Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Urinary albumin excretion (UAE) was evaluated in 26 subjects with essential hypertension and no diabetes (5 men, 21 women; 19 whites and 7 blacks), with creatinine clearance (Ccreat) > or = 75 ml/min/1.73 m2, in individualized treatment with various antihypertensive drugs. Clinical and laboratorial data were the following: mean age, 53 +/- 2 years (SEM); duration of hypertension, 14.9 +/- 2.2 years; body mass index (BMI), 26.8 +/- 0.7; arterial blood pressure, 142 +/- 4/89 +/- 3 mmHg; serum creatinine, 0.8 +/- 0.03 mg/dL; Ccreat, 99.3 +/- 3.8 ml/min/1.73 m2 and UAE, 9.3 +/- 1.5 micrograms/min. No significant difference was found when data were evaluated for gender and race. Microalbuminuria, defined as UAE > 13.9 micrograms/min, was found in 19% of the hypertensives (range: 16.3 to 28.1 micrograms/min). UAE correlated positively and significantly with systolic (r = 0.6309; P = 0.0005), diastolic (r = 0.4146; P = 0.0352), and mean blood pressure (r = 0.5000; P = 0.0093). The correlation between UAE and systolic pressure was stronger than with diastolic pressure. There was a positive and significant correlation between BMI and UAE values (r = 0.5623; P = 0.0028), and between BMI values with those of systolic (r = 0.5271; P = 0.0057) and mean blood pressure (r = 0.3930; P = 0.470). No correlation was found between UAE and age, duration of hypertension or Ccreat. Systolic, diastolic and mean blood pressures were significantly higher in microalbuminuric than in non microalbuminuric hypertensives. Obese hypertensives presented higher mean values of UAE, systolic, diastolic and mean pressures than non obese.
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PMID:Microalbuminuria in essential hypertensives in treatment for hypertension. 959 80

An insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene significantly influences circulating ACE levels and plays a role in the development of target organ damage, that is, left ventricular hypertrophy in essential hypertension (EH), and microalbuminuria in diabetes mellitus. We have examined the role of the I/D polymorphism in essential hypertensive patients with renal involvement. The study was divided in two independent protocols. In protocol 1, we retrospectively analyzed the ACE genotypes in 37 essential hypertensive patients with a clinical and histopathological diagnosis of nephroangiosclerosis. In protocol 2, ACE genotypes as well as microalbuminuria and renal hemodynamic parameters were investigated in 75 patients with EH with normal renal function and a strong family history of hypertension. As control group, 75 healthy subjects with BP < 130/85 mm Hg and no family history of cardiovascular diseases were studied. The ACE variants were determined by PCR and the genotypes were classified as DD, DI and II. In protocol 1, patients with nephroangiosclerosis displayed a significant difference in the genotype distribution (57% DD, 27% DI, 16% II) when compared to the control population (25% DD, 64% DI, 11% II; P < 0.001). There was no significant difference in genotype distribution between hypertensive patients with normal renal function (protocol 2; 33% DD, 59% DI, 8% II) and the control group. There were no differences in age, blood pressure, microalbuminuria and duration of the disease among the three genotypes in the EH group from protocol 2. Taken together, these findings suggest that the DD genotype of ACE is associated with histopathologic-proven kidney involvement in patients with EH and that this polymorphism could be a potential genetic marker in hypertensives at risk of renal complications.
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PMID:Angiotensin converting enzyme gene I/D polymorphism in essential hypertension and nephroangiosclerosis. 960 7

As hypertensive target-organ damage has been associated with diminished diurnal blood pressure (BP) variation in adults, we compared diurnal BP patterns of hypertensive adolescents with left ventricular hypertrophy with normotensive and hypertensive adolescents with normal left ventricular mass. In addition, the frequency of microalbuminuria (Malb), hyperfiltration, and reduced renal functional reserve (RFR) was evaluated in adolescents with normal BP and untreated borderline and mild essential hypertension. Thirty-three normotensive (NT) adolescents, 14.5+/-2.1 years (mean +/- SD), and 29 untreated borderline and mildly hypertensive (HT) adolescents, 14.6+/-2.4 years, wore the SpaceLabs 90207 ambulatory BP monitor for 24 h. Left ventricular mass was measured by M-mode echocardiography and then indexed (LVMI) to the cube of height. Creatinine clearance (Clcr) and urine Malb was measured on 24 h collection and RFR by change in creatinine clearance after an oral protein load. Diurnal BP change was expressed as the absolute and percent day-night BP fall and cusum derived plot height (CPH) and circadian alteration magnitude (CDCAM). Groups were compared using analysis of covariance with adjustments for race, gender, and body mass index. All NT and 19 HT subjects (HT-1) had normal LVMI at 22.2+/-5.3 and 25.8+/-3.8 g/m3, respectively. Ten HT (HT-2) had increased LVMI of 36.9+/-5.2 g/m3. No significant difference was found for absolute or percent day-night BP fall or CDCAM between groups. Nocturnal systolic BP was correlated most closely with LVMI (r = 0.41, p = .001). Clcr, Malb, and RFR did not differ between the groups. In conclusion, adolescents with borderline and mild essential hypertension and left ventricular hypertrophy have similar levels of diurnal BP fall, urine Malb excretion, and RFR compared to normotensive and hypertensive adolescents with normal left ventricular mass.
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PMID:Influence of diurnal blood pressure variations on target organ abnormalities in adolescents with mild essential hypertension. 960 78

