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Biomedical subjects

M Marre

Publications and source records attributed to M Marre.

At least 73 records · Page 4Linked to original sources
PubMed1997

Contribution of genetic polymorphism in the renin-angiotensin system to the development of renal complications in insulin-dependent diabetes: Genetique de la Nephropathie Diabetique (GENEDIAB) study group.

Diabetic nephropathy is a glomerular disease due to uncontrolled diabetes and genetic factors. It can be caused by glomerular hypertension produced by capillary vasodilation, due to diabetes, against constitutional glomerular resistance. As angiotensin II increases glomerular pressure, we studied the relationship between genetic polymorphisms in the renin-angiotensin system-angiotensin I converting enzyme (ACE), angiotensinogen (AGT), and angiotensin II, subtype 1, receptor-and the renal involvement of insulin-dependent diabetic subjects with proliferative retinopathy: those exposed to the risk of nephropathy due to diabetes. Of 494 subjects recruited in 17 centers in France and Belgium (GENEDIAB Study), 157 (32%) had no nephropathy, 104 (21%) incipient (microalbuminuria), 126 (25 %) established (proteinuria), and 107 (22%) advanced (plasma creatinine > or = 150 micromol/liter or renal replacement therapy) nephropathy. The severity of renal involvement was associated with ACE insertion/deletion (I/D) polymorphism: chi2 for trend 5.135, P = 0.023; adjusted odds ratio attributable to the D allele 1.889 (95% CI 1.209-2.952, P = 0.0052). Renal involvement was not directly linked to other polymorphisms. However, ACE I-D and AGT M235T polymorphisms interacted significantly (P = 0.0166): in subjects with ACE ID and DD genotypes, renal involvement increased from the AGT MM to TT genotypes. Thus, genetic determinants that affect renal angiotensin II and kinin productions are risk factors for the progression of glomerular disease in uncontrolled insulin-dependent diabetic patients.

Adult↗
PubMed1997

Microalbuminuria as a predictor of a drop in glomerular filtration rate in subjects with non-insulin-dependent diabetes mellitus and hypertension.

UNLABELLED: Hypertension and non-insulin-dependent diabetes mellitus (NIDDM) are two major risk factors for end-stage renal failure. The value of microalbuminuria (urinary albumin excretion [UAE]: 30-300 mg/24 h) as an indicator of the glomerular filtration rate (GFR) is not known in these patients. METHODS: The relationships between microalbuminuria and GFR in subjects with NIDDM and hypertension were studied cross-sectionally (Study I) and longitudinally (Study II). RESULTS: In study I, 205 NIDDM subjects with hypertension (151 with normoalbuminuria [UAE < 30 mg/24 h] and 54 with microalbuminuria) were studied. The GFR of subjects with normoalbuminuria (97 +/- 30 ml/min) (mean +/- SD), and microalbuminuria (97 +/- 27 ml/min; NS) were similar. Study II examined 51 of the subjects with normoalbuminuria and 21 with microalbuminuria 22 months (range 13-57) later. The GFR of subjects with microalbuminuria (-10 +/- 19 ml/min) declined more than in those with normoalbuminuria (+4 +/- 17 ml/min; Student's t-test: p = 0.0022). The predictive value of microalbuminuria for a drop in GFR was independent of the antihypertensive treatment used, the follow-up time, or changes in UAE. The only variable linked to GFR loss in subjects with microalbuminuria was an increase in diastolic blood pressure (p = 0.0298). CONCLUSION: Microalbuminuria is a risk factor for a drop in GRF in NIDDM subjects with hypertension, and a reduction in blood pressure is the only effective way to prevent a loss of GFR in subjects with microalbuminuria.

Albuminuria↗
PubMed1997

Multiple antibody status in type 1 diabetic patients and subjects at various risk with islet-cell antibodies.

