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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In non-insulin-dependent diabetes mellitus (NIDDM) patients, microalbuminuria predicts early mortality, predominantly from cardiovascular disease. Increased free radical activity and abnormalities in hemostasis have been implicated in the development of vascular disease. Therefore, we measured markers of free radical activity (nonperoxide-conjugated diene isomer of linoleic acid [PL-9,11-LA'] and lipid peroxides expressed as malondialdehyde [MDA]) along with the hemostatic variables: fibrinogen, von Willebrand factor (vWf), plasminogen activator inhibitor (PAI-1), tissue plasminogen activator (t-PA), and plasmin activity (B beta 15-42) in 24 NIDDM patients (12 patients with microalbuminuria and 12 without microalbuminuria) and in 12 age-matched control subjects. There were no differences in linoleic acid (PL-9,12-LA) concentrations between the three groups. PL-9,11-LA' was elevated in the microalbuminuric patients compared with control subjects (P less than 0.05), but there was no difference between the two diabetic groups. MDA was elevated in the microalbuminuric diabetic patients compared with those patients without microalbuminuria (P less than 0.05) and control subjects (P less than 0.001). MDA was also increased in the patients without microalbuminuria compared with control subjects (P less than 0.01). Except for B beta 15-42, all the hemostatic variables were increased (P less than 0.05) in the diabetic patients compared with control subjects. The microalbuminuric diabetic patients had further increases in vWf (P less than 0.03) and t-PA (P less than 0.03) compared with patients with microalbuminuria. Our study suggests that there is an increase in free radical activity and abnormalities in hemostatic variables favoring a hypercoagulable state in NIDDM, especially in those with microalbuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Free radical activity and hemostatic factors in NIDDM patients with and without microalbuminuria. 162 64

The standard risk factors--dyslipidaemia, hypertension and smoking--provide little help in explaining the raised cardiovascular risk in diabetes. It can be calculated that intervening for disturbances of these risk factors could do little to rectify the loss of life expectancy of around 10 years for a middle-aged diabetic man. Three new risk factors are discussed, which together may contribute to some of the excess cardiovascular risk in diabetes. Plasminogen activator inhibitor is an inhibitor of fibrinolysis which is elevated in concentration in diabetic subjects, and may increase both the incidence of thrombotic events and the risk of reinfarction after the initial infarct. Recent work also suggests that high activity of this substance may impair pharmacological fibrinolysis. Proinsulin-like molecules are elevated in concentration in diabetic patients and correlate with levels of a number of other risk factors. Whilst these correlations may represent cause and effect for plasminogen activator inhibitor, there is no evidence that changes in levels of proinsulin-like molecules influence levels of other risk factors. Microalbuminuria provides a powerful indicator of cardiovascular risk in both diabetic and non-diabetic subjects, but whilst the mechanisms for this association are unclear, they are again unlikely to be mediated through changes in levels of standard risk factors. Recent observations of an association between short stature and microalbuminuria suggest that intrauterine or early infant nutrition may represent a common antecedent, these having also been shown to predict both components of the insulin resistance syndrome and cardiovascular disease in adult life.
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PMID:Coronary heart disease in diabetes mellitus: three new risk factors and a unifying hypothesis. 760 43

Microalbuminuria, i.e., slightly elevated urinary albumin excretion rate (UAER), notifies increased risk for atherosclerotic disease and may reflect an early generalized vascular abnormality in healthy subjects. This study was designed in order to examine whether such abnormality is associated with a shift of the haemostatic balance in prothrombotic direction. The following haemostatic factors were measured in two representative groups of clinically healthy subjects, 28 with microalbuminuria (UAER of 6.6-150 micrograms/min) and 60 age- and sex-matched controls with normoalbuminuria (UAER < 6.6 micrograms/min): Coagulation factors: blood platelet count and mean volume, plasma Factor VII antigen concentration and coagulant activity, and plasma concentrations of prothrombin fragment 1 + 2, thrombin-antithrombin III complexes, fibrinogen, and fibrinopeptide A; fibrinolytic and endothelial factors: plasma concentrations of tissue plasminogen activator antigen and plasminogen activator inhibitor type 1 antigen; and endothelial factor: plasma von Willebrand factor antigen concentration. The fibrinolytic and endothelial factors were measured both before and after 10 minutes of venous occlusion of the arm. None of the haemostatic factors were significantly altered in the microalbuminuric group. Plasma fibrinogen concentration tended to be elevated but not statistically significant ((mean (95% C.I.) 7.8 (7.2-8.3) vs. 7.2 (6.9-7.5) mumol/l; p < 0.1). Neither did any of the haemostatic factors correlate with UAER in regression analyses. It is concluded that the haemostatic balance is unaltered in healthy subjects with microalbuminuria. It is unlikely that a prothrombotic state is present as an intermedial factor early in a causal chain between microalbuminuria and atherosclerotic vascular disease.
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PMID:Aspects of haemostatic function in healthy subjects with microalbuminuria--a potential atherosclerotic risk factor. 777 57