Microalbuminuria has been associated with a cluster of metabolic and nonmetabolic risk factors, suggesting that it might indicate the presence of generalized microvascular damage in patients with essential hypertension. To explore whether microalbuminuria is associated with early target organ damage, two groups of essential hypertensive patients, with (n = 17) (HtAlb+) and without (n = 16) (HtAlb-) microalbuminuria, and a control group (C) of healthy normotensive subjects (n = 20) were studied. The study groups, selected among participants of a large epidemiologic trial, were carefully matched for several potentially confounding variables such as gender, age, duration of hypertension, and body mass index. Albumin excretion rate was evaluated by radioimmunoassay in three nonconsecutive timed overnight collections after 3 weeks of pharmacologic wash-out. Left ventricular mass was assessed by M-B-mode echocardiography, carotid wall thickness by a high resolution ultrasound scan, and renal vascular impedance by Doppler scan. Office as well as 24-h ambulatory pressure monitoring (Takeda TM-2420) were also evaluated. There was no difference between the two hypertensive groups for office and 24-h blood pressure levels except for a lower daytime/nighttime systolic blood pressure ratio in the group with microalbuminuria. Microalbuminuric patients showed signs of early organ damage as compared to normoalbuminuric patients and normal subjects, namely greater left ventricular mass indices (LVMI 167+/-7 g/m2 in HtAlb+; 139+/-9 g/m2 in HtAlb-; 118+/-5 g/m2 in C, P < .001) and increased wall thickness of common carotid arteries (intima plus media thickness 12.5+/-0.2 mm in HtAlb+; 11.7+/-0.3 mm in HtAlb-; 11.2+/-0.2 mm in C, P < .001) as well as higher intrarenal vascular resistance (mean resistive index 0.62+/-0.01 in HtAlb+; 0.59+/-0.01 in HtAlb-; 0.59+/-0.01 in C, P < .05). In conclusion, microalbuminuria is an early marker of diffuse target organ damage in essential hypertension and therefore can be useful to identify patients for whom more aggressive preventive strategies or additional treatment measures are advisable.
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PMID:Microalbuminuria is an early marker of target organ damage in essential hypertension. 960 81

The molecular variants M235T and T174M of the angiotensinogen gene have been linked to essential hypertension in some populations, but there are discrepancies about this association in other studies. We studied 75 patients with essential hypertension (BP > 160/100 mm Hg) from our outpatient clinic, aged 55+/-1 years, 30 men, systolic BP 182+/-2.5, diastolic BP 109+/-1 mm Hg (mean +/- SEM), and a family history of the disease. Target organ damage was evaluated by measuring urinary albumin excretion rate, left ventricular hypertrophy, and fundoscopy. As a control group, 75 healthy subjects with BP < 130/85 mm Hg and with no family history of cardiovascular disease were selected. M235T and T174M angiotensinogen genotypes were determined by PCR and subsequent digestion of the products with SfaNI and NcoI, respectively. The frequency (q) of genotypes of the variant M235T in the patients with essential hypertension was MM 0.31, MT 0.41, and TT 0.28, not significantly different (P = .93) from that of the controls (MM 0.28, MT 0.44, and TT 0.28). For the variant T174M, the genotype frequencies in hypertensives were TT 0.83, TM 0.15, and MM 0.02, which was not significantly different (P = .89) from that of the controls (TT 0.86, TM 0.12, and MM 0.02). Similarly, there was no evidence for association between angiotensinogen genotypes and hypertension in subjects aged < or = 40 years old (n = 24) or with severe (stage III) hypertension (n = 31). Within the group of patients with essential hypertension, there were no differences in genotype distribution between patients with and without retinopathy (n = 31), left ventricular hypertrophy (n = 37), or microalbuminuria (n = 14). This study shows that M235T and T174M variants are not associated either with essential hypertension or with target organ damage in a Spanish sample.
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PMID:Angiotensinogen gene M235T and T174M polymorphisms in essential hypertension: relation with target organ damage. 960 82