The frequency of 37/40 kD antibodies and their association with other pancreatic humoral markers were studied in 109 recently diagnosed Type 1 diabetic patients and 116 subjects with islet-cell antibodies (ICA) at various risk for this disease (64 relatives of Type 1 diabetic patients, 23 schoolchildren with no family history of diabetes, and 29 patients with Graves' disease). At the time of diagnosis, 37/40 kD antibodies were detected in 45% of Type 1a and 77% of Type 1b diabetic patients (p = 0.03). Antibodies to glutamic acid decarboxylase (GAD) and/or 37/40 kD were present with the same frequency as ICA (86%). The frequency of 37/40 kD antibodies was not significantly different between the 3 groups at risk, in contrast with GAD antibodies which were found at a lower frequency in schoolchildren (p < 0.02). Frequencies of other pancreatic markers (ICA cross-reactive with mouse pancreas and insulin autoantibodies) and the combination of ICA with at least two other markers were significantly higher in relatives than in the other groups at risk (p < 0.02). Out of 116 ICA-positive non-diabetic subjects, 10 developed diabetes. All 10 displayed 37/40kD and/or GAD antibodies during the prediabetic phase. In 8 of these 10 patients, ICA was combined with at least two other markers, whereas this association was detected in only 17 of the remaining 106 subjects who did not progress to diabetes (p < 10(-4). Thus, 37/40 kD antibodies were found in about half of Type 1 diabetic patients, and with a higher-frequency in Type 1b than 1a. In ICA-positive non-diabetic subjects, our date confirm that a combination of multiple antibodies, including GAD antibodies and 37/40 kD antibodies, can enhance the predictive value for diabetes. Comparison of ICA-positive relatives of diabetic patients, schoolchildren and patients with Graves' disease revealed distinct frequencies and combinations of markers of diabetes. This might reflect different patterns of progression among these 3 groups.

Animals↗
PubMed1997

Proposed criteria for the diagnosis of diabetes: evidence from a French epidemiological study (D.E.S.I.R.).

The American Diabetes Association and a working group of the International Diabetes Federation and the World Health Organisation are considering the possibility of lowering the level of fasting glucose for diagnosis of diabetes from 7.8 mM to 7.0 mM (126 mg/dl) and adding a "hyperglycaemia" category (6.1-6.9 mM). This report studied the resulting change in the frequency of diabetes in the French D.E.S.I.R. cohort and evaluated cardiovascular risk factors according to the proposed limits. The frequency of treated diabetes was 1.0% in this cohort of more than 5,000 French men and women 30 to 64 years of age, 0.7% had a fasting glucose > or = 7.8 mM versus 1.6% for the proposed > or = 7.0 mM. Using the new criteria, 3.8% of men and 1.6% of women would be diabetic. For many cardiovascular risk factors, men with fasting glucose > or = 7.8 mM had a significantly higher risk than those in the (7.0-7.7 mM) range, whereas no significant differences were found for women. There were few differences between the (7.0-7.7 mM) and (6.1-6.9 mM) ranges, but highly significant differences were apparent for both sexes between the normoglycaemic (< 6.1 mM) and hyperglycaemic (6.1-6.9 mM) categories. The percentage of men with two or more of ten risk factors increased with fasting glucose: 36% in the normoglycaemic (< 6.1 mM) and 49% in the hyperglycaemic (6.1-6.9 mM) categories; 73% with fasting glucose in (7.0-7.7 mM) versus 90% with fasting glucose > or = 7.8 mM. In women, the corresponding percentages were lower: 26% and 60%, 32% versus 64% respectively. The major increase in cardiovascular risk factors would appear to occur at 6.1 mM, for men, whereas the increase in the combination of risk factors was at the more conservative cut-off of 7.0 mM.

Adult↗
PubMed1996

[Nephropathy in non-insulin-dependent diabetics].

In the USA, diabetic nephropathy is involved in 34% of cases of end stage renal failure. In Europe, five-year survival of diabetics with end renal failure is 31%, compared with 55% in the non diabetic population. Three phenomena are involved in the development of nephropathy in non-insulin-dependent diabetic patients: glomerular hyperfiltration, elevation of urinary albumin excretion and high blood pressure, the latter sometimes being present before the discovery of diabetes. Even if control of blood sugar is improved, various prospective studies have failed to demonstrate any benefic effect in terms of reducing renal failure in non-insulin-dependent diabetic patients. Some data indicate that angiotensin-converting enzyme inhibitors can reduce the amount of proteinuria and slow the progression of diabetic nephropathy in insulin-dependent diabetic patients, but data remain controversial in non-insulin-dependent diabetic patients. Specifically, in these patients, there is no evidence pointing to an advantage of lowering blood pressure with angiotensin converting enzyme-inhibitors to reduce morbidity or mortality.

Diabetes Mellitus, Type 2↗
PubMed1996

Differential beta-cell response to glucose, glucagon, and arginine during progression to type I (insulin-dependent) diabetes mellitus.

