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)

Patients who develop diabetic nephropathy, one of the leading causes of end-stage renal diseases in Western communities, have an increased red cell Li+/Na+ countertransport (CT). Li+/Na+ CT is a membrane function which exchanges intracellular Li for extracellular Na in vitro. High Li+/Na+ CT reflects abnormal kinetic properties of red cell membrane Na/H exchange. A widespread abnormality of Na/H exchange could play a major role in the pathogenesis of diabetic nephropathy as well as of cardiovascular diseases since Na/H exchange is involved in the regulation of cell pH and cell volume; in the cellular response to hormones, mitogens, and growth factors; and in the renal reabsorption of Na and bicarbonate. Li+/Na+ CT is under genetic control and raised in a subgroup of patients with essential hypertension. Among these patients, high Li+/Na+ CT is associated with increased glomerular filtration rate, filtration fraction, proximal fractional Na reabsorption, microalbuminuria, plasma renin activity, and kidney and cardiac volume. Increased Li+/Na+ CT is often associated with hyperlipidemia, hyperuricemia, reduced insulin sensitivity, and obesity. The whole of these observations may explain why patients with diabetes or essential hypertension and increased Li/Na CT are at risk of early renal and cardiac impairment.
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PMID:Red blood cell Li+/Na+ exchange in patients with diabetic nephropathy and essential hypertension: therapeutic implications. 851 86

A cohort of 227 untreated essential hypertensive patients from north-western Italy was studied in order to evaluate the prevalence of micro- and macroalbuminuria and their relationship with other cardiovascular risk factors. Albuminuria was evaluated as the albumin to creatinine ratio (Alb/Cr) in three non-consecutive first morning samples. The prevalence of microalbuminuria and macroalbuminuria was 10% and 2.2%, respectively. Albuminuric patients showed higher blood pressure, serum creatinine, triglycerides and uric acid as well as a greater prevalence of retinopathy. Stepwise multiple regression analysis demonstrated that only a small part of variations in albuminuria was explained by changes in blood pressure. Duration of disease did not seem to influence microalbuminuria. The presence of hypertensive retinopathy was associated with greater albuminuria, longer duration of hypertension, and higher prevalence of major ECG changes, but not with higher blood pressure levels. Microalbuminuria, rather than a consequence of elevated blood pressure levels, seems to be a marker of a syndrome featuring, among other characteristics, essential hypertension. Furthermore, microalbuminuria must be considered as an independent cardiovascular risk factor.
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PMID:Prevalence of micro- and macroalbuminuria and their relationship with other cardiovascular risk factors in essential hypertension. 852 98

In patients with essential hypertension, the presence of microalbuminuria carries an increased risk for cardiovascular morbidity and mortality. The mechanisms responsible for this association are not clear. Microalbuminuria could signal the presence of generalised atherosclerosis. To determine the extent of atherosclerosis, we measured by B-mode ultrasound imaging the thickness of the intima and media layers of the carotid artery in 30 hypertensive patients with microalbuminuria, 30 patients without microalbuminuria and 30 normotensive healthy subjects. In hypertensive patients with microalbuminuria, urinary albumin excretion (55 +/- 4.7 mg/24 h) was greater (P < 0.01) than in patients without microalbuminuria (12 +/- 0.9 mg/24 h) and in healthy subjects (7.1 +/- 0.52 mg/24 h). In hypertensive patients with microalbuminuria, the thickness of the carotid artery (0.78 +/- 0.02 mm) was greater (P < 0.01) than in patients without microalbuminuria (0.69 +/- 0.01 mm) and in healthy subjects (0.64 +/- 0.02 mm). In hypertensive patients with microalbuminuria, the mean insulin area-under-the curve (59,703 +/- 4,874 pmol/L x 2 h) and glucose area-under-the curve (928 +/- 40.0 mmol/L x 2 h) were significantly greater (P < 0.005) than in patients without microalbuminuria (38,774 +/- 4,104 pmol/L x 2 h and 803 +/- 34.7 mmol/L x 2 h, respectively), and in normotensive healthy subjects (27,557 +/- 2563 pmol/L x 2 h and 837 +/- 31.2 mmol/L x 2 h, respectively). Serum levels of total cholesterol, triglycerides and lipoprotein(a) were higher in hypertensives with than in those without microalbuminuria. The thickness of the carotid artery was significantly correlated with microalbuminuria, blood pressure, cholesterol, serum triglycerides and insulin area-under-the curve. In conclusion, this study shows that hypertensive patients with microalbuminuria have an increased thickness of the carotid intima and media layers suggesting a greater degree of atherosclerosis. Measurements of urinary albumin excretion may be important in the evaluation of patients with essential hypertension.
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PMID:Increased thickness of the carotid artery in patients with essential hypertension and microalbuminuria. 857 99

