Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal artery stenosis (RAS) may cause hypertension, azotemia, episodes of flash pulmonary edema and congestive heart failure. Renal artery angioplasty and stenting was performed in 207 patients from 1991 to 1997. Thirty-nine of these patients (19%) underwent renal artery stenting for the control of recurrent episodes of congestive heart failure and flash pulmonary edema. All patients had angiographic evidence of severe (>70%) bilateral RAS (n = 18) or severe RAS to a solitary functioning kidney (n = 21). Sixteen patients (41%) were male and 23 (59%) were female, mean age 69.9 years (range 50-85 years). Of the 18 patients with bilateral RAS, 12 (66.6%) underwent bilateral stenting. Mean blood pressure decreased from 174/85 +/- 32/23 mmHg to 148/72 +/- 24/14 mmHg (p < 0.001). Mean number of blood pressure medications decreased from 3 +/- 1 to 2.5 +/- 1 (p = 0.006). Twenty-eight patients (71.8%) had improvement in blood pressure control. The mean serum creatinine decreased from 3.16 +/- 1.61 to 2.65 +/- 1.87 (p = 0.06). Six of 39 patients (15.4%) used angiotensin converting enzyme (ACE) inhibitors prior to stenting whereas 19 of 39 patients (48.7%) used ACE inhibitors poststenting (p = 0.004). Twenty of 39 patients (51.4%) demonstrated improvement in serum creatinine, 10 of 39 patients (25.6%) had stabilization of serum creatinine and nine of 39 patients (23%) demonstrated worsening. The number of hospitalizations due to congestive heart failure in the year preceding renal artery stenting was 2.4 +/- 1.4 and poststenting was 0.3 +/- 0.7 (p < 0.001). The New York Heart Association Functional Class decreased from 2.9 +/- 0.9 prestenting to 1.6 +/- 0.9 poststenting (p < 0.001). Thirty of 39 patients (77%) had no hospitalizations for congestive heart failure during a mean follow-up period of 21.3 months. Nine patients expired during the course of follow up; eight of the nine patients died within the first year after renal artery stenting. Renal artery stenting decreased the frequency of congestive heart failure, flash pulmonary edema, and the need for hospitalization in most patients. Blood pressure was markedly improved in the majority of patients with improved or stabilized renal function. Evaluation for RAS is important in hypertensive patients who present with recurrent congestive heart failure or flash pulmonary edema.
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PMID:Clinical benefit of renal artery angioplasty with stenting for the control of recurrent and refractory congestive heart failure. 1271 Aug 43

High-altitude pulmonary oedema (HAPE) is a potentially fatal condition affecting fit and previously well individuals at altitudes in excess of 3000 m. This article discusses the mechanisms of HAPE, considers the contribution of hypoxic pulmonary vasoconstriction and alterations in sodium transport to the pathological process. It discusses the various biochemical mediators such as nitric oxide (NO), endothelin-1 (ET-1), and the renin-angiotensin-aldosterone system (RAS) that may be involved and considers possible oxygen-sensing mechanisms involved in hypoxic adaptation such as hypoxia-inducible factor-1 (HIF-1). Those who have had HAPE once run an unpredictable but significant risk of recurrence; therefore, there may be a constitutional or genetic component in its aetiology. This paper considers the possible involvement of genes that may be involved in physiological adaptation to hypoxia (e.g., angiotensin-1 [AT(1)]-converting enzyme [ACE], tyrosine hydroxylase, serotonin transporter [5-HTT], and endothelial NO synthase [eNOS] genes). As yet, no formal association has been identified between an identified genetic polymorphism and HAPE, but genetic variation provides a possible mechanism to explain interindividual variation in response to hypoxia and enhanced or reduced performance at altitude.
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PMID:The genetic basis of high-altitude pulmonary oedema. 1476 4