Morbidity and mortality through coronary atherosclerosis are higher in Type 2 diabetic patients than in nondiabetic subjects, roughly by a factor of 2 in males and 3 in females. Methodological problems in attempting to weigh the relative effects of each factor make it difficult to accurately interpret the numerous epidemiological data already available. Three issues are discussed here:--Do diabetics have more "classic" risk factors than nondiabetics? The incidence of hypertension, lipid disorders, and even smoking is practically consistently higher in diabetics, with "diabetic" lipid disorders (decreased HDL cholesterol and hypertriglyceridemia) topping the list.--Do diabetics have specific risk factors which could explain the observed increase in coronary morbidity and mortality? The answer would appear to be yes, as patent microalbuminuria--between 30 and 300 mg/24 hours--is found, as well as retinopathy and an increase in fibrinogen and PAI1 plasminogen activator inhibitor. Recent genetic studies have highlighted the role of Lp (a), and particularly that of angiotensin converting-enzyme gene polymorphism (DD allele).--What are the respective roles of hyperglycalmia and elevated levels of circulating insulin? In contrast to the importance of insulin in nondiabetics as demonstrated in longitudinal studies, insulin appears to play a marginal or even nil role in diabetics once the disease is established. It is probably glycaemia itself which remains the fundamental factor, even though the mechanisms leading from hyperglycemia to macrovascular complications remain unknown.
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PMID:[Cardiovascular risk factors in type 2 diabetes]. 782 79

The major risk factors appear to explain only a small proportion of the excess risk of coronary heart disease in patients with Non-Insulin-Dependent Diabetes Mellitus (NIDDM). Among novel risk markers that have been-proposed to explain the susceptibility of NIDDM subjects to coronary heart disease are insulin resistance, elevated concentrations of proinsulin-line molecules, plasminogen activator inhibitor, and microalbuminuria. Several prospective studies have shown that hyperinsulinemia predicts coronary heart disease, perhaps independently of established risk factors. Some of this excess risk may be through the dyslipidemia, or the elevation in activity of plasminogen activator inhibitor, an inhibitor of fibrinolysis, which relate to hyperinsulinemia. However proinsulin-like molecules show similar relationships with both risk factors and with prevalent coronary heart disease as does insulin, despite low concentrations of these molecules in the circulation, suggesting a causative relationship is improbable. Furthermore, the link between insulin resistance and microalbuminuria, a powerful predictor of vascular disease in its own right, is poorly understood through known mechanisms. This clustering leads to the possibility of a link with coronary heart disease through other mechanisms. It is proposed that the pathogenesis of this link is endothelial dysfunction, which may predicate both impaired insulin action, through effects of blood flow and insulin transport, and the associated dyslipidemia, impaired fibrinolysis, microalbuminuria, and atherogenesis. In terms of etiology, the links of all these risk factors with evidence of growth retardation in early life may suggest a role of the thirfty phenotype hypothesis-impaired organogenesis resulting from poor maternal nutrition during pregnancy.
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PMID:The Deidesheimer meeting: significance of classical and new risk factors in non-insulin-dependent diabetes mellitus. 910 95

