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Introduction: Microalbuminuria is considered as a marker of endothelial dysfunction and is associated with an increase in cardiovascular risk. The aim of this study was to evaluate this parameter as a potential marker of artery rigidity and left ventricle (LV) function., Subjects and Methods: We included 375 subjects referred to a health assessment center. They were 228 men and 147 women aged in means of 52.7 and 53.1 years, respectively. Among this population, 57 had type 2 diabetes, 28 of them with hypertension, 65 were hypertensive but free of diabetes, and 39 were free of diabetes but exhibited a metabolic syndrome (NCEP-ATP III). Urinary albumin excretion rate (UAER) was determined. Artery rigidity was evaluated by pulse pressure of the brachial artery (plethysmographic method), pulse pressure of the radial artery and aorta and pulse wave velocity (PWV) measured by aplanation tonometry (SphygmoCor). LV afterload was appreciated by LV telesystolic pressure and coronary perfusion by the diastolic area/systolic area ratio for aortic pressure curve (Buckberg index)., Results: UAER correlated with PWV in the overall population (p<0.0001) and in the diabetic sub-group (p<0.001). In the overall population UAER correlated with LV telesystolic pressure (p=0.006) but not with Buckberg index. In the overall population and the diabetic subgroup, the artery rigidity indexes correlated strongly with LV telesystolic pressure, and radial and aortic pulse pressure correlated negatively with Buckberg index., Conclusion: These data suggest that 1) microalbuminuria may be considered as a marker of artery rigidity, in line with experimental data which indicate the deleterious role of endothelial dysfunction on artery compliance; 2) artery rigidity is a potent determinant of LV afterload and coronary perfusion, in particular in diabetic patients.

It is difficult to summarize in a few pages the wealth of information appeared during the year 2005 in the field of epidemiology and cardiovascular prevention. The general epidemiological data on the evolutionary tendencies of coronary mortality and morbidity make it possible to underline the effectiveness of the control of the great risk factors within the framework of the primary prevention. Although lipids and diabetes have still this year held the front of the scene through many trials, this analysis is also focused on smoking, subject more and more tackled in the cardiologic journals, and to which a larger attention should be paid in our daily practice. The Paris Prospective Study I brought new data concerning the early identification of the subjects at risk of sudden death, starting from the analysis of the evolution of heart rate profile during and after exercise. Is the concept of metabolic syndrome a phenomenon of mode or does it constitute in itself an autonomous prognostic factor beyond the risk related to the plurality of the factors which define it? The cardiologist will have to be interested more and more in the living conditions of his patients and in particular with the environmental factors such as the air pollution, who seems to have a considerable impact on the incidence of the acute coronary events. Lastly, the ADMA (asymmetric dimethylarginine), seems a possible new marker of cardiovascular risk, but its real prognostic interest remains to be defined.

A sympathetic hyperactivity is a common feature in hypertension, type 2 diabetes (T2D), ageing and obesity-induced hypertension. This increase in sympathetic activity may lead to an elevation of arterial rigidity. By contrast, cardiac parasympathetic impairment is observed in these pathologies. Recently we showed in a model of rats with massive obesity (ventromedial hypothalamic lesions) that an enhanced vagal activity may be protective against hypertension. The aim of the present study was to evaluate the influence of an increase in sympathetic activity and a change in vagal activity on arterial rigidity and hypertension in T2D patients. Fourteen hypertensive T2D patients aged 54 +/- 2 years were compared to 22 elderly normotensive subjects (75 +/- 1 years: 11 controls and 11 T2D) and 34 middle aged normotensive subjects (43 +/- 1 years; 17 controls and 17 T2D). Cardiovascular vagosympathetic activity was investigated by spectral analysis of heart rate (HR) and blood pressure (BP) (Finapres) during 6 min at a controlled breathing rate (12 cycles/min). BP and the low frequencies of systolic BP (LF-SBP) were significantly (p<0.01) higher in hypertensive T2D and elderly patients. Pulse pressure (PP) and the high frequencies of HR (HF-HR) were lower in hypertensive T2D patients. PP was positively correlated to LF-SBP (r=0.58; p=0.03) only in hypertensive T2D patients. Diastolic BP was negatively correlated to HF-HR in elderly control subjects (r=-0.63; p=0.03) but not in hypertensive T2D patients. The present results suggest that: sympathetic nervous system activity is enhanced in subjects over 70 years without any aggravating effect of T2D and in middle-aged hypertensive patients with type 2 diabetes; the increase in pulse pressure, an index of arterial rigidity, in elderly subjects may result from sympathetic override; the decrease in the cardiac sympathovagal balance, mainly due to a high vagal activity, may be protective against the occurrence of hypertension in patients with type 2 diabetes.