There is increasing evidence that essential hypertension is associated with a panoply of metabolic abnormalities. Included in these abnormalities are insulin resistance, dyslipidemia, enhanced coagulation, and decreased fibrinolytic activity, microalbuminuria, and platelet abnormalities and endothelial dysfunction. Visceral obesity appears to be the most common and predictive underlying factor for all of these metabolic abnormalities accompanying hypertension as well as increased cardiovascular disease (CVD) risk. As the prevalence of obesity is increasing, there is cause for concern that CVD increases will parallel this risk factor, particularly in especially high-risk populations, such as African-American women. Other important risk factors, such as increased oxidative stress, may require special therapeutic strategies, including the use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin blockers as cornerstones of antihypertensive drug therapy.
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PMID:Diabetic vascular disease and hypertension. 982 85

The kidney can suffer the consequences of a persistently elevated blood pressure. In fact end-stage renal failure caused by essential hypertension appears to be one of the most prevalent etiologies in patients entering a dialysis program. Blood pressure control is needed in order to prevent the progressive loss of renal function. Target blood pressure control has been established at values as low as 125/75 mm Hg for patients with proteinuria above 1 g/day. Attainment of this target level usually requires the combination of two or more drugs. However, the possibility that differences exist among the different classes of antihypertensive drugs beyond their capacity to simply lower blood pressure remains to be clearly elucidated. The fact that the presence of chronic renal failure is also accompanied by an enhanced cardiovascular risk potentiates the need to explore the renoprotective and cardiovascular protective capacity of the different classes of antihypertensive drugs, in patients with essential hypertension and some degree of renal involvement, characterized by the presence of microalbuminuria, proteinuria and/or an elevated serum creatinine.
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PMID:Therapeutic implications and new perspectives for essential hypertension and renal damage. 983 83

Microalbuminuria is frequently seen in patients with established essential hypertension, and is a predictor of a higher risk for cardiovascular and probably renal dysfunction. The presence of microalbuminuria has been shown to correlate with the other cardiovascular risk factors commonly seen in hypertensive patients. This fact indicates that the detection of an increased urinary albumin excretion could probably be the best index of an increased global cardiovascular risk in a given patient. Blood pressure control is accompanied by a fall in the content of albumin in urine. Agents with the capacity to block the renin-angiotensin system have shown a capacity to decrease urinary albumin excretion, which is independent of their ability to lower blood pressure. Whether or not a decrease in urinary albumin excretion is accompanied by an improved renal and cardiovascular prognosis in hypertensive patients remains to be elucidated.
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PMID:Microalbuminuria in essential hypertension. 983 84

During the last few years there has been a renewed interest in blood-pressure (BP)-induced kidney damage, owing to a progressive increase in the incidence and prevalence of hypertension and vascular diseases as a cause of end-stage renal disease (ESRD). The need to prevent ESRD demands continued efforts so as to identify early those people with hypertension who are at risk and to provide them with effective antihypertensive therapy. This review analyses what is needed in terms of surrogate endpoints for monitoring kidney damage and what is known about the impact of antihypertensive treatments in reducing the BP burden on the kidney in non-diabetic subjects. Although glomerular filtration rate (GFR) and proteinuria are useful surrogate endpoints for patients with nephropathy and GFR below or close to the threshold value for renal insufficiency, it is clear that monitoring changes in either GFR or proteinuria does not provide a sensitive endpoint for subjects with the mildest forms of renal disease, e.g. essential hypertensive patients who are at risk of developing kidney damage. In this case microalbuminuria may be useful, although unequivocal evidence demonstrating that microalbuminuria is a risk marker for developing renal insufficiency in non-diabetic renal diseases has not existed until now, and whether a decrease in microalbuminuria is of prognostic significance in patients with essential hypertension remains to be demonstrated. The beneficial effects of the antihypertensive agents on microalbuminuria are also proportional to BP reduction. If a large enough BP reduction is achieved there seem to be, at most, only minimal differences among the antihypertensive drug classes. Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers have additional beneficial effects on microalbuminuria independent of the BP reduction, owing to their direct role in glomerular haemodynamics. The heterogeneity in the changes in urinary albumin excretion during antihypertensive treatment may be related to the different factors involved in the presence of microalbuminuria or structural end-organ damage, or both.
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PMID:Renal protection by antihypertensive drugs: insights from microalbuminuria studies. 988 2


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