The allele 235T (a threonine in place of a methionine at position 235) of angiotensinogen has been found to be associated with a predisposition to essential hypertension. We investigated whether this allele also confers increased susceptibility to nephropathy in patients with insulin-dependent diabetes mellitus (IDDM). A group of 380 patients who had had IDDM for 15 to 20 years were genotyped at the angiotensinogen 235 locus. Included were 75 patients with normoalbuminuria (albumin excretion rate < 30 micrograms/min), two series of patients with microalbuminuria (n = 30 and n = 136), and two series with overt proteinuria (n = 41 and n = 98). Allele 235T frequency was higher among cases with microalbuminuria (0.41 in the two series combined) or overt proteinuria (0.40) than in the normoalbuminuria group (0.36). However, this difference was not statistically significant with this sample size (chi 2 = 1.2, P = NS with 2 df). Under a recessive model, allele 235T homozygotes had a 1.6-fold risk of developing nephropathy relative to carriers of other genotypes, but this value was not significantly different from 1(95% CI = 0.8 to 3.5). The strength of the association did not improve after stratification by degree of glycemic control. With respect to the hypertension in these IDDM patients, no association with allele 235T was found. Allele 235T frequencies in normotensive and hypertensive individuals were 0.363 and 0.353, respectively, among normoalbuminuric IDDM individuals (chi 2 = 0.01, P = NS) and 0.411 and 0.414 among microalbuminuric IDDM subjects (chi 2 = 0.0, P = NS). We conclude that the angiotensinogen polymorphism M235T might influence susceptibility to nephropathy in insulin-dependent diabetes, but its effect, if any, is rather small and independent of hypertension.
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PMID:Angiotensinogen polymorphism M235T, hypertension, and nephropathy in insulin-dependent diabetes. 862 Dec 7

We studied the relationship among albuminuria, factor VII (FVII) hyperactivity, and endothelial cell damage in 6 elderly hypertensive subjects. The plasma levels of activated FVII (FVIIa), FVII coagulant activity, FVII antigen (FVIIag), von Willebrand factor (vWF), and thrombomodulin were measured to assess FVII hyperactivity and endothelial cell damage, and urinary albumin excretion rate (UAE) was calculated using 12-hour nighttime (7 pm to 7 am) urine collection (mean for 2 consecutive nights). We performed 24-hour ambulatory blood pressure monitoring in all 61 hypertensive patients and classified them into a white-coat hypertension group (n=12) and a sustained hypertension group (n=49). For the levels of FVII, vWF, and thrombomodulin, there were no differences between the white-coat hypertension group and normotensive control subjects (n=25). In the sustained hypertensive group, only the microalbuminuric subgroup (UAE, 15 to 300 microgram/min: n=30) showed significant elevation compared with the normotensive group for the level of FVIIa (mean [95% confidence interval]: 4.0 [3.6 to 4.4] versus 3.0 [2.6 to 3.3] ng/mL, P<.001), the FVIIa/FVIIag ratio (an indicator of activation of FVII zymogen to FVIIa) (1.33 [1.19 to 1.50] versus 1.04 [0.92 to 1.19], P<.01), the level of vWF (188 [165 to 214] % versus 144 [129 to 160] %, P<.01), and thrombomodulin (11.7 [10.3 to 13.3] versus 9.3 [8.5 to 10.3] ng/mL, P<.01). In contrast, none of these levels in the normoalbuminuric hypertensive group (UAE <15 microgram/min, n=19) differed from that in the normotensive control group. These results suggest that among elderly hypertensives, only those with microalbuminuria show enhancement of FVII activation and endothelial cell damage, while patients with white-coat hypertension and normoalbuminuric hypertensives do not show these accompanying abnormalities. Thus, increased levels of FVII activity and markers of endothelial cell damage might account for the higher risk of cardiovascular events in essential hypertension with microalbuminuria.
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PMID:Factor VII hyperactivity and endothelial cell damage are found in elderly hypertensives only when concomitant with microalbuminuria. 863 Jun 73