In diabetes, endothelium-dependent dilation of large and small coronary arteries is impaired, which results in a mismatch between myocardial metabolic demand and coronary blood flow. It has been proved that deferoxamine, an iron chelator that inhibits Fenton and Haber-Weiss reactions, restores a normal response to cold pressor test and flow increase in angiographically normal epicardial coronary arteries of diabetic patients. This result suggests that nitric oxide could be inactivated by reactive oxygen species. The aim of this study was to assess the effects of deferoxamine on coronary microcirculation vasomotion when myocardial oxygen demand is increased by sympathetic stimulation elicited by cold pressor test in type 2 diabetic patients. In 17 patients with angiographically normal coronary arteries and without any other coronary risk factors, coronary blood flow has been measured using quantitative angiography and intracoronary Doppler at baseline and during a cold pressor test, before and after intravenous administration of 500 mg deferoxamine. Increase in rate-pressure product, an estimate of myocardial metabolic demand, was similar before and after deferoxamine (+21.1 +/- 8.7% vs +20.5 +/- 8.9%, respectively), but coronary blood flow increase was significantly higher after deferoxamine (+6.3 +/- 12.9% vs +31.8 +/- 16.7%, respectively, p < 0.001), and coronary resistance was increased before deferoxamine and decreased after (+14.8 +/- 21.9% vs -7.9 +/- 10.9%, respectively, p < 0.001). Moreover, before deferoxamine, the negative correlation between coronary blood flow and rate-pressure product changes before deferoxamine (R = 0.518, P < 0.05) was turned in a positive relationship after deferoxamine (r = 0.546, p < 0.05). In conclusion, in type 2 diabetic patients, endothelium-dependent dilation of the coronary microcirculation is restored when iron-catalysed oxidative reactions are inhibited by deferoxamine, which restores the normal matching between myocardial oxygen demand and coronary blood flow.

Several studies have well demonstrated that obesity is associated with changes in cardiovascular vagosympathetic activity. The aim of the present work was to evaluate this activity in normotensive and in mildly hypertensive obese patients, and to correlate this activity with clinical and biological indexes of insulin resistance. Heart rate (HR) and systolic blood pressure (sBP) were examined by spectral analysis in 70 normotensive obese patients (group 1), 32 mildly hypertensive obese patients (group 2), and 21 controls. The high frequency peak of HR variations at a controlled breathing rate (vagal activity) was significantly reduced in both groups (p < 0.001). The mid frequency peak of sBP in the standing position (sympathetic activity) was similar in both groups and in the control group. In groups 1 and 2, the high frequency peak correlated negatively with age (p = 0.005 and 0.034 respectively). In group 1, the mid frequency peak correlated positively with fat mass, fasting plasma insulin and triglyceride levels, and insulin resistance index (p < or = 0.03). In group 2, the mid frequency peak correlated positively with fasting insulin and insulin resistance index (p = 0.006 and 0.007 respectively). This study shows that, in obese patients: 1. cardiac vagal activity is reduced in normotensive and mildly hypertensive subjects; 2. vascular sympathetic activity is unchanged in means but may be increased as a consequence of adiposity, hyperinsulinemia and insulin resistance, and this increase is likely to be involved in the increase of blood pressure.

An increase in arterial rigidity is associated with a poor cardiovascular prognosis. Several studies have suggested that an increase in sympathetic activity may be involved in essential hypertension. We have recently shown that vagal control of heart rate (HR) variations during standardised tests is altered in normotensive obese and diabetic patients. The aim of the present study was to compare cardiovascular vagosympathetic activity in obese and type 2 diabetic patients, either normotensive or hypertensive, and to investigate the relationship between pulse pressure (an index of arterial rigidity) and sympathetic activity in this population. Seventy normotensive obese and 32 mildly hypertensive obese patients, 18 normotensive type 2 diabetic patients and 14 mildly hypertensive type 2 diabetic patients were compared with 21 control subjects. Finapres studied HR and blood pressure variations. In the four groups, during a 6-min period at a controlled breathing rate, the high frequency peak of HR variations was significantly reduced (p < 0.001). The mid-frequency peak of systolic BP variations in the standing position, which depends on sympathetic activity, did not differ significantly between the four groups and control subjects. In obese and diabetic hypertensive patients, this peak correlated significantly with pulse pressure measured in the lying position (r = 0.379; p = 0.043 and r = 0.81; p < 0.0001, respectively). This study 1, confirms that vagal control of HR variations is reduced to a similar extent in obese and diabetic patients; and 2, suggests that cardiovascular sympathetic activity is relatively increased in these patients without significant difference between normotensive and hypertensive patients, but interestingly that the increase in arterial rigidity is associated with a higher sympathetic activity.

