Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a case of juxtaglomerular cell tumor, which excessively produced renin, resulting in secondary hypertension. A 25-year-old woman complained of headache and nausea. Hypertension and elevation of plasma renin activity were found by physical and laboratory examination. US and CT showed a space occupying lesion at upper pole of the right kidney. Angiography showed a hypovascular area at the corresponding area of the right kidney. Renin-secreting renal tumor of the right kidney was diagnosed and right nephrectomy was performed. Postoperatively, blood pressure and plasma renin activity became normalized and symptoms ameliorated. The juxtaglomerular cell tumor was pathologically confirmed and localization renin in the tumor cells was shown by immunohistochemical study. Forty one cases of juxtaglomerular cell tumor have been reported, since Robertson reported the first case. We discussed the clinical and pathological characteristics of the disease in this report.
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PMID:[Renin-secreting renal tumor. A case report]. 834 32

Hypertension in children is not a common problem. When it is found, however, a pathologic cause can often be identified. The endocrine causes of hypertension in children are generally rare. We have reviewed the diverse and rare endocrine causes of hypertension in the pediatric population. Table 3 lists features of these conditions that assist in their diagnosis. In all patients with hypertension, a thorough history and physical examination may point to the diagnosis of endocrine or other causes of secondary hypertension. For a more detailed approach to these diagnoses, other reviews may be helpful. A phased laboratory evaluation similar to that suggested by Ogborn and Crocker facilitates in the evaluation of secondary hypertension. The critical screening tests from an endocrine point of view are plasma sodium, potassium, calcium, renin activity, and thyroid function tests, including T4, T3, and thyroid stimulating hormone. Measurement of a 24-hour urine collection for aldosterone, metanephrine, and catecholamines may be warranted if the previously mentioned studies are unrevealing. More specific studies also may be suggested by these preliminary evaluations and the history and physical examination. Further investigations should be done with the additional guidance of a pediatric endocrinologist.
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PMID:Endocrine causes of hypertension in children. 841 3

A case of a 62-year old male with malignant hypertension was described. The clinical picture was dominated by the presence of cachexia, polyuria and polyneuropathy. Laboratory examinations revealed highly elevated sedimentation rate, hyponatremia and hypokalemia. Secondary hypertension as well as other diseases with similar clinical symptoms were excluded basing in diagnostic procedures. The authors discuss pathophysiological mechanisms on the base of abnormally elevated activity of the renin-angiotensin-aldosterone system. Unusual body weight loss (approximately 20 kgs), polyneuropathy and irreversible lesion of renal tubules without renal function impairment are emphasized.
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PMID:[A difficult diagnostic case of malignant hypertension]. 847 45

We have examined cardiovascular pressor responsiveness to infused norepinephrine (NE) as related to endogenous plasma NE and plasma renin and to platelet free cytosolic (Ca2+) in 36 patients with early-stage kidney disease and 27 matched normal subjects. The 27 hypertensive patients and the normal subjects did not differ in blood volume, plasma renin, and NE; however, the hypertensive patients had a higher exchangeable body sodium content. Basal plasma NE levels, the relationship between plasma NE measured during NE infusion and the corresponding NE infusion rate, as well as the total plasma clearance for NE did also not differ significantly between the two study groups. In contrast, the threshold or pressor doses of infused NE significantly decreased in the patients with kidney disease. Antihypertensive pharmacotherapy with (Ca2+) channel blockers and/or loop diuretics normalized blood pressure and cardiovascular NE hyperresponsiveness and reduced blood volume, exchangeable body sodium, and platelet free cytosolic (Ca2+). In contrast, experimental digitalisation as a model for in vivo sodium/potassium adenosine triphosphatase inhibition augmented NE responsiveness and raised platelet free cytosolic (Ca2+). Incubation of platelets from normal subjects with plasma ultrafiltrate from hypertensive patients gave evidence for an endogenous factor capable to raise free cytosolic (Ca2+) and to act synergistically with digoxin. Hypertension secondary to early-stage kidney disease is related to an impairment of sodium excretion leading to an expansion of blood volume and exchangeable body sodium. This may result in increased secretion of endogenous factors, leading to alterations of cytosolic (Ca2+) homeostasis of vascular smooth muscle cells followed by elevated peripheral resistance and thus blood pressure.
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PMID:Hypertension secondary to early-stage kidney disease: the pathogenetic role of altered cytosolic calcium (Ca2+) homeostasis of vascular smooth muscle cells. 849 19