Diabetic nephropathy in Jewish insulin-dependent diabetes mellitus (IDDM) patients has been found to correlate to their ethnic origin. It has also been found that increased sodium-lithium countertransport (SLC) in erythrocytes, as a genetic marker for essential hypertension, may identify those patients at risk for diabetic nephropathy. The purpose of this study was to investigate a possible correlation between this genetic marker and the ethnic origin of Jewish IDDM patients and their parents and the risk for developing diabetic nephropathy. Although SLC was slightly increased in IDDM patients with microalbuminuria, SLC was not correlated with the existence of diabetic nephropathy nor with the ethnic origin and blood pressure of these Jewish IDDM patients. Thus, other genetic factors may play a role in the different prevalence of diabetic nephropathy in Jewish IDDM patients of different ethnic origin.
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PMID:Sodium-lithium countertransport: a predictor of diabetic nephropathy in Jewish insulin-dependent diabetes mellitus patients of different ethnic origin? 863 45

Epidemiologic and clinical studies suggest an association between hyperinsulinemia (and insulin resistance) and hypertension. This relationship is not present in secondary forms of hypertension and may persist despite adequate antihypertensive therapy. Normotensive offspring of hypertensive parents are also, as a group, insulin resistant and hyperinsulinemic. The association of hyperinsulinemia (and insulin resistance) with hypertension is more marked in the obese but present in lean hypertensive as well. Physiological mechanisms by which insulin might increase blood pressure include sympathetic nervous system stimulation and enhancement or renal sodium reabsorption. Evidence exists linking both of these mechanisms to hypertension. Insulin is also independently associated with myocardial infarction and microalbuminuria, two long term complications of high blood pressure. Experimentally induced decreases in insulin resistance and hyperinsulinemia, furthermore, have been associated with decreased blood pressure. In summary, the evidence suggests that hyperinsulinemia (and insulin resistance) exerts a pro-hypertensive effect that may be important in the pathogenesis of hypertension and hypertensive complications in some patients with essential hypertension.
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PMID:Insulin sensitivity in the pathogenesis of hypertension and hypertensive complications. 874 25