Cardiac autonomic neuropathy (CAN) is frequent in subclinical stages. Its prognostic value has been demonstrated. Cardiac autonomic neuropathy induces different functional cardiac changes, especially a reduction in left ventricular contractility and changes in ventricular repolarisation. It is also associated with changes in the daily variations in blood pressure. The association of CAN and silent myocardial ischaemia significantly worsens the prognosis. The investigation of CAN in the greatest number of diabetic patients is therefore justified. The study of heart rate variations during deep respiration, active orthostatism or Valsalva manoeuvre, is still the reference. This method is simple, reproducible and may be carried out in the clinical setting in 10 to 15 minutes. The results must be strictly interpreted with rigour with respect to age. Orthostatic hypotension is a late sign of sympathetic nervous system disease. Spectral analysis of blood pressure variations on orthostatism or the study of cutaneous blood flow during activating the sympathetic system tests of greater sensitivity, should be developed. The demonstration of subclinical CAN should lead to the careful use of drugs which may induce orthostatic hypotension and certain antiarrhythmics, to search for disorders of ventricular repolarisation and for silent myocardial ischaemia in diabetics with several risk factors.

Diabetes is a cause of serious myocardial disease related to an increased incidence of coronary artery disease, probably aggravated by cardiac autonomic neuropathy (CAN). In its incipient form, CAN hardly changes the sinus rhythm with an increase in nocturnal heart rate but without an appreciable effect on the indices of variability. In more advanced forms, "CAN+", there are not only changes in the heart rate variability but also in ventricular repolarisation. It is classical to underline the value of the corrected QT interval but this index has little real value. The "QT dispersion", comparing the duration of ventricular repolarisation on the surface leads, is no better a marker from the theoretical point of view. The dynamics of ventricular repolarisation on the other hand seem to be much more indicative of ventricular myocardial disease. They are studied by evaluating the QT-heart rate relationship and its increase distinguishes clearly CAN diabetics from CAN+ diabetics. In addition, in the latter subjects, diurnal physiological increase in the heart rate dependency of the QT interval (QT/RR slope) disappears or even inverse. It is probably this phenomenon which is responsible for the traditionally increased risk of ventricular arrhythmias and particularly sudden death in diabetics with autonomic neuropathy.

The rat with ventromedian hypothalamus lesions (VMH) is characterized by massive obesity, hyperinsulinemia, increase in parasympathetic tonus and sympathetic depression. The aim of this study was to examine in this model the hemodynamic changes and the baroreflex response and to compare the data with the evaluation of beta adrenergic sensitivity. In VMH rats and Sham operated rats hemodynamic parameters were followed until 8 weeks after operation. Heart rate (HR) and blood pressure (BP) were monitored each week during 24 hours by a telemetric system, a catheter being implanted in aorta. In VMH, HR was significantly lower by the first week (p = 0.02) and until the last measurement. Systolic BP increased progressively in the two groups but was higher in VMH only at 8 weeks (p = 0.03). Compared with Sham rats, 5 days after operation, the percentage of HR acceleration in response to atropine and isoprenaline was significantly higher in VMH, whereas HR response to sodium nitroprussiate was similar in the two groups. Plasma epinephrine and norepinephrine levels were significantly higher in VMH rats. The density of cardiac beta receptors decreased from 15 days to 3 months after operation, similarly in VMH and Sham rats. The affinity of cardiac beta receptors remained stable during the same period and very similar in VMH and Sham rats. This study suggests that in VMH rats 1. bradycardia results mainly from an increase in parasympathetic tone; 2. the increase in reflex tachycardia described in normal rats after insulin infusion needs a normal activity of the sympathetic nervous system; 3. catecholamine levels may be increased despite sympathetic depression, probably as a result of an increase in adrenomedullary secretion possibly due to endogenous hyperinsulinemia; 4. the lack of hypertension in this model including a massive obesity is likely to result from the proper vasodilatory effect of insulin.

