UMLS:C0020538 - FACTA Search

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Query: UMLS:C0020538 (hypertension)
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Recent large-scale epidemiological studies demonstrate that blood concentrations of immunoreactive insulin predict the development of NIDDM and IDDM and are associated with the risk of several degenerative diseases, such as coronary and peripheral vessel atherosclerosis, hypertension, and dyslipidemia. The reliability of these measurements is dependent on a biological assay that has not been well standardized between laboratories. Recognizing this, the American Diabetes Association organized a task force to assess comparability of blood insulin measurements between laboratories and to suggest techniques to improve comparability. The task force found that identical serum and plasma samples measured in different laboratories produced widely disparate values that were unacceptable for population comparisons. Use of a single reference standard did little to improve comparability. Assay characteristics such as linearity, recovery, accuracy, and cross-reactivity to proinsulin and its primary conversion intermediates varied among the laboratories, and they did not readily explain differences in the measurements made from assay to assay. Use of the same assay kit in different laboratories did not always ensure comparable measurements. Linear regression of assay results from one laboratory to an arbitrarily chosen reference assay greatly improved comparability and demonstrated the potential value in comparing each assay to a reference method. The task force report defines acceptable assay characteristics and proposes a three-step process of insulin assay proficiency and comparability. A central reference assay and ongoing sample exchange will be needed to allow reliable comparisons of insulin measurements made in different laboratories. Rigorous quality control and continuous quality improvement are needed to maintain reliability of the insulin measurement.
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PMID:Report of the American Diabetes Association's Task Force on standardization of the insulin assay. 854 70

Microalbuminuria in both insulin-dependent (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) is a marker for insulin resistance. Microalbuminuria is also associated with hypertension, itself an insulin-resistant state. Therefore, in order to examine the independent relationships of microalbuminuria with blood pressure and insulin resistance, we measured ambulatory blood pressure (Takeda TM-2420), insulin resistance (modified Harano method), and urinary albumin excretion rate (overnight urine collection) in 36 subjects with NIDDM. Albumin excretion correlated with 24-h systolic blood pressure (r = 0.49, p = 0.003), and insulin sensitivity (r = -0.39, p = 0.007). Microalbuminuric subjects had reduced insulin sensitivity compared with normoalbuminuric subjects [Mean (SD) 2.95 (0.33) versus 4.67 (0.56) ml.kg-1.min-1; p = 0.013]. In multivariate analysis including ambulatory blood pressure and insulin resistance, urinary albumin excretion was associated primarily with insulin resistance, with smaller contributions from glycated hemoglobin and male gender. These data suggest that microalbuminuria in NIDDM, although associated with hypertension, is also independently associated with insulin resistance.
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PMID:Insulin resistance in non-insulin-dependent diabetes mellitus is associated with microalbuminuria independently of ambulatory blood pressure. 857 34

Genotypic abnormalities of the renin-ANG system have been suggested as a risk factor for the development of diabetic nephropathy. Cleavage of angiotensinogen is the rate-limiting step in the activation of the renin-ANG system. The TT genotype of a polymorphism encoding threonine instead of methionine (M235T) has been associated not only with increased plasma angiotensinogen concentration but also with essential hypertension. In addition, a polymorphism in the angiotensinogen gene substituting methionine for threonine (T174M) has been associated with hypertension in nondiabetic populations. We studied the relationship between these polymorphisms in the angiotensinogen gene in IDDM patients with diabetic nephropathy (121 men, 74 women, age 40.9 +/- 10 years, diabetes duration 27 +/- 8 years). There was no difference in M235T genotype distribution between IDDM patients with diabetic nephropathy and those with normoalbuminuria: 73/97/25 (37/50/13%) vs. 67/95/23 (36/52/12%) had MM/MT/TT genotypes, respectively. No difference in distribution of T174M genotypes between nephropathic and normoalbuminuric IDDM patients was observed either: 148/44/1 (77/23/0.5%) vs. 141/42/2 (76/23/1%) had TT/TM/MM genotypes, respectively. In patients with nephropathy, systolic blood pressure was higher (161 +/- 22 mmHg [mean +/- SD]) in patients carrying TT genotype of the M235T angiotensinogen polymorphism as compared with patients with MM or MT genotypes (150 +/- 23 mmHg; P = 0.03). We conclude that neither the M235T nor the T174M polymorphism in the angiotensinogen gene contributes to genetic susceptibility to diabetic nephropathy in white IDDM patients, whereas the TT genotype of the M235T is associated with elevated blood pressure in patients with diabetic nephropathy.
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PMID:Angiotensinogen gene polymorphisms in IDDM patients with diabetic nephropathy. 859 44

