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)

The development of hypertension is associated with the presence of cardiovascular structural alterations. The principal target organs of hypertensive disease are the heart, brain, kidney and eye. Although left ventricular hypertrophy is an initially useful and well tolerated adaptive mechanism because it tends to reduce wall stress, it may subsequently lead to impaired cardiac function and even heart failure. Vascular structural alterations include reduced compliance, the appearance of atheromatous lesions in the large arteries, and hypertrophy or remodelling of small artery walls, and may be involved in the onset of retinal, renal and brain lesions. Technological progress now enables us to evaluate cardiovascular structural alterations early on as well as to monitor their natural history and the modifications induced by antihypertensive therapy. There is no question as to capacity of antihypertensive therapy to reduce the incidence of stroke, heart failure, renal failure and severe hypertensive retinopathy. Although a number of drugs are able to lower blood pressure, ACE-inhibitors and calcium entry blockers more effectively bring about the regression of left ventricular hypertrophy and, probably, also the retrocession of structural alterations in small resistance arteries; they seem to have a beneficial effect on structural alterations in large arteries as well. Although the regression of left ventricular hypertrophy could be associated with an improved prognosis, no data are available yet on the prognostic significance of the presence and regression of vascular structural alterations.
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PMID:[The organ damage in arterial hypertension]. 856 78

The activity of the renin-angiotensin-aldosterone system is thought to play a significant role in the development of target organ damage in essential hypertension. An insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene has recently been associated with increased risk for left ventricular hypertrophy and coronary heart disease in the general population. The D allele is associated with higher levels of circulating ACE and therefore may predispose to cardiovascular damage. The study presented here was performed to investigate the association between the ACE genotype, microalbuminuria, retinopathy, and left ventricular hypertrophy in 106 patients with essential hypertension. ACE gene polymorphism was determined by polymerase chain reaction technique. Microalbuminuria was evaluated as albumin-to-creatinine ratio (A/C) in three nonconsecutive first morning urine samples (negative urine culture) after a 4-wk washout period. Microalbuminuria was defined as A/C between 2.38 to 19 (men) and 2.96 to 20 (women). Hypertensive retinopathy was evaluated by direct funduscopic examination (keith-Wagener-Barker classification) and left ventricular hypertrophy by M-B mode echocardiography. The distribution of the DD, ID, and II genotypes was 27, 50, and 23%, respectively. The prevalence of microalbuminuria, retinopathy, and left ventricular hypertrophy was 19, 74, and 72% respectively. There were no differences among the three genotypes for age, known duration of disease, body mass index, blood pressure, serum glucose, uric acid, and lipid profile. DD and ID genotypes were significantly associated with the presence of microalbuminuria (odds ratio, 8.51; 95% confidence interval, 1.07 to 67.85; P = 0.019), retinopathy (odds ratio, 5.19; 95% confidence interval, 1.71 to 15.75; P = 0.005) and left ventricular hypertrophy (odds ratio, 5.22; 95% confidence interval, 1.52 to 17.94; P = 0.016). Furthermore, patients with DD and ID genotypes showed higher levels of A/C (3.6 +/- 0.9, DD; 2.6 +/- 0.7, ID; 0.9 +/- 0.2 mg/mmol, II; P = 0.0015 by analysis of variance) and increased left ventricular mass index (152 +/- 4.7, DD + ID versus 133 +/- 5.7 g/m2, II; P = 0.01) compared with II patients. The D allele was significantly more frequent in patients with microalbuminuria (odds ratio, 2.59; 95% confidence interval, 1.24 to 5.41; P = 0.013) and in those with retinopathy (odds ratio, 2.44; 95% confidence interval, 1.21 to 4.90; P = 0.015). Multiple regression analyses performed among the entire cohort of patients demonstrated that ACE genotype significantly and independently influences the presence of retinopathy, left ventricular hypertrophy, and microalbuminuria. In conclusion, the D allele of the ACE gene is associated with microalbuminuria as well as with retinopathy and left ventricular hypertrophy, and seems to be an independent risk factor for target organ damage in essential hypertension.
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PMID:The deletion polymorphism of the angiotensin I-converting enzyme gene is associated with target organ damage in essential hypertension. 898 33

Microalbuminuria is usually defined as a urinary albumin excretion of 30-300 mg/24 h (i.e. 20-200 micrograms/min) measured, in view of the short-term variation of 15-30%, in at least 2 out of 3 urine samples. An alternative definition is: an albumin-creatinine ratio of 2-20 mg/mmol creatinine. Microalbuminuria is an indicator of an enhanced risk of chronic kidney failure and cardiovascular disease in diabetic patients and of cardiovascular disease in the elderly general population. It is not known whether these relationships exist in essential hypertension as well. In essential hypertension there is, however, a relationship between microalbuminuria and endothelial dysfunction, impaired regulation of renal haemodynamics and an increased risk of left ventricular hypertrophy and hypertensive retinopathy. By screening for microalbuminuria a group of patients can be distinguished who have a relatively high risk for the presence of complications of hypertension. It is not certain, however, that more intensive treatment of such patients (e.g. with ACE inhibitors) is useful. Consequently, for the time being, screening of patients with essential hypertension for microalbuminuria is of little practical importance.
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PMID:[Microalbuminuria in essential hypertension: of limited value as an indicator of patients with a high risk for complications]. 954 76

