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Introduction: The aim of the study was to assess the age-specific, sex-specific, and region-specific average sodium and potassium intake and its association with anthropometric characteristics in a sample of the Italian adult hypertensive population., Methods: A total of 1232 hypertensive patients were recruited consecutively by 47 centers recognized by the Italian Society of Hypertension. The enrolled participants were on stable antihypertensive treatment. Anthropometric indices, blood pressure, 24-h urinary sodium, and potassium excretion were measured and used as proxy for the average daily sodium and potassium intake., Results: The average sodium intake was 172  mmol (or 10.1  g of salt/day) among men and 138 (or 8.1) among women, with no difference among geographical areas. Over 90% of men and 81% of women had a consumption higher than the recommended standard dietary intake of 5  g/day. The average potassium intake was 63 and 56  mmol, respectively in men and women, again without geographical differences, nearly 92% of men and 95% of women having an intake lower than the recommended intake (100  mmol/day or 3.9  g/day). There was a significant trend to a gradual decrease in sodium intake with age in both sexes (P <0.001). There was also a direct association between BMI and sodium intake in both sexes, this association being independent of age (P < 0.001)., Conclusion: In this national sample of the Italian hypertensive population, dietary sodium intake was largely higher and potassium intake much lower than the recommended intakes, and this was true for all geographical areas. Overweight and obese hypertensive patients had particularly high sodium intakes.

Hypertension is a common manifestation of antiphospholipid syndrome (APS). Antiphospholipid antibodies (aPL) have been described in patients with hypertension secondary to renal artery stenosis (RAS). Twenty-six patients with RAS and 25 patients with severe essential hypertension (diastolic blood pressure > 110 mmHg or > or = 3 hypertensive drugs) were studied and compared to 61 age- and sex-matched healthy subjects. Serum samples were tested for lupus anticoagulant (LA), anticardiolipin (aCL) IgG and IgM, antiprothrombin (aPT) IgG and IgM, anti-beta2glycoprotein 1 (abeta2GP1) IgG and IgM. aPL were negative in all patients with RAS. Two patients with essential hypertension had positive aPL (8%) (LA in one patient confirmed in a second assay and abeta2GP1-IgG in the other patient confirmed one year later together with aCL IgG positivity). Among healthy subjects, one case (1.6%) was found to be positive for LA, aCL IgM, abeta2GP1 IgM, aPT IgG, aPT IgM. In conclusion, the association between RAS and aPL seems to be casual rather than an expression of an elective thrombotic localization ofAPS. The positive finding of aPL in 8% of patients with essential hypertension, a frequency higher than that of the control population, deserves further studies in larger series to better explore the relationship between aPL and hypertension.

The kidneys are a major target of PAPS. The histologic lesions of PAPS nephropathy are vascular; among them thrombotic microangiopathy (TMA) is the most characteristic. It is still not clear in the literature whether the nephropathy can be the unique manifestation of PAPS in the absence of other thrombotic processes; that is: do the renal microthrombotic lesions allow to make the diagnosis of PAPS in presence of anti-phospholipid antibodies (APA)? With this purpose we present three clinical cases. The first patient had severe hypertension C4 hypocomplementemia, thrombocytopenia, and mitralic valve insufficiency. LAC and anti-cardiolipin antibodies at high titre were positive. The histologic picture was characterized by basement membrane reduplication and arteriolar mucoid degeneration, which are features of early phase of TMA. The second patient had severe hypertension. The detection of anti-cardiolipin antibodies was performed several times and resulted positive three times, four months after the diagnosis as well. The renal histologic features were consistent with late lesions of TMA. The third patient had severe hypertension, rapidly progressive renal failure, tricuspidal valve insufficiency and two positive anti-phospholipid antibodies determinations three weeks apart (in two occasions anti-cardiolipin and in one occasion LAC as well were found). The renal lesions were characteristic for TMA. In conclusion we think that patients with TMA and antiphospholipid antibodies can be considered affected by PAPS, as the thrombotic process is represented by thrombosis in preglomerular arterioles, which leads to TMA.

The purpose of this study was to assess the management of both hypertension and micro/macroalbuminuria in a cohort of type II diabetic patients. In the first 6 months of the year 2000, 5815 diabetic patients were identified through prescriptions for antidiabetic drugs in our sanitary district (191 568 inhabitants). In all, 65% (3810) of these type II diabetic patients were also given prescriptions for antihypertensive drugs. A total of 400 diabetic patients were randomly selected and 171 entered the study (gender: 94/77 M/F; age: 66.6+/-8 years; diabetes duration: 12+/-9 years): 100 patients (group DT) were treated with antihypertensive drugs and 71 (group DU) were untreated. Blood pressure, urine albumin-to-creatinine ratio (ACR), and glycated haemoglobin were measured in the two groups. A total of 80% (57/71) of DU patients were hypertensive (BP>/=130/85 mmHg). Specifically, 24.4% had diastolic hypertension (BP>/=85 mmHg) and 79% systolic hypertension (BP>/=130 mmHg). Only 63% (100/157) of the hypertensive patients were treated with antihypertensive drugs (two drugs/patient on average, range 1-5). In addition, only 13% of the DT patients were adequately controlled (BP<130/85 mmHg), while the others had above target blood pressure levels (14%: 130-139/85-89 mmHg; 40%: 140-159/90-95 mmHg, and 33%>/=160/95 mmHg). Angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) were included in the antihypertensive medical regimen in 70% of the DT patients (ACE-I: 62%; ARB: 8%; diuretics: 39%; dihydropyridine calcium antagonists: 38%; alpha-blockers: 20%, beta-blockers: 17%; clonidin: 8%; nondihydropyridine calcium antagonists: 5%). Only 33% of type II diabetic patients underwent a screening for microalbuminuria as assessed on clinical records. The same percentage of micro- and macroalbuminuric patients (13.5%) was observed in the DT group, whereas 25% micro vs 3% macro were found in the DU group. In all, 73% of microalbuminuric patients were not on ACE-I/ARB. Hypertensive type II diabetic patients were often left untreated and only a minority of those treated were optimally controlled. The importance of an elevated systolic pressure is underestimated and the number of antihypertensive drugs prescribed insufficient. Screening and treatment of albuminuria are inadequate.