The objectives of the study were to assess the effects of moderate sodium restriction on blood pressure in insulin-dependent diabetic (IDDM) patients with nephropathy and high normal or mildly hypertensive blood pressure (primary objective), and to document possible associated changes of exchangeable body sodium, body volumes, components of the renin-angiotensin-aldosterone system, atrial natriuretic peptide, and catecholamines (secondary objective). Sixteen patients with untreated systolic blood pressure > or = 140 < 160 mmHg and/or diastolic blood pressure > or = 85 < 100 mmHg were included in a double-blind, randomized, placebo-controlled trial. After a 4-week run-in period on their usual diet and a 2-week dietary training period to reduce sodium intake to about 90 mmol/day, eight patients received 100 mmol/day sodium supplement (group 2) and eight patients a matching placebo (group 1) for 4 weeks while continuing on the reduced-sodium diet. Patients were examined at weekly intervals. Main response variables were mean values of supine and sitting systolic and diastolic blood pressure as measured in the clinic and by the patients at home. The differences in blood pressure between the beginning and the end of the blinded 4-week study period were calculated and the differences in changes between the two patient groups were regarded as the main outcome parameters. During the blinded 4-week study period, average urinary sodium excretion was 92 +/- 33 (mean +/- SD) mmol/day in group 1 and 199 +/- 52 mmol/day in group 2 (p = 0.0002). The differences in blood pressure changes between the two patient groups were 3.9(-1.2 to 9) mmHg [mean (95% confidence intervals)] for systolic home blood pressure, 0.9(-3.7 to 5.5) mmHg for diastolic home blood pressure, 4.9(-3.3 to 13.1) mmHg for clinic systolic blood pressure and 5.3(1 to 9.7 mmHg, p = 0.02) for clinic diastolic blood pressure. Combining all patients, there were relevant associations between changes of urinary sodium excretion and blood volume (Spearman correlation coefficient r = 0.57), blood pressure and angiotensin II (diastolic: r = -0.7; systolic: r = -0.48), and exchangeable body sodium and renin activity (r = -0.5). In conclusion, in this study of IDDM patients with nephropathy and high normal or mildly hypertensive blood pressure, a difference in sodium intake of about 100 mmol/day for a period of 4 weeks led to a slight reduction of clinic diastolic blood pressure. Studies including larger numbers of patients with various stages of nephropathy and hypertension are needed to definitely clarify the effects of sodium restriction in IDDM.
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PMID:Effects of dietary sodium on blood pressure in IDDM patients with nephropathy. 863 74

Hypertension is both an exacerbating factor for, and a consequence of, diabetic renal disease. In diabetic patients, hypertension is associated with increased total body sodium secondary to impaired renal excretion, and increased vascular reactivity, notably to catecholamines and angiotensin II. The mechanisms causing these changes are discussed. Control of hypertension will slow the progression of diabetic renal disease and the inexorable decline in GFR. A number of studies now suggest that in proteinuric IDDM and NIDDM patients angiotensin converting enzyme inhibitors (ACE-I) may have additional reno-protective effects in addition to their hypotensive action. In addition ACE-I will reduce proteinuria and delay the onset of diabetic nephropathy in normotensive microalbuminuric IDDM and NIDDM patients. Use of ambulatory blood pressure monitoring indicates that such patients may not be truly 'normotensive'. On-going studies seem to suggest that the most reno-protective blood pressure is the lowest one achievable, as long as the patient remains asymptomatic. Further studies are required to assess the impact of blood pressure control, and especially ACE-I, on the incidence of end-stage renal failure. In addition, more direct comparisons between different pharmacological agents in early diabetic renal disease would be useful.
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PMID:The management of hypertension in diabetes: with special reference to diabetic kidney disease. 873 20

Diabetic nephropathy can be regarded mainly as a type of microangiopathy, but is a disease that may also include aspects of macroangiopathy. This is especially true of renal disease in non-insulin dependent diabetes mellitus (NIDDM), which is characterized not only by diabetic glomerulosclerosis, but also by atherosclerosis. We performed morphological studies on the kidney, using computed tomography (CT), focusing on such points as: (1) abdominal aortic calcifications at the level of kidney, (2) calcifications in the renal artery, and (3) wedge-shaped defects on the renal surface. We noted that these findings became more prominent in NIDDM patients during end-stage renal failure than during normal renal function, and were significantly more common in those two NIDDM groups than in age-matched nondiabetic patients without hypertension, hyperlipidemia or gout. NIDDM patients exhibited these features more frequently than IDDM patients.
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PMID:[Computed tomographical evaluation of diabetic nephropathy]. 875 67