A 47-year-old woman was admitted to our hospital for evaluation of general fatigue and dyspnea. She had been diagnosed with progressive systemic sclerosis (PSS) when she was 39 years of age, on the basis of Raynaud's phenomenon, proximal sclerosis, and pigmentation of the skin. On admission, her blood pressure was 206/128 mmHg. Funduscopy revealed grade III (Keith & Wagener) hypertensive retinopathy. Laboratory data showed positivity for anti-nuclear antibody and anticardiolipin beta 2 glycoprotein I antibody, and the plasma level of renin activity (PRA) was abnormally high. Chest X-ray and UCG revealed massive pericardial effusion. On the second hospital day, she was operated on for pericardiodiaphragmatic fenestration. The volume of pericardial effusion amounted to more than 2000 ml. Post operative malignant hypertension persisted. Laboratory data showed thrombocytopenia, hemolytic anemia, and acute renal failure. We diagnosed scleroderma renal crisis (SRC) associated with antiphospholipid syndrome. Following the initiation of angiotensin converting enzyme inhibitor (ACE-I) combined with calcium antagonist and alpha-one blocker, her blood pressure and PRA decreased. She also had been treated with aspirin 81 mg daily. These therapies were effective in recovering the platelet count and stopped the progression of anemia and renal failure. Although either the finding of large pericardial effusion or SRC is associated with poor prognosis in PSS, this case has had a good clinical course. In this case, the findings suggested that anti-phospholipid antibody may have contributed to the pericarditis and SRC.
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PMID:[A case of scleroderma renal crisis with massive pericardial effusion and positivity on antiphospholipid antibody test]. 965 14

We report a case whose renal failure was due to malignant hypertension and in whom steroid facilitated the recovery of renal function. The patient, a 41-year-old man, was admitted to our hospital because of malaise and macrohematuria. On admission, his blood pressure was 270/160 mmHg. The plasma renin activity (PRA) and aldosterone were markedly elevated. Chest X-ray, echo cardiography and electrocardiogram revealed marked hypertrophy. Hypertensive retinopathy and arteriosclerotic change were noted on ophthalmoscopy. Because of renal dysfunction (blood urea nitrogen 45.6 mg/dl, serum creatinine 4.9 mg/dl with massive proteinuria and increased FENa, renal biopsy was performed on the 8th clinical day. The specimens showed slight proliferation of mesangial cells with mesangiolysis and interstitial cell infiltration, in addition to marked arteriosclerosis and partial collapse of the glomerular tuft. After the administration of a Ca antagonist and angiotensin converting enzyme inhibitor (ACE-I), his mean blood pressure decreased to 100-130 mmHg, and urinary protein decreased as well. Nevertheless, renal dysfunction remained unchanged during the following 3 weeks. Thus, prednisolone (PSL, 30 mg/day) was administered on the 22nd clinical day and renal function improved thereafter without a significant change in blood pressure. The improved renal function was maintained after PSL tapered off on the 184th clinical day. It is suggested that PSL might be the therapy of choice in malignant hypertension, when the renal function has not been improved by anti-hypertensive treatment alone.
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PMID:[A case of malignant hypertension in whom steroid improved renal function]. 1065 31

Hypertensive crises can be divided into two categories as hypertensive emergency and hypertensive urgency. Most authorities have defined hypertensive emergency as a situation that requires immediate reduction in blood pressure (BP) with parenteral agents because of acute or progressive target organ damage, whereas hypertensive urgency is a situation with markedly elevated BP but without severe symptoms or progressive target organ damage, wherein the BP should be reduced within hours, often with oral agents. Adolescent with hypertension should be suspected of having renovascular hypertension in spite of other causes. This case is presenting a 16-year-old boy with hypertensive crises due to suspected renovascular hypertension. His blood pressure was 240/120 at admission with hypertensive retinopathy grade III and there was increase in creatinine after administering ACE-inhibitor but his renal arteriography revealed normal, other physical examination and laboratory findings was normal. Regarding these findings, the conclusion was this patient got essential hypertension. As many hypertensive crises occur in any ages, clinicians should aware the possibility of renovascular hypertension in young patients with hypertensive crises. An early detection and urgent treatment are needed to prevent the implication of progressive target organ damage.
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PMID:Hypertensive crises in the adolescent: evaluation of suspected renovascular hypertension. 2358 9