension were classified as excellent in six patients, good in nine, and poor in four. Native renal-vein renin ratios of patients with excellent or good responses were not statistically different when compared with those of poor responders.
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PMID:Selective posttransplantation bilateral native nephrectomy. Indications and results. 635 7

We present here results of studies on four patients (three men, one woman) who had had cadaver renal transplants and in whom renal artery stenosis and hypertension developed. Erythropoietin-dependent erythrocytosis developed in association with these changes in the three men. All patients had stable renal function and the hypertension was well controlled. Absolute erythrocytosis thought to be secondary to local renal hypoxia due to decreased renal blood flow developed in two of the men. Erythrocytosis developed in the other man but his RBC mass was at the upper limit of normal. In these patients, we suspect that the erythropoietin-dependent erythrocytosis is secondary to intrarenal hypoxia due to renal artery stenosis. Erythrocytosis or elevated erythropoietin levels failed to develop in the woman despite severe renal artery stenosis. Possible reasons for this discrepancy are discussed.
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PMID:Renal artery stenosis with erythrocytosis after renal transplantation. 699 30


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