The aim of study was to analyse factors that modified the survival time of 125 patients with diabetes mellitus and 121 patients with normal tolerance glucose to whom amputations of a lower limb in consequence of gangrene were performed. The prospective study were started on 5th January 1989 and finished 31st December 1993. Among the examined patients with NIDDM were 66 men in the age from 53 to 88 years (mean age 66.8 +/- 8.5 (+/-SD) years) and 48 women in the age from 58 to 91 years (mean age 71.8 +/- 9.1 years). Among the examined patients with IDDM were 6 men in the age from 40 to 65 years (mean age 55.7 +/- 9.7 years) and 5 women in the age from 34 to 72 years (mean age 53.7 +/- 13.6 years). The mean duration of NIDDM among men was 14.1 +/- 8.6 years, among women - 13.6 +/- 10.2 years and the mean duration of IDDM among men was 26.1 +/- 6.7 years, among women-26.0 +/- 10.8 years. In that period among patients with diabetes mellitus 80 patients died (64 percent), and among patients with normal glucose tolerance-died 39 patients (32 percent). In the analysis of survival time of patients with diabetes mellitus after nontraumatic amputation of a lower limb the following factors were the essential predictors of death: age (p = 0.0001), duration of diabetes (p = 0.03), arterial hypertension (p = 0.006), peripheral arterial disease (p = 0.0007), diabetic nephropathy (p = 0.0065). Among patients with normal tolerance glucose only the age was the essential predictor of death (p = 0.0001). The necessity of performance of amputation of a lower limb among patients with diabetes mellitus provides information on unsuccessful course of disease.
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PMID:[The fate of patients with diabetes mellitus after amputation of a lower limb as a consequence of gangrene]. 875 41

A longitudinal study for six months was conducted to demonstrate the influence of enalapril therapy on microalbuminuria in a group of patients with IDDM without arterial hypertension. An evaluation was also considered of its possible activity on other biochemical parameters, particularly plasma lipid levels. Thirty-four patients with IDDM were selected, with a mean age of 26.1 +/- 7.2 years and a mean clinical course of 11.8 +/- 5.6 years. Arterial blood pressure (ABP) was confirmed lower than 140/85 mmHg in all cases. Patients were administered 5 mg/day of enalapril and if a decrease in microalbuminuria higher than 25% was not achieved at the end of the first month of therapy, the dose was doubled (10 mg/day). No significant differences were found in ABP and in HbA1c throughout the study period. Albumin excretion in the initial period was 125.1 +/- 79.28 mg/24 h, at one month in the follow-up 47.6 +/- 44.1 mg/24 h, at three months 23.8 +/- 18.1 mg/24 h, and at the end of the 6th month 15.33 +/- 6.9 mg/24 h, all differences being significant. Renal function parameters and Na+ and K+ measurements remained unchanged for the follow-up period. No significant changes were detected for lipid and lipoprotein values for the length of the study. We conclude that therapy with enalapril in insulin-dependent diabetic patients without hypertension has an important effect on microalbuminuria during the first month of therapy; a stabilization in the normal range was reached in the third and sixth months of follow-up. No changes in arterial blood pressure nor in renal function were observed. Plasma lipid values were in the normal range throughout the study. Therefore, treatment for microalbuminuria with the ACEI assayed was efficient, in absence of arterial hypertension and irrespective of the metabolic control obtained. Future long-term studies are needed to evaluate the possible delay in the emergence of renal insufficiency.
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PMID:[Effect of enalapril on microalbuminuria and lipid profile of normotensive type I diabetes mellitus patients]. 876 69

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

An increased activity of Na+/H+ antiport has been reported in leukocytes and fibroblasts from insulin-dependent diabetic (IDDM) patients with nephropathy. To test whether a similar abnormality is present in fibroblasts from non-insulin-dependent diabetic (NIDDM) patients with microalbuminuria and hypertension, we examined intracellular pHi and Na+/H+ antiport activity, using the pH sensitive dye 2', 7'-bis (2-carboxyethyl-5(6)-carboxyfluorescein (BCECF), in cultured skin fibroblasts obtained from 34 NIDDM patients, divided into four groups based upon whether they had microalbuminuria or hypertension, or both: Group 1, nine NIDDM patients with microalbuminuria and hypertension. Group 2, nine NIDDM patients with hypertension and normal albumin excretion rate. Group 3, seven NIDDM patients with microalbuminuria and normal blood pressure. Group 4, nine NIDDM patients with normal blood pressure and normal albumin excretion rate. Nine normal subjects served as control group. Resting pHi was more alkaline in fibroblasts from Group 1 (7.22 +/- 0.03; p < 0.05), Group 2 (7.21 +/- 0.02; p < 0.05) and Group 3 (7.19 +/- 0.02, p = 0.17) than in Group 4 and normal subjects. This was due to higher Vmax values of Na+/H+ antiport activity in cultured fibroblasts from Group 1 (52.1 +/- 5.3 mmol H+/min; p < 0.05), Group 2 (57.7 +/- 8.3; p < 0.05) and Group 3 (60.6 +/- 7.4, p < 0.05) than those from Group 4 (31.2 +/- 3.6) or control subjects (31.3 +/- 3.5). The intracellular pH for half-maximal activation, Hill coefficient and buffering power capacity was similar in all the groups. These data suggest that in vitro phenotypic abnormalities of long-term cultured fibroblasts from NIDDM patients with microalbuminuria and/ or hypertension are likely to be, at least in part, independent of the degree of metabolic control in vivo and to be an intrinsic feature of these cells.
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PMID:Abnormal Na+/H+ antiport activity in cultured fibroblasts from NIDDM patients with hypertension and microalbuminuria. 878 68

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