The objective of the present study was to assess the relationship between microalbuminuria (Malb) and left ventricular hypertrophy (LVH), when levels of ambulatory BP was token in to account as a confounder factor. Patients with essential hypertension, aged 25 to 50 years old, never treated with antihypertensive drugs, were included in the study. The inclusion criteria were: (a) absence of diabetes, renal disease or urinary tract infection; (b) urinary albumin excretion (UAE) estimated in urine of 24 hours in two separate days; (c) echocardiography suitable for measurement of left ventricular mass (LVM); and (d) good quality ambulatory blood pressure monitoring during 24 hours. UAE was measured using a immunonephelometric assay (Behring Institute) and Malb was considered when UAE 30 to 300 mg/24 hours during the two days. LVM was calculated by the Devereaux formula and referred to height (LVMI g/m). AMBP was performed using an oscilometric device (Spacelabs 90202 or 90207) during a regular working day. Readings were programmed every 20 minutes between 6 a.m. to midnight and thereafter every 30 minutes. The average BP during a 24 hour period was calculated. One hundred and fifty one patients (96 male, mean age 37 +/- 8 years, body mass index 27.7 +/- 3.7 g/m2) were included. The average values of office BP was 148 +/- 15/96 +/- 8 mm Hg, and the average BP during 24 hours was 137 +/- 13/88 +/- 12 mm Hg. UAE was 30.1 +/- 52.3 mg/24 hr and the LVMI 140.6 +/- 44.1 g/m. The percentage of Malb patients was 28% and those with LVH 34%. A significant relationship between UAE and office and ambulatory SBP and DBP was observed. LVMI was also significantly related to ambulatory SBP and DBP, a relationship that was not found for office BP. In a multiple regression model, significant relationship between UAE and LVMI emerged, independent of diastolic ambulatory BP, age and sex (P < 0.04). In conclusion; we observed a significant relationship between UAE and LVMI, in part, independent of blood pressure. The fact that Malb is associated with the presence of LVH, supports the idea that Malb is a risk marker in essential hypertensive patients.
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PMID:Microalbuminuria, left ventricular mass and ambulatory blood pressure in essential hypertension. 874 18

Hypertension and diabetes co-exist more commonly than would be expected from their individual prevalences. Elevated blood pressure is most commonly due to coexisting essential hypertension, or diabetic renal disease. Early stages of diabetic renal disease can be identified by detecting microalbuminuria. Standard measures of blood pressure are not necessarily raised, but 24-hour ambulatory measures frequently identify a loss of nocturnal drop in blood pressure. Treating hypertension aggressively is important in slowing the inexorable decline in glomerular filtration rate. In diabetes there appears to be no 'J'-shaped relationship between blood pressure and cardiovascular events, thus removing any concern about attaining low blood pressures as long as the patient is asymptomatic. Morbidity and mortality in these patients is usually associated with cardiovascular events, and it is important to assess the effect of drugs on left ventricular hypertrophy and metabolic parameters. Many drugs are effective at lowering blood pressure, but angiotensin-converting enzyme inhibitors may have an additional renoprotective action. alpha-Adrenergic antagonists may improve lipid profiles and calcium antagonists are probably lipid neutral, making these drugs useful alternatives. Dihydropyridine calcium antagonists (eg, nifedipine) may augment protein-uria, and hence non-dihydropyridine calcium antagonists (eg, verapamil, diltiazem) would be preferred. beta-Blockers and thiazide diuretics have the disadvantage of causing a deterioration in glycaemic and lipid profiles, but can be useful on occasions.
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PMID:The diabetic patient with hypertension. 876 97

Recent studies have suggested that an inherited predisposition to essential hypertension may increase susceptibility to nephropathy for patients with IDDM. Essential hypertension has been linked to the angiotensinogen (AGT) gene in genetic linkage studies in American and European populations. A molecular variant (M235T), which has a functional effect, has been described with highest plasma AGT levels being associated with the TT genotype. In a case-control study, we have evaluated the role of this functional genetic marker in patients with IDDM and nephropathy and in IDDM patients without nephropathy. We studied 195 IDDM patients, of whom 95 had established diabetic nephropathy; the remaining 100 patients, who had no evidence of microalbuminuria, served as control subjects. All patients were whites born in Northern Ireland. The point mutation in the AGT gene was analyzed using restriction typing. The background frequency of the M235T variant was assessed in 80 healthy blood donors, and the TT genotype was present in 9%. This genotype occurred in 8% of control IDDM patients without nephropathy and 19% of IDDM patients with nephropathy (P = 0.025). The odds ratio for diabetic nephropathy associated with the TT genotype was 2.7 (95% CI 1.04-7.52). There was no relationship between blood pressure and AGT genotypes in the control group. We cannot exclude the possibility that the observed association in the nephropathy group is due to an association between AGT genotype and hypertension. This evidence may help to explain the predisposition to diabetic nephropathy afforded by hypertension and merits further investigation.
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PMID:A molecular variant of angiotensinogen is associated with diabetic nephropathy in IDDM. 877 23


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