Essential hypertension accounts for 95% of all cases of hypertension. A small number of patients (between 2% and 5%) have a reversible disease as the cause for raised blood pressure. Unilateral and bilateral renal artery stenosis may be responsible for secondary hypertension. Diagnosis and treatment of renal artery stenosis are of a great importance. Revascularization of ischemic kidney may correct blood pressure control and preserve renal function. Much data suggest close pathophysiological relation between renal artery stenosis, ischemic nephropathy and development of hypertension. However, it should be stressed that not every renal artery stenosis leads to hypertension and ischemic nephropathy. Therefore diagnosis of renal artery stenosis in hypertensive patient is not always equivalent with renovascular hypertension. The true prevalence of renal artery stenosis is unknown. In unselected population it accounts for less than 1% of hypertensive patients. Renovascular etiology of hypertension may be suggested by abrupt onset of hypertension, resistant and malignant hypertension or recurrent pulmonary edema of unknown etiology. Physical examination may reveal bruits over major vessels, including the abdominal aorta and renal arteries. The principle aim of the renal artery stenosis investigation is to confirm presence and size of vessel obstruction and its association with hypertension. Typical evaluation is based on imaging techniques and physiological studies. Former include: doppler duplex ultrasonography, conventional angiography, intraarterial and intravenous digital subtraction angiography, computed axial tomography, magnetic resonance angiography and intravascular ultrasonography. Functional studies are occasionally used. These are renal scintigraphy, evaluation of plasma renin activity in renal veins and evaluation of plasma rennin activity after ACE inhibition. Treatment of patients with renal artery stenosis and hypertension should restore vessel patency and inhibit its occlusion. Revascularization should elicit an improvement in or normalization of blood pressure control and renal function. Therapeutic approach include percutaneous renal artery angioplasty (PTRA), with or without stenting, revascularization by surgery and pharmacotherapy. PTRA is currently the first choice option. In general, it is simpler and similarly effective as surgical reconstruction. In some cases PTRA is completed with stent placement. It prevents immediate recoil but does not completely eliminate restenosis of revascularized artery. Surgical bypass is currently reserved for patients in whom PTRA and stenting fail and in patients with extensive atherosclerotic lesions. Patients with renal artery stenosis and hypertension should be provided with pharmacological treatment according to current recommendations. Specific procedures to limit associated risk factors of atherosclerosis should also be introduced.
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PMID:[Renovascular hypertension: is it only the top of the iceberg?]. 1497 69

An acute respiratory insufficiency as a result of pulmonary oedema is regarded as a life threatening emergency event. Diagnostic classification differentiates between cardiogenic and non-cardiogenic lung oedema. Symptomatic treatment of the impaired gas exchange often precedes a causal therapy of the underlying disease. For this purpose non-invasive ventilation, in parallel with efficient medical interventions, has come into focus. Moreover, this therapeutic intervention can prevent from the necessity of endotracheal intubation in the majority of cases. Rapid restoration of arterial oxygenation along with medical support of the cardiac function (i.e. by nitrates, diuretics, ACE-inhibitors, etc.) results in improved myocardial oxygen-delivery and reduced oxygen-consumption. This article reviews mainly the pathophysiology of cardiogenic lung edema, while most of the currently discussed therapeutic implications also apply to other entities of lung edema.
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PMID:[Pulmonary edema]. 1505 5

This article provides information and a commentary on trials relevant to the pathophysiology, prevention and treatment of heart failure, presented at the European Society of Cardiology Congress 2007. Unpublished reports should be considered as preliminary data, as analyses may change in the final publication. In the 3CPO study, non-invasive ventilation produced a more rapid resolution of symptoms in patients hospitalised with acute cardiogenic pulmonary oedema; but had no effect on survival, compared to standard oxygen therapy. The ALOFT study showed that the selective oral renin inhibitor aliskiren reduces plasma BNP levels and is well tolerated in patients with heart failure receiving ACE inhibitors or ARBs, although the study was not powered to show clinical benefit. In the PROSPECT study, no echocardiographic measure of mechanical dyssynchrony was identified that was useful for identifying patients more or less likely to respond to CRT. Low dose atorvastatin reduced the incidence of sudden cardiac death in a small placebo controlled study of patients with advanced chronic heart failure.
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PMID:Clinical trials update from the European Society of Cardiology Congress 2007: 3CPO, ALOFT, PROSPECT and statins for heart failure. 1789 Jan 52