A failure of coronary blood flow to increase during cold pressor test has been shown in patients with coronary atherosclerosis and impaired metabolic coronary vasodilatation in response to atrial pacing has been demonstrated in diabetic patients without significant epicardial artery stenoses. This study was designed to evaluate coronary microvascular adaptation to increased myocardial oxygen demand in response to sympathetic stimulation in diabetic patients with angiographically normal coronary arteries. Microvascular coronary adaptation to increased myocardial oxygen demand due to sympathetic stimulation evoked by the cold pressor test has been examined in 22 type 2 diabetic patients and in 15 control subjects with angiographically normal coronary arteries and no other risk factors. Coronary blood flow was calculated by measuring mean flow velocity in left anterior descending coronary artery by intracoronary Doppler and cross sectional area of the artery by digital angiography. Results show that despite a similar increase in rate-pressure product in the 2 groups (+22.6 +/- 12.4% in diabetic patients and +31.8 +/- 8.2% in control subjects, NS), coronary blood flow increase in left anterior descending artery was significantly lower in diabetic patients than in control subjects (+14.7 +/- 19.8% vs +75.5 +/- 13.5%, respectively, p = 0.0001). In addition, when there was a positive correlation between the 2 parameters in control subjects (R = 0.651, p < 0.01), there was no relationship in diabetic patients (R = 0.054). In conclusion, this study demonstrates that vasodilatation of coronary microcirculation in response to sympathetic stimulation evoked by cold pressor test is impaired in type 2 diabetic patients without epicardial artery lesions. This microvascular impairment during sympathetic stimulation may explain exercise-induced myocardial perfusion abnormalities observed in these patients and may impair microcirculatory coronary vasodilatation during current life stress episodes such as exercise, mental stress or cold exposure.

We have previously shown that alterations of vagal control of heart rate variations are found in more than half of non diabetic obese subjects (Int J Obes 1995) and are associated with a more severe insulin resistance in noninsulin dependent diabetic patients (Metabolism 1998). The aim of this study was to examine whether parasympathetic alterations are also associated with a more severe insulin resistance in non diabetic obese subjects. 245 obese subjects (BMI = 34.2 +/- 0.4 kg/m2) aged 38.6 +/- 0.8 years, with a normal oral glucose tolerance test were included. Parasympathetic activity was evaluated by heart rate variations during three standardised tests: Valsalva, deep-breathing and active lying-to-standing, with age being taken into account. The Valsalva maneuver was abnormal in 17.5%, the deep-breathing test in 18% and the lying-to-standing test in 30.3% of the cases. One hundred and thirty subjects (52.1%) had at least one abnormal test. Compared with those with three normal tests, the obese subjects with parasympathetic alterations had very similar BMI and blood pressure, but significantly higher values of heart rate (75.5 +/- 1.4 vs 71.3 +/- 1.1 beats/min, p = 0.02), fasting blood glucose (5.0 +/- 0.1 vs 4.8 +/- 0.1 mmol/L, p = 0.03) and plasma insulin (98 +/- 6 vs 82 +/- 4 pmol/L, p = 0.03). In the whole series of obese subjects, heart rate variations during the deep-breathing and lying-to-standing tests correlated negatively with blood glucose (p = 0.001 and p = 0.03 respectively), and during the deep-breathing test they correlated negatively with the waist/hip ratio (p = 0.004). This data suggests that cardiac parasympathetic alterations should take part in the insulin-resistance syndrome and might account for the poor cardiovascular prognosis linked to this syndrome.