Background: Aim of this study is to evaluate the treatment and control of arterial hypertension in patients with type 2 diabetes., Methods: We identified 5815 diabetic patients in our health-care district (191,568 inhabitants) through prescriptions for insulin and/or hypoglycaemic drugs in the first 6 months of 2000; 3810 of them (65%) also had prescriptions for antihypertensive drugs. We evaluated a randomly selected sample of 171 patients with type 2 diabetes, 100 of whom were receiving antihypertensive drugs (94 males and 77 females, mean age 66.6 +/- 8 years, mean diabetes duration 12+/-9 years)., Results: Fifty-seven out of 71 patients not treated with antihypertensive drugs (80.3%) had a BP = 130/85 mmHg; 24.4% of them had a diastolic BP = 85 mmHg and 79% had a systolic BP = 130 mmHg. Thirteen out of 100 treated patients (13%) had a BP < 130/85 mmHg. Among the patients treated with antihypertensive drugs 36% received one drug, 36% two drugs and 28%=3 drugs; mean 1.98 +/- 0.9 drugs/patients. Among the patients treated with monotherapy 36.1% received ACE-inhibitors, 36.1% dihydropyridinic calcium-antagonists, 11.1% alpha-blockers, 11%, diuretics, 2.8% non-dihydropyridinic calcium-antagonists, and 2.8% angiotensin II antagonists. Patients treated with two antihypertensive drugs received more frequently an ACE-inhibitor plus a diuretic (31%) or an ACE-inhibitor plus an alpha-blocker (23%) or an ACE-inhibitor plus a dihydropyridinic calcium-antagonists (20%). A diuretic was used in 40% of the patients with two antihypertensive drugs and in 78% of those with >= 3 drugs., Conclusions: Many hypertensive type 2 diabetic patients are left untreated and only a minority of those treated reach optimal blood pressure control. The importance of an elevated systolic pressure is underestimated, and the number of antihypertensive drugs prescribed is suboptimal.

Background: To evaluate the metabolic effects of modification of sodium intake in patients with essential hypertension., Methods: Thirteen patients with essential hypertension (10 M, median age 51 yrs, range 21-64) followed in random order a low-sodium and a high-sodium diet (50 mmol Na/day vs 250 mmol/day for two weeks each). At the end of each diet an evaluation was made of 24 hour blood pressure (ABPM, Spacelabs 90207) and serum concentration of: glucose, total and HDL cholesterol, uric acid, lipoproteins A, B, Lp(a), total proteins, albumin., Results: Twenty-four hours systolic and diastolic BP were significantly higher at the end of high sodium diet than of low sodium diet [respectively 132 mmHg (120-161) vs 128 mmHg (109-150); p = 0.008 and 84 mmHg (71-99) vs 81 mmHg (70-95); p = 0.008)]. No significant variations were found as regards serum glucose and lipidic parameters between low and high sodium diets. Serum uric acid was significantly higher following low sodium diet [5.9 mg/dl (4.5-8) vs 4.6 mg/dl (3.4-6.5); p = 0.003)], as well as serum total proteins [7.2 g/dl (6.9-8.2) vs 7 g/dl (6.5-7.8); p = 0.027)]. A significant direct correlation was found between changes of uric acid and total proteins from low to high sodium diet (Spearman's rho = 0.57; p = 0.04)., Conclusions: In patients with essential hypertension a moderate dietary sodium restriction, able to reduce significantly 24 hours arterial pressure, does not worsen serum glucose nor lipids concentration.

Background: The tenet that peritoneal dialysis is capable of either normalizing or improving blood pressure control in uraemic patients is based on outdated or monocentric experiences. Therefore, we assessed the prevalence of hypertension and the efficacy of antihypertensive therapy in a large, multicentric cohort of patients on peritoneal dialysis., Methods: Twenty seven out of the 50 centres belonging to the Italian Co-operative Peritoneal Dialysis Study Group took part in the study. The main patient selection criteria were: peritoneal dialysis therapy for at least 3 months and no peritonitis or changes in dialysis technique for at least 1 month. Clinical blood pressure was measured according to WHO/ISH guidelines. Ambulatory blood pressure monitoring was carried out using a SpaceLabs 90207 recorder. Hypertension was defined according to WHO/ISH criteria and staged according to the criteria of the Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure (JNC), 5th Report. Ambulatory blood pressure monitoring recordings were used to evaluate white-coat hypertension, blood pressure load and the dipping phenomenon., Results: Five hundred and four subjects were evaluated. Hypertension was prevalent in 88.1% of the population, and 362 out of 444 hypertensive patients were on antihypertensive therapy. JNC staging revealed that 188 patients had moderate to severe hypertension. Blood pressure load was pathological in 77.3% of the patients receiving antihypertensive treatment. White-coat hypertension was identified in 9.1% of the hypertensive patients not on antihypertensive therapy, and 53.1% of the patients were non-dippers., Conclusions: The study demonstrates that hypertension is a dramