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)

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

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