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

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.
 ...
PMID:Microalbuminuria in essential hypertensives in treatment for hypertension. 959 80

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.
 ...
PMID:Angiotensinogen gene M235T and T174M polymorphisms in essential hypertension: relation with target organ damage. 960 82

Glomerular hyperfiltration, which is expected to occur after uninephrectomy, could potentially damage the non-transplanted donor kidney in living donor transplantation. We therefore prospectively measured renal function (inulin and PAH clearance), albumin excretion and blood pressure in the donors of 30 consecutive living donor kidney transplants before uninephrectomy (n = 29) and 1 week (n = 27) and 1 year (n = 16) after. Hyperfiltration was defined as: (post-nephrectomy inulin clearance)/(0.5 x pre-nephrectomy inulin clearance); hyperperfusion was defined in an analogous way for PAH clearance. Hyperfiltration averaged 128 +/- 5% [SEM] and hyperperfusion 133 +/- 6% 1 week after uninephrectomy. Hyperfiltration was nearly unchanged (126 +/- 7%) 1 year after nephrectomy, whereas hyperperfusion had significantly decreased to 118 +/- 8% (P < 0.02). There was no significant change in blood pressure after nephrectomy, and no new cases of hypertension were observed during the 1-year follow-up. The degree of hyperfiltration did not correlate with donor age. Microalbuminuria > 30 mg/24 h was found in two donors 1 week after nephrectomy (one of which normalized at 1 year) and in one additional donor 1 year after nephrectomy. The degree of hyperfiltration did not correlate with albumin excretion rate. In conclusion, no adverse consequences of hyperfiltration were demonstrable during the 1-year observation period, but the prognostic role of occasional microalbuminuria should be further investigated.
 ...
PMID:Glomerular hyperfiltration after unilateral nephrectomy in living kidney donors. 1462 63

The assessment of the postprandial state in diabetes mellitus has gained importance due to postprandial hyperglycemia being considered as an independent risk factor for cardiovascular disease. Hyperglycemia may contribute to vascular dysfunction through the alteration of the nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway. The authors assessed the NO/cGMP pathway in the fasting and postprandial state in 20 type 1 diabetic patients (age: 34.1 +/- 2.6 years, body mass index (BMI): 24.1 +/- 1.3 kg/m (2), duration of diabetes: 16 +/- 2.2 years, HbA (1C): 8.3 +/- 0.4 %, [x +/- SEM], 10 without, 10 with late complications) and 20 matched control subjects (age: 39.7 +/- 1.9 years, BMI: 25.3 +/- 1.1 kg/m (2)). In the fasting state NO end product (nitrite/nitrate) levels did not differ between the diabetic and control group, cGMP levels were found to be significantly lower in the diabetic group (2.5 +/- 0.2 vs. 4.6 +/- 0.6 nmol/l, p = 0.01). A higher level of lipid peroxidation end products (TBARS) was found in diabetic subjects (6.7 +/- 0.4 vs. 5.0 +/- 0.3 micro mol/l, p = 0.004). The diabetic subgroup without late complications had significantly higher nitrite/nitrate levels compared to the patients with complications (57.8 +/- 6.6 vs. 30.4 +/- 4.3 micro mol/l, p = 0.006), their TBARS and cGMP levels were similar. The control subjects responded to the test meal with an increase in the cGMP levels (4.6 +/- 0.6 to 5.5 +/- 0.6 nmol/l, p = 0.02), while in the diabetic group no change was detected. Postprandial nitrite/nitrate levels decreased in both groups, they were significantly lower in the diabetic group. There was no difference between postprandial nitrite/nitrate, cGMP, or glucose levels in the diabetic subgroups. Postprandial glucose levels showed a significant negative correlation with cGMP levels in the diabetic group (r = - 0.50, p = 0.02). The results suggest that in subjects with type 1 diabetes mellitus NO might have an impaired ability to induce cGMP production in the fasting state prior to the development of late specific complications or microalbuminuria under hyperglycemic conditions. Postprandial hyperglycemia is suggested to interfere with endothelial NO action, as shown by the decreased nitrite/nitrate and unchanged cGMP plasma levels in the diabetic group. The impairment of the NO/cGMP pathway both in the fasting and postprandial state that was shown in patients without diabetic complications may be an early sign of hyperglycemia induced vascular damage in type 1 diabetes mellitus.
 ...
PMID:Impairment of the NO/cGMP pathway in the fasting and postprandial state in type 1 diabetes mellitus. 1514 72

Microalbuminuria can be present in 25-100% of patients with essential hypertension and is associated with increased incidence of cardiovascular events. Our goal was to evaluate the effect of a commonly used calcium channel blocker, amlodipine, and an angiotensin converting enzyme inhibitor, lisinopril on urinary albumin excretion in patients with mild to moderate essential hypertension. We screened 324 patients with essential hypertension for microalbuminuria and documented it in 120 patients. These 120 patients with microalbuminuria were randomly divided into two groups of 60 each, matched for age, sex, arterial pressure, creatinine clearance, and urinary albumin excretion so as to receive amlodipine or lisinopril. We prospectively measured their urinary albumin excretion and creatinine clearance prior to treatment and, four and eight weeks after treatment with amlodipine or lisinopril. Mean arterial pressure (mean +/- SD) at baseline, after four weeks, and after eight weeks was 113.01 +/- 4.38,104.93 +/- 3.12, and 98.89 +/- 1.75 mmHg (P < 0.0000); and 114.13 +/- 7.11, 106.52 +/- 3.50, and 100.89 +/- 2.80 mmHg (P < 0.0000) in amlodipine and lisinopril groups, respectively. Urinary albumin excretion (mean +/- SEM) at baseline, after four, and after eight weeks was 79.30 +/- 3.74, 62.03 +/- 3.61, and 52.02 +/- 3.05 (P < 0.0000); and 73.96 +/- 4.10, 72.39 +/- 3.74, 66.12 +/- 3.94 (P = 0.1742) in lisinopril and amlodipine groups, respectively. Lisinopril but not amlodipine, reduced the urinary albumin excretion significantly despite their similar antihypertensive efficacy. The clinical and prognostic significance of these observations need to be established.
 ...
PMID:Effect of amlodipine and lisinopril on microalbuminuria in patients with essential hypertension: A prospective study. 2053 65


<< Previous 1 2 3 4