The pathogenesis of high-altitude pulmonary edema (HAPE) has been at least partially attributed to the local dysregulation of the renin-angiotensin-aldosterone system (RAAS) cascade. To address this issue, we conducted the largest nested case-control study to-date to explore the association between variations in RAAS genes and HAPE in Chinese population. We recruited 140 HAPE patients and 144 controls during the construction of Qinghai-Tibet railway and genotyped 10 gene polymorphisms evenly interspersed in 5 RAAS candidate genes. The data were analyzed by haplotype and multifactor dimensionality reduction (MDR). The single-locus analysis showed that CYP11B2 C-344T and K173R and ACE A-240T polymorphisms were significantly associated with HAPE after Bonferroni correction (P<0.005). The linkage analysis constructed a linkage block including C-344T and K173R polymorphisms in complete linkage disequilibrium with each other, while occurred with significantly different frequencies between HAPE and control groups. The gene-gene interaction analysis found the overall best model including ACE A-240T and A2350G and CYP11B2 C-344T polymorphisms with strong synergistic effect. This model had a maximum testing accuracy of 68.61% and a maximum cross validation consistency of 9 out of 10 (P=0.004). The homozygous genotype combination of -240AA, 2350GG and -344TT conferred high genetic susceptibility to HAPE, which was further strengthened by haplotype analysis. Our results add evidence for synergistic effect of RAAS gene polymorphisms on HAPE susceptibility. Moreover, we proposed a promising data-mining analytical approach (MDR) for detecting and characterizing gene-gene interactions.
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PMID:Synergistic effect of the genetic polymorphisms of the renin-angiotensin-aldosterone system on high-altitude pulmonary edema: a study from Qinghai-Tibet altitude. 1798 91

Diagnosis of renal artery stenosis (RAS) should be discussed in numerous clinical situations including refractory high blood pressure (HBP), HBP in a polyvascular patient, degradation of renal function following renin angiotensin inhibitor or flash pulmonary edema. Ultrasound-doppler coupled with gadolinium-enhanced MR or CT angiography has proven adequate for most patients with RAS. Digital subtraction angiography should be limited to revascularisation procedures. Functional testing are not sensitive or specific enough because the degree of renin activation differs widely among patients with RAS. Renal percutaneous angioplasty induces a light to moderate decrease in blood pressure, has no effect on renal function but allows to reduce the number of anti-hypertensive drugs. Stenting completed angioplasty is worthwhile in most patients with atherosclerotic RAS. ACE inhibitors decrease mortality and increase renal function in patients with RAS.
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PMID:[Why screening for a renal artery stenosis?]. 1803 19

Oxidative stress (OS) is a keystone in the pathology of the ischemia reperfusion sequence (acute coronary syndromes, cardiac surgery, transplantation). In heart failure, the implication of OS is less understood. This study was intended to evaluate OS in acute heart failure. Criteria for inclusion were consecutive patients hospitalized in our cardiology department for a first pulmonary edema that revealed a dilated cardiomyopathy (DCM). Exclusion criteria included known cardiomyopathy, smoker, acute coronary syndrome, and treatment with angiotensin converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARAII). OS was evaluated in blood samples: thiobarbituric acid-reactive substances (TBARS), total antioxidant status (TAS), plasma alpha-tocopherol, vitamin A, and beta-carotene. Standard biochemical parameters including CRP, fibrinogen, lipid, and creatinine were assayed. Ten patients (80% men, mean age 55.3 +/- 7.9 years) were included and followed during a 6 month period. The etiologies of DCM were alcohol (n = 3), anti-cancer drugs (n = 2), valvulopathies (n = 2), or idiopathic (n = 3). In acute heart failure, TBARS were elevated (1.69 micromol/L; normal value 0.6-4.2 micromol/L) and TAS status was decreased (0.96 mmol/L; normal value 1.3-1.9 pmol/L). OS was more important when patients had atrial or ventricular arrhythmia. Nevertheless, liposoluble antioxidant parameters (beta-carotene, vitamin A, alpha-tocopherol) had a usual value. At the term of the follow-up, patients returned to a stable condition, OS markers revealed normal values, and every Holter ECG showed no supraventricular or ventricular arrhythmias. In acute heart failure, oxygen-free radicals are increased. We thus hypothetized that a modification in OS could be responsible for arrhythmias and complications of acute heart failure.
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PMID:Oxidative stress in patients with acute heart failure. 1839 53