A 13 year old girl with hypertension (170/140 mmHg), hyperkalemia (7.3 mmol/L), hyperchloremic metabolic acidosis and normal glomerular filtration rate (creatinine clearance 128 mL/min/1.73 m2), had low plasmatic renin activity (0.20 ng/mL/h), the levels of plasma aldosterone was low (5.5 ng/100mL) and very low transtubular potassium concentration gradient. Other forms of the secondary hypertension were discarded. The patient was treated with salt restriction, oral salbutamol and furosemide, with satisfactory evolution. At present her blood pressure is 130/85 mmHg and potassium, plasmatic levels of 5.3 mmol/L.
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PMID:[Gordon's syndrome. Report of a case]. 850 4

Hypertensive crisis is a medical emergency presenting with a severely increased blood pressure. The condition is associated with a state of increased vasoconstriction, coexisting hyponatriaemia and hypovolaemia. Besides the absolute level of blood pressure evidence of organ damage is also important in initial judgement of the case. Hypertensive crises are most commonly seen in younger patients with essential hypertension and in patients with secondary hypertension. It is unknown why a patient with hypertension suddenly develops a hypertensive crisis, but the renin-angiotension system seems to play an important role. Untreated, the disease will lead to irreversible end-organ damage. Hypertensive crises may be divided into "hypertensive emergencies" with evidence of severe new and/or progressive end-organ damage, requiring careful reduction of blood pressure within an hour, and "hypertensive urgencies" with no evidence of end-organ damage or complications where reduction of blood pressure to a safe level must be achieved within a few hours.
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PMID:[Hypertensive crises. 1. Pathogenesis and symptomatology]. 875 95

The objectives of this study were to assess relations between ACE gene I/D polymorphism, essential hypertension, plasma renin activity and aldosterone in white (European descent) and black (Afro-Caribbean descent) peoples. Measurements were carried out on a total of 320 subjects (210 white: 116 men, 94 women; 110 black: 65 men, 45 women); all were on their usual sodium intake; none was on anti-hypertensive therapy and none had secondary hypertension. Genomic DNA was isolated from blood cells and ACE I/D genotype was established using polymerase chain reaction. Plasma hormones were measured by radioimmunoassay and blood pressure (BP) with an ultrasound sphygmomanometer. All subjects were grouped into normotensive, borderline and hypertensive according to WHO guidelines. The distribution of the I/D genotype in the white people was approximately 1:2:1; by contrast, in the Afro-Caribbean people there was a significantly higher frequency of the D allele (chi 2P = 0.04). Within the white people there was no significant association between ACE genotype and high BP; however, within the black people there was a positive association between the frequency of the D allele and increasing BP ( chi 2 for trend P = 0.03). In either group, there were no associations between ACE I/D genotype and plasma renin activity and aldosterone suggesting that ACE genotype does not contribute to the expression of the circulating renin-angiotensin system. This study highlights differences in ACE I/D polymorphism between white and black peoples and suggests the possibility of racial differences in the association between ACE genotype and BP.
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PMID:Angiotensin converting enzyme gene I/D polymorphism, blood pressure and the renin-angiotensin system in Caucasian and Afro-Caribbean peoples. 864 88

To investigate the role of aldosterone and the renin-angiotensin system in cardiac structure, we performed echocardiography in patients with secondary hypertension. The relation between blood pressure or hormonal influences and left ventricular hypertrophy has not been well established in secondary hypertension. Sixteen patients with primary aldosteronism and 11 with unilateral renovascular hypertension who had completely normalized blood pressure after operation or percutaneous transluminal angioplasty were evaluated by echocardiography before and after surgery or other interventional treatment. Blood pressure was not statistically different between the groups before treatment and was normalized after treatment in both groups. Left ventricular hypertrophy was mild in both groups before treatment, and its degree was not statistically different between the groups. At the end of the follow-up period, all parameters of primary aldosteronism and left ventricular mass index in patients with unilateral renovascular hypertension were significantly reduced. In patients with primary aldosteronism, changes in end-diastolic left ventricular internal dimension correlated positively with changes in left ventricular mass index (r=.58,P<.01). In patients with unilateral renovascular hypertension, changes in mean blood pressure and left ventricular mass index were significantly correlated (r=.77,P<.01). The expanded plasma volume induced by an excess of aldosterone and high blood pressure may play an important role in the increase of left ventricular mass in primary aldosteronism. In unilateral renovascular hypertension, high blood pressure mainly contributes significantly to increased left ventricular mass. Therefore, different factors may modulate the development of left ventricular hypertrophy in patients with secondary hypertension.
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PMID:Comparison of changes in cardiac structure after treatment in secondary hypertension. 869 32