Acute insulin responses to glucose (AIRG), glucagon (AIRGln), and arginine (AIRArg) were evaluated prospectively in nine subjects positive for islet-cell antibodies (ICAs) who later progressed to type I diabetes or impaired glucose tolerance (IGT) (progressors), 64 ICA-positive subjects at risk who did not develop type I diabetes, 365 ICA-negative relatives of diabetic patients who also remained free of the disease, and 89 control subjects. Seven progressors already had a low AIRG at entry into the study, and the other two became low responders 3 to 9 months before diabetes or IGT, with a progressive decline of AIRG over serial intravenous (IV) glucose tolerance tests. At entry into the study, the group of progressors displayed lower AIRG, AIRGln, and AIRArg than the other three groups (P<.001). However, AIRArg was less altered than AIRG. During the course of the prediabetic phase, there was a progressive decline in AIRG and AIRGln analyzed as a function either of time (P<.006) or of basal glycemia (P<.05), ie, two different ways of estimating worsening of the disease process. Conversely, there was no significant decrease in AIRArg with time or with increasing basal glycemia, so that AIRArg was not totally blunted in these prediabetic subjects even a few months before the onset of diabetes. The persistence of a substantial response to arginine, ie, higher than the fifth control percentile, even at a late stage, was confirmed in five of nine diabetic patients tested either at onset of the disease or during non-insulin-receiving remission. Whereas AIRG deteriorates during prediabetes, AIRArg appears to be less altered with time and increased basal glycemia, remaining substantial even at the onset of the disease. This reinforces the supposition that the prediabetic state may be associated with a glucose-specific beta-cell functional abnormality in addition to a decreasing beta-cell mass.

Adolescent↗
PubMed1996

Loss of the nocturnal decline in blood pressure in subjects with essential hypertension and microalbuminuria.

BACKGROUND: Microalbuminuria, a marker of early renal damage, predicts mortality in non-diabetic subjects. The loss of circadian blood pressure regulation is associated with the severity of essential hypertension and has been reported in hypertension due to renal disease. We therefore looked for a possible link between microalbuminuria and the smaller decrease in nocturnal blood pressure that occurs in essential hypertension.METHODS: The 24 h ambulatory blood pressure of 52 subjects with essential hypertension was measured and their urine tested for microalbuminuria (urinary albumin excretion of 30-300 mg/24 h). RESULTS: The subjects with (n = 10) and without (n = 42) microalbuminuria were comparable in clinical characteristics, antihypertensive treatments and serum creatinine. They had significantly different night-time systolic, diastolic and mean blood pressure decreases on ambulatory blood pressure monitoring. Two-factor analysis of variance showed that the day-night blood pressure decrease was linked to microalbuminuria status. The day-night blood pressure change of subjects with microalbuminuria differed from that of subjects without microalbuminuria independently from the daytime blood pressure level. CONCLUSION: Subjects with essential hypertension and microalbuminuria show a loss of nocturnal blood pressure decline. Whether microalbuminuria indicates a subtype of essential hypertension due to renal disease or severe hypertension with early renal damage remains to be clarified.

Journal Article↗
PubMed1996

[Decrease of nocturnal blood pressure in type II diabetic subjects with microalbuminuria].

The aim of this study was to evaluate the circadian blood pressure variations in subjects with or without microalbuminuria (Urinary Albumin Excretion (UAE) between 30 and 300 mg/24 h. Forty-nine non-insulin dependent diabetic subjects with essential arterial hypertension and without proteinuria (UAE < 300 mg/24 h) were consecutively recruited. Systolic (SBP) and Diastolic Blood Pressure (DBP) have been measured using a SpaceLabs 90207 ambulatory blood pressure monitor, every 15 minutes during daytime (7:00 a.m. to 22:00 p.m.) and every 30 minutes during nighttime (22:00 p.m. 7:00 a.m.). UAE has been measured by nephelometry on three 24 h urine collections. The group with microalbuminuria (n = 16) was not different from the group with normoalbuminuria (n = 33) for age, sex ratio, body mass index, known diabetes duration, proportion of anti-hypertensive treatment, serum creatinine and HbA1c. Daytime blood pressures (SBP/DBP: 144 +/- 15/83 +/- 8 vs 137 +/- 13/84 +/- 9 mmHg) and nighttime DBP (75 +/- 7 vs 74 +/- 9 mmHg) were comparable between both groups. In contrast, the nighttime SBP was higher in subjects with microalbuminuria than in those without (139 +/- 17 vs 129 +/- 17 mmHg; p = 0.016). If dippers are the subjects with a nocturnal blood pressure reduction (SBP and/or DBP) below 4%, there is a relationship between "non dippler" subjects and those with microalbuminuria (Chi-squared test = 5.67; p = 0.017). In conclusion, hypertensive non-insulin dependent diabetic subjects with microalbuminuria have a loss of nocturnal blood pressure decrease.

Aged↗
PubMed1995

Relationship between fat intake and glomerular filtration rate in normotensive insulin-dependent diabetic patients.