Several epidemiological and experimental studies suggest that essential arterial hypertension is associated with hyperinsulinism and insulin resistance in obese subjects and also in subjects with normal body weight. Undernutrition remains frequent in adult Vietnamese people and mean body mass index is around 18.5 kg/m2 in Vietnam. The aim of this study was to look for insulin resistance in hypertensive Vietnamese subjects, despite a markedly lower BMI in Vietnam than in occidental countries. One hundred and eight hypertensive patients (51 men and 57 women) over 40 years (mean = 65.4 years) were compared with 36 healthy subjects (23 men and 13 women) over 40 years (mean = 63.8 years). Hypertensive patients had significantly higher BMI (20.5 +/- 0.3 (SEM) kg/m2 vs 18.4 +/- 0.4 kg/m2; p < 0.01), thicker triceps skinfold (1.26 +/- 0.07 cm vs 0.71 +/- 0.07 cm; p < 0.001) and not significantly different waist/hip ratio (0.88 +/- 0.01 vs 0.85 +/- 0.01). Blood glucose at fasting and 2 hours after 75 g glucose taken orally were similar in hypertensive and normotensive subjects. Plasma insulin at fasting and 2 hours after glucose were significantly higher in hypertensive patients (44.4 +/- 5.1 pmol/L vs 21.6 +/- 3.2 pmol/L; p < 0.05 and 271.1 +/- 21.6 pmol/L vs 139.1 +/- 15.2 pmol/L; p < 0.001). Thus, despite under-nutrition, hypertensive Vietnamese patients have a moderate but significant increase in BMI and fat mass without predominant abdominal localization, and a state of insulin-resistance, compared with normotensive healthy subjects.

Several studies suggest alterations of parasympathetic and sympathetic control in obesity. We have already shown that more than 40% of non diabetic obese subjects have alterations of parasympathetic control of heart rate (HR) variations. The present study aimed to investigate parasympathetic and sympathetic cardiovascular control by using spectral analysis. Sixty-two non diabetic obese subjects were compared to 38 sex-matched healthy controls. Spectral analysis was performed by Anapres system and identified two particular peaks: the one of high frequency (0.20-0.25 Hz) for heart rate variations during controlled breathing which depends on parasympathetic activity, the other of low frequency (around 0.10 Hz) for systolic BP variations in the standing position which mainly depend on sympathetic activity. In control subjects the amplitude of the high frequency peak (r = -0.556, p < 0.0001) but not the amplitude of the low frequency peak correlated negatively with age. In the obese subjects both the high and low frequency peaks correlated negatively with age (r = -0.249; p = 0.05 and r = -0.289, p = 0.036 respectively) and did not correlate with body mass index. The high frequency peak was significantly lower than in controls (4.80 +/- 3.37 (SD) vs 8.38 +/- 4.14; p < 0.0001). In the 25 obese subjects over 40 years the low frequency peak was also significantly lower than in controls (10.00 +/- 3.10 vs 11.95 +/- 4.25; p < 0.05). This study suggests that 1) age must be taken into account when interpreting the cardiovascular parameters under vagosympathetic control; 2) in non diabetic obese subjects vagal activity is decreased and in those over 40 years sympathetic activity is also decreased.

Unlabelled: Acetylcholine produces coronary artery (CA) constriction in diabetic patients suggesting an impairment of endothelium-dependent dilation. To examine the mechanism of this abnormal response. 2 physiological tests, i.e. cold pressor test (CPT) and coronary flow-increase induced by 10 mg papaverine (PAP) injection in the distal left anterior descending CA (dLAD), were performed before (1) and after (2) either i.v. L-arginine (L-arg, 625 mg/min x 10 min) or i.v. desferrioxamine (DFX, 50 mg/min x 10 min) in 15 normotensive nonsmoker diabetic patients with angiographically normal CA and normal cholesterol. Dimensions of the proximal LAD (pLAD) were measured by quantitative angiography. [table: see text] Before administration of L-arg or DFX, CPT induced a decrease of pLAD diameter, and PAP injection in dLAD dit not modify pLAD diameter. In the 7 diabetic patients receiving L-arg, responses to CPT and PAP were not modified. Conversely in the 10 patients receiving DFX, pLAD dilated in response to the 2 tests. Intracoronary isosorbide dinitrate, an endothelium-independent dilator, produced similar dilation in the 2 groups (+20 +/- 8% and +16 +/- 6%, respectively)., Conclusions: 1) responses of angiography normal CA to CPT and to flow increase are impaired in diabetic patients; 2) abnormal responses are not improved by L-arg suggesting that a deficit in substrate for NO synthesis is not involved; 3) DFX restores a vasodilator response to the 2 tests suggesting that inactivation of NO by superoxide radicals might be partly responsible of the impairment of CA dilatation in diabetic patients.