Understanding the pathophysiology, diagnosis, and management of renovascular hypertension (RVH) is of paramount importance due to the severity of hypertension (HT) and renal insufficiency (RI). Moreover, adequate treatment by surgery and/or endovascular intervention can improve HT and revert RI. The comprehension of the pathophysiology of RVH had its origin on the experiments of Goldblatt which led to the recognition of the renin dependent, volume dependent, and mixed types. A continuum seems to exist, from an acute phase, supported by the endocrine renin angiotensin aldosterone system, evolving towards a chronic phase sustained by the local renin angiotensin system. The involved vasoconstrictor and mitogenic mechanisms may contribute to the arterial remodeling. The most common forms of pathology, i.e. atherosclerosis, fibromuscular dysplasia (FD), and Takayasu's arteritis, and their natural history, are described. The prevalence of RVH, ranging from 0.2% to more than 25%, depending on the clinical situation, is evidenced. Clinical symptoms and signs and the most important diagnostic tests are pointed out: functional tests (captopril test, postcaptopril renography, scintigraphy, and renin determinations) and anatomical tests (intravenous digital angiography and intrarterial angiography). New imaging techniques are also referred. A diagnostic work-up based on the index of clinical suspicion is described. The therapeutic goal is the resolution of the two main problems of RVH: hypertension and ischemic nephropathy. Revascularization is becoming mandatory either by percutaneous transluminal angioplasty mostly for FD and atheromatous non-ostial stenoses, or by surgery, which is preferred for patients with ostial or peripheral stenoses, aneuryms, occlusions and concomitant aortic disease. A better knowledge of RVH allows, not only diagnosis and treatment of one of the most frequent types of secondary hypertension, but also the control of the resulting ischemic nephropathy.
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PMID:[Renovascular arterial hypertension. From physiopathology to therapy]. 870 4

Patients with secondary hypertension frequently display abnormal circadian blood pressure profiles, characterized by a failure to decrease blood pressure at night. The transgenic TGR(mRen-2)27 rat strain, developing fulminant hypertension after the mouse salivary Ren-2 renin gene has been integrated into its genome, provides a fundamental model of genetic hypertension. Because of an inverse circadian blood pressure profile and an unchanged rhythmic pattern of heart rate compared with the normotensive Sprague-Dawley (SPR) strain, it was proposed to serve as an animal model of genetic hypertension. It was the aim of the present study to investigate the circadian rhythmicity in renal function of the transgenic rat to determine whether hypertension and disturbed circadian blood pressure profile would affect kidney function. Urinary water, electrolyte, and protein excretion, as well as glomerular filtration rate and renal plasma flow, were determined in unrestrained freely moving transgenic hypertensive (TGR) and SPR normotensive control rats by collecting urine and arterial blood every 4 h. Significant and similar circadian rhythms were found in renal excretion and hemodynamics in both normotensive and hypertensive strains. Peaks occurred in the active dark period, whereas troughs were found in daytime for all parameters. However, it has to be pointed out that, although the circadian profiles were not grossly perturbed in hypertensive animals, some small differences between SPR and TGR strains did exist in renal function. These discrepancies were precisely related to acrophase, showing a slight phase delay, and also to relative amplitude in TGR. This study demonstrates that the inverted circadian blood pressure profile affected only slightly the circadian rhythms in kidney function in TGR compared with SPR. These findings support the notion that time-dependent changes in systemic blood flow may be of greater importance for circadian regulation of kidney function than systemic blood pressure.
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PMID:Circadian rhythms in renal function in hypertensive TGR(mRen-2)27 rats and their normotensive controls. 889 93


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