Increased plasma plasminogen activator inhibitor type 1 (PAI-1), coagulation factor VII (FVII) and fibrinogen levels have been recognized as risk factors for cardiovascular disease. Because a substantially high incidence of cardiovascular disease has been reported in diabetic patients with nephropathy compared with those without nephropathy, we measured plasma levels of PAI-1, FVII activity and fibrinogen in non-insulin-dependent diabetic patients (NIDDM) with normoalbuminuria (without nephropathy), microalbuminuria (incipient nephropathy) and macroalbuminuria (overt nephropathy). PAI-1 and FVII levels were significantly increased in NIDDM with overt nephropathy compared with NIDDM without nephropathy. Fibrinogen levels were comparable between the patients with normo-, micro- and macro-albuminuria. Univariate regression analysis indicated that PAI-1 and FVII levels were significantly correlated with the albumin excretion rate (AER) in urine. PAI-1, FVII and fibrinogen levels were significantly correlated with the degree of insulin resistance estimated by the steady state plasma glucose concentration (SSPG) during the continuous infusion of glucose, insulin and octreotide. PAI-1 levels were correlated with plasma triglyceride (TG) levels. Multiple regression analysis revealed that AER was significantly associated with PAI-1 and FVII levels, whereas TG lost significant correlation with PAI-1 when AER, SSPG and plasma TG were entered as independent variables. SSPG retained an independent correlation with fibrinogen, PAI-1 and FVII levels. These results suggest that elevated plasma levels of PAI-1 and FVII in NIDDM patients with nephropathy are directly associated with renal damage, whereas insulin resistance widely regulates hemostatic components in NIDDM patients, irrespective of the presence of nephropathy.
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PMID:Albuminuria is directly associated with increased plasma PAI-1 and factor VII levels in NIDDM patients. 918 10

Vascular complications are the main cause of morbidity in diabetes mellitus. To evaluate lipoprotein and hemostatic parameters and their relationship with clinically detectable microangiopathy, we studied 58 insulin-dependent diabetes mellitus patients and 60 controls matched for age, sex, and body mass index. Thirteen patients presented clinically detectable microangiopathy (8 retinopathy and 5 both retinopathy and microalbuminuria). A cross-sectional study of lipid profile, coagulation parameters, and a flow-cytometric evaluation of tissue factor expression in normal monocytes induced by patient plasma were performed. Patients were re-evaluated for microangiopathy in a 3-year median follow-up. Patients showed triglyceride enrichment in low (P = 0.00002) and high density lipoproteins (P = 0.004) and increased levels of D-dimer (P < 0.00001), prothrombin fragment 1 + 2 (P < 0.00001), and thrombin-antithrombin III complex (P = 0.0001). Patients with clinically detectable microangiopathy had increased type 1 plasminogen activator inhibitor (P = 0.00001), thrombomodulin (P = 0.02), and induced monocyte tissue factor expression (P < 0.00001). Nine patients developed clinically detectable microangiopathy in the follow-up and the only predictive variable was increased induced tissue factor expression. In conclusion, in these patients elevated thrombin and fibrin generation reflects a hypercoagulable state but clinically detectable microangiopathy seems related to endothelial cell injury markers and to increased induced tissue factor expression on monocytes.
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PMID:Thrombomodulin and induced tissue factor expression on monocytes as markers of diabetic microangiopathy: a prospective study on hemostasis and lipoproteins in insulin-dependent diabetes mellitus. 932 50

The high incidence of cardiovascular morbidity and mortality in non-insulin-dependent diabetes mellitus with albuminuria cannot be fully explained by the presence of standard cardiovascular risk factors. We assessed some pathogenic factors of diabetic vascular atherosclerotic damage in 72 non-insulin-dependent diabetes mellitus patients controlled by diet alone and 60 healthy controls. Our study aim was to assess the early onset of these alterations and to correlate them with the presence of microalbuminuria. We determined their incidence in two carefully selected groups of diabetic patients without clinical signs of cardiovascular risk and complications, where diet alone achieved glycometabolic balance. Microalbuminuric patients had an alterated oxide-reductive balance and elevated values of plasminogen activator inhibitor, tissue plasminogen activator, von Willebrand factor, endothelin-1 and betathromboglobulin compared with the normoalbuminuric diabetics and controls. Our findings support the hypothesis that a state of endothelial dysfunction characterized by altered oxide-reductive balance, modified hemostasis and changes in the endothelial barrier properties occurs much earlier in non-insulin-dependent diabetic patient especially in diabetics with microalbuminuria. In addition, alterations in the oxide-reductive balance, and hemostasis occur early and may be an underlying cause of microangiopathic complications in microalbuminuric diabetics.
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PMID:Early endothelial alterations in non-insulin-dependent diabetes mellitus. 968 51