Numerous anatomical and functional changes occurring in the aging kidney lead to reduced glomerular filtration rate, lower renal blood flow and impaired renal autoregulation. The elderly are especially vulnerable to the development of renal dysfunction and in this population acute renal failure (ARF) is a common problem. ARF is often iatrogenic and multifactorial; common iatrogenic combinations include pre-existing renal dysfunction and exposure to nephrotoxins such as radiocontrast agents or aminoglycosides, use of NSAIDs in patients with congestive cardiac failure and use of ACE inhibitors and diuretics in patients with underlying atherosclerotic renal artery stenosis. The aetiology of ARF is classically grouped into three categories: prerenal, intrinsic and postrenal. Prerenal ARF is the second most common cause of ARF in the elderly, accounting for nearly one-third of all hospitalized cases. Common causes can be grouped into true volume depletion (e.g. decreased fluid intake), decreased effective blood volume (e.g. systemic vasodilation) and haemodynamic (e.g. renal artery stenosis, NSAID use). Acute tubular necrosis (ATN) is the most common cause of intrinsic ARF and is responsible for over 50% of ARF in hospitalized patients, and up to 76% of cases in patients in intensive care units. ATN usually occurs after an acute ischaemic or toxic event. The pathogenesis of ATN involves an interplay of processes that include endothelial injury, microvascular flow disruption, tubular hypoxia, dysfunction and apoptosis, tubular obstruction and trans-tubular back-leak. Vasculitis causing ARF should not be missed as this condition is potentially life threatening. The likelihood of a postrenal cause for ARF increases with age. Benign prostatic hypertrophy, prostatic carcinoma and pelvic malignancies are all important causes. Early identification of ARF secondary to obstruction with renal imaging is essential, and complete or partial renal recovery usually ensues following relief of the obstruction.A comprehensive medical and drug history and physical examination are all invaluable. Particular attention should be paid to the fluid status of the patient (skin turgor, jugular venous pressure, lying and standing blood pressure, urine output). Urinalysis should be performed to detect evidence of proteinuria and haematuria, which will aid diagnosis. Fractional excretion of sodium and urine osmolality may be measured but the widespread use of diuretics in the elderly gives rise to unreliable results. Renal imaging, usually ultrasound scanning, is routinely performed for assessment of renal size and to exclude urinary obstruction. In some cases, renal biopsy is necessary to provide specific diagnostic information. The general principles of managing ARF include treatment of life-threatening features such as shock, respiratory failure, hyperkalaemia, pulmonary oedema, metabolic acidosis and sepsis; stopping and avoiding administration of nephrotoxins; optimization of haemodynamic and fluid status; adjustment of drug dosage appropriate to glomerular filtration rate; early nutritional support; and early referral to nephrologists for diagnosis of ARF cause, timely initiation of dialysis and initiation of specific treatment. The treatment of prerenal and ATN ARF is largely supportive with little evidence of benefit from current pharmacological therapies. Despite advances in critical care medicine and renal replacement therapy, the mortality of ARF has not changed significantly over the last 40 years, with current mortality rates being up to 75%.
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PMID:Management of acute renal failure in the elderly patient: a clinician's guide. 1854 Jun 87

Acute renal failure (ARF) is seen mostly in Plasmodium falciparum infection, but P vivax and P. malariae can occasionally contribute for renal impairment. Malarial ARF is commonly found in non-immune adults and older children with falciparum malaria. Occurance of ARF in severe falciparum malaria is quite common in southeast Asia and Indian subcontinent where intensity of malaria transmission is usually low with occasional microfoci of intense transmission. Since precise mechanism of malarial ARF is not known, several hypotheses including mechanical obstruction by infected erythrocytes, immune mediated glomerular and tubular pathology, fluid loss due to multiple mechanisms and alterations in the renal microcirculation, etc, have been proposed. Increased fluid administration, oxygen toxicity, and yet unidentified factors may contribute to pulmonary edema, acute respiratory distress syndrome (ARDS), multiorgan failure and death. Mainstay of treatment consists of appropriate antimalarial drug therapy, fluid replacement, and renal replacement therapy. Loop diuretics can convert an oliguric renal failure to non-oliguric renal failure without affecting outcome of the disease though the conversion reduces the risk of volume overload. There is little evidence on beneficial effect of vasoactive drugs. Nephrotoxic drugs such as ACE inhibitors, NSAIDs, aminoglycosides, cephalosporins should be avoided. Currently, high quality intensive care, early institution of renal replacement therapy, and avoidance of nephrotoxic drugs are standard practice of the prevention and management of ARF.
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PMID:Renal failure in malaria. 1859 37


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