The present study was designed to evaluate the frequency of an increase in the urinary albumin excretion rate (UAER) and the factors involved in this parameter in non-diabetic obese patients; 122 non-diabetic obese patients were investigated. None had proteinuria or history of nephropathy or uropathy. Fourty of them had moderate hypertension. Compared with a group of 22 lean controls, UAER was significantly higher in the obese patients (19.0 +/- 2.0 (SEM) mg/24 h vs 3.2 +/- 0.6 mg/24 h, p < 0.001). UAER was elevated (> 20 mg/24 h) in 29 patients (23.7%). Prevalence of microalbuminuria was not significantly different in hypertensive than in normotensive patients. However UAER was significantly higher in the 32 patients with a family history of hypertension (29.6 +/- 6.3 mg/24 h vs 15.3 +/- 1.5 mg/24 h, p < 0.002). In patients with microalbuminuria, body weight was significantly higher (100.3 +/- 3.9 kg vs 91.8 +/- 1.9 kg, p < 0.05), plasma albumin was significantly lower (38.3 +/- 0.6 g/l vs 40.3 +/- 0.3 g/l, p < 0.005) and the estimated value of fractional albumin clearance was significantly higher. These results show the high frequency of microalbuminuria in non-diabetic obese patients. They suggest that UAER level may be an index of family hypertension in obese patients and that microalbuminuria is part of a widespread abnormality of the capillary permeability.

Hypertensive and diabetic mellitus diseases are known to increase stiffness of the arterial wall. However these alterations probably involve different mechanisms. To this end, we compared the effect of hypertension and diabetes on large artery caliber and elasticity at real pressure conditions and at the same level of pressure. Nine poorly controlled non insulino-dependent diabetic men without hypertension and 9 non-diabetic essential hypertensive men underwent measures of lumen diameter (pulsed Doppler) and segmental compliance (Bramwell and Hill formula; pulse wave velocity) at the brachial artery. Isobaric diameter and compliance were deduced from a non linear model, comparing diameter and pressure on one part, and compliance and pressure on the other. Pulse wave velocity was similarly increased in both diseases (11.5 +/- 1 vs 12.8 +/- 1 m/s; NS; respectively in diabetes and hypertension). Both measured and isobaric diameters were smaller in diabetic patients (4.05 +/- 0.2 vs 5.03 +/- 0.2 mm, p less than 0.1% for the measured diameters respectively in diabetes and hypertension and 4.06 +/- 0.2 vs 5.01 +/- 0.2 mm, p less than 1% for isobaric diameters). The measured and isobaric compliances were not significantly different (2.38 +/- 0.4 vs 2.08 +/- 0.2 cm/mmHg10(-4), NS, for the measured compliance respectively in diabetes and hypertension; 2.28 +/- 0.4 vs 2.4 +/- 0.2, NS for the isobaric compliance). After correction of the effect of mechanical arterial stretch induced by the different blood pressure level of the two groups, significant reduction of diameter in diabetic subjects persisted and isobaric and measured compliances remained unchanged between groups.

The relation between hypertension and diabetic nephropathy is complex. Nephropathy is probably involved in the elevated blood pressure found in diabetic patients. In maturity onset diabetes, patients may also have hypertension which is associated with obesity or essential hypertension. It has been suggested that in both types of diabetes, hypertension enhances the development of diabetic nephropathy. Moreover, an aggressive antihypertensive treatment seems able to reduce rate of decline in kidney function in insulin-dependent diabetic patients with patent nephropathy. In this work, creatinine clearance and microalbuminuria in 20 diabetic patients (mostly with maturity-onset-diabetes) with known moderate and effectively treated hypertension were therefore measured and the results were compared with those for 18 normotensive diabetic patients and 22 controls. Duration of diabetes was from one to 26 years (mean: 11 years) and duration of hypertension was from one to 35 years (mean: 10 years). Patients and controls had normal serum creatinine and proteinuria below 0.1 g/l. Microalbuminuria was measured by immunonephelometric assay using specific antiserum (sensitivity = 1.5 mg/l; intra and interassay coefficients: 6.5% and 8% respectively). The highest value was observed in hypertensive diabetic patients with retinopathy (group 1). But hypertensive patients without retinopathy (group 2) and normotensive patients also had significantly increased microalbuminuria. In group 1, microalbuminuria was significantly higher than in group 2. The creatinine clearance was reduced in groups 1 and 2 versus normotensive diabetics, but hypertensive patients were older.(ABSTRACT TRUNCATED AT 250 WORDS)