Glomerular hyperfiltration is a candidate marker for diabetic nephropathy in insulin-dependent diabetic patients since it can reflect elevated glomerular capillary pressure, a cause of glomerulosclerosis. We studied the potential contribution of several dietary components to glomerular hyperfiltration during a cross-sectional study of 110 consecutive normotensive, non-proteinuric insulin-dependent patients with respect to glomerular filtration rate (GFR) and food intake. GFR was measured using the 51Cr-EDTA plasma disappearance technique. Glomerular hyperfiltration was defined as GFR > 137 ml.min-1 1.73 m-2 (mean +2 SD of age-matched healthy controls). Food intake was recorded with a computer-assisted programme. Thirteen patients displaying glomerular hyperfiltration ingested more protein (1.60 +/- 37 vs 1.38 +/- 0.34 g.kg-1 body weight.day-1; p = 0.032) and more fat (1.70 +/- 0.54 vs 1.39 +/- 0.44 g.kg-1 body weight.day-1; p = 0.022) than other subjects, although their total energy intakes were similar. Univariate regression analysis showed that GFR was positively related to both protein (r = 0.28; p = 0.003) and fat (r = 0.25; p = 0.007) intakes and negatively related to age (r = -0.29; p = 0.002). Stepwise multivariate regression analysis indicated 2 independent determinants for GFR: age (F = 15.26) and fat intake (F = 13.15). Excess fat intake may contribute to glomerular hyperfiltration in insulin-dependent diabetes.

Adolescent↗
PubMed1995

[Prevalence of microalbuminuria in French type 2 diabetics followed by their general practitioner].

Microalbuminuria is a risk marker for cardiovascular morbidity and mortality in Type 2 diabetes. We studied microalbuminuria among French Type 2 diabetic patients in general practice, because we set-up a trial using cardiovascular events as end-points. Two thousand twenty four volunteer patients were studied for Urinary Albumin Concentration (UAC) during outpatient visit to general practitioners. The UAC was measured on first samples. If UAC was positive (> or = 20 mg/l), a second sample was requested. If UAC was positive two times, persistently elevated UAC was identified (micro or macroalbuminuria). Clinical characteristic, cardiovascular antecedents and risk factors were studied. One hundred five first samples were excluded due to urinary infection; 1,217 others displayed normal UAC (< 20 mg/l); 63.4%; group N), 557 microalbuminuria (20-200 mg/l; 29.0%, group mu), and 145 others macroalbuminuria (> 200 mg/l; 7.6%; group M). Among subjects with positive first sample, 26.5% had persistent albuminuria. There was no intergroup difference for age, but males were more frequent in groups mu or M than N (p < 10(-4)). Blood pressure and body mass index varied between groups. Smokers and alcoholic subjects were more frequent in groups mu and M than N (p = 0.037 and p = 0.0003 respectively), as were cases with myocardial infarction (p = 0.0026), lower limb arteritis (p < 10(-4)), and laser-treated diabetic retinopathy (p = 0.0002). Antihypertensive treatments were taken by 61% of the subjects. Elevated UAC (micro or macroalbuminuria) is frequent among french Type 2 diabetic patients cared by their general practitioners, and is associated with a high cardiovascular risk profile.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Value of ambulatory blood pressure monitoring in type I (insulin-dependent) diabetic patients with incipient diabetic nephropathy.

Ambulatory blood pressure monitoring (ABPM) is currently proposed for measuring blood pressure in type I, insulin-dependent diabetic subjects with incipient diabetic nephropathy. However, the value of this method, in comparison with conventional ones in detecting blood pressure differences between normotensive type I, insulin-dependent diabetic subjects with or without microalbuminuria, is questionable. We obtained systolic, diastolic, and mean blood pressures (SBP/DBP/MBP) in 10 hospitalized normotensive type I, insulin-dependent diabetic subjects with microalbuminuria, and in 29 others without, using a mercury sphygmomanometer (method 1) and an automatic device (Dinamap; method 2) to obtain morning (9 to 11 AM) measurements, and ABPM (SpaceLabs 90207; method 3) to obtain daytime (7 AM to 10 PM) and nighttime (10 PM to 7 AM) measurements. During the daytime, SBP/DBP/MBP values were higher in microalbuminuric than in normoalbuminuric patients, whatever the blood pressure measurement method used (P = .034/.061/.033, two-factor ANOVA). Analysis of 24-h ABPM also showed higher SBP/DBP/MBP in microalbuminuric than in normoalbuminuric patients (P = .022/.040/.016), and demonstrated a defect in nocturnal SBP decrease in microalbuminuric compared with normoalbuminuric patients (P = .028). Stepwise multiple regression analysis indicated nocturnal SBP as the only independent factor determining for microalbuminuria (F = 6.72). Thus ABPM, in relation to other methods, indicates above all that the most relevant blood pressure change in type I insulin-dependent diabetic subjects with microalbuminuria is a defect in nocturnal SBP decrease.

Adult↗