Angiotensin converting enzyme inhibitors (ACE-I) are a mainstay for the treatment of heart failure, and of diabetic microalbuminuria. Recently ACE-I have been found to decrease plasma levels of circulating vascular cell adhesion molecule-1 (cVCAM-1) in patients with congestive heart failure. As increased cVCAM-1 levels are pathognomonic for diabetics with microangiopathy, we investigated the effects of ACE-I on plasma levels of cVCAM-1, intercellular adhesion molecule (cICAM-1), and cE-selectin in microalbuminuric diabetics. In addition, the effects of ACE-I on plasma levels of plasminogen activator inhibitor (PAI-1) and of tissue plasminogen activator (TPA) were studied. Fosinopril (10 mg/day) was administered over 12 weeks to 11 microalbuminuric patients with non-insulin-dependent diabetes mellitus (NIDDM). As expected, baseline plasma concentrations of cE-selectin, cICAM-1, and cVCAM-1 were markedly higher in patients than in healthy control subjects (n = 82; P < .001). PAI-1 levels in NIDDM were similar to those in control subjects, whereas TPA levels were about 25% lower in patients than in control subjects (P = .013). Serum levels of cVCAM-1 decreased by -19% (CI: -25% to -13%) after treatment with fosinopril (P = .003) and were no longer different from those of the control group. In contrast, plasma levels of cE-selectin, cICAM-1, PAI-1, and TPA were unaffected. As expected microalbuminuria decreased by -44% (CI: -65 to -22; P = .004). In conclusion, fosinopril lowered cVCAM-1 levels along with microalbuminuria in NIDDM. This may represent a novel mechanism of action of ACE-I in diabetes-associated endothelial dysfunction. Whether decreased VCAM-1 expression is responsible for the observed reduction in microalbuminuria, deserves further investigation.
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PMID:Fosinopril decreases levels of soluble vascular cell adhesion molecule-1 in borderline hypertensive type II diabetic patients with microalbuminuria. 1009 Mar 51

The aim of our study was to estimate selected parameters of hemostasis and fibrinolysis in diabetic patients with vascular complications and obesity. The investigation was carried out in 23 type 1 diabetic subjects aged 17-56 ys, in 25 type 2 diabetic patients aged 41-69 ys and in 38 healthy persons: 16 "young"--aged 32.5 +/- 13.2 ys and 22 "old"--aged 56.2 +/- 9.4 ys. The following parameters were determined: glycaemia, HbA1c, blood level fibrinogen, euglobulin clot lysis time, plasminogen activator inhibitor (PAI-1) activity, microalbuminuria, triglyceride, total, HDL- and LDL-cholesterol concentration. Plasma fibrinogen level was elevated in type 2 diabetic subjects, and the highest concentrations were noted in patients with retinopathy or arterial hypertension, in overweight persons and--surprisingly--in type 1 diabetic subjects with nephropathy and coronary vascular disease (CVD). There were also positive correlations between fibrinogen level and systolic blood pressure (r = 0.3413, p < 0.02), diastolic blood pressure (r = 0.3809, p < 0.002) and microalbuminuria (r = 0.3552, p < 0.05). The mean euglobulin clot lysis time was prolonged in type II diabetics in comparison to the control group, especially in obese subjects. The highest activity of PAI-1 was found in overweight controls (28.87 +/- 6.24 Au/ml, p < 0.002). PAI-1 activity was also slightly increased in type 1 diabetic patients, especially with the symptoms of diabetic neuropathy, nephropathy or CHD, in comparison to the other groups. Our results seem to confirm the disturbed balance between coagulation and fibrinolysis--towards and increased risk of a prothrombotic state --in both--obese and diabetic patients--especially with advanced vascular complications.
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PMID:[Some parameters of hemostasis and fibrinolysis in diabetic patients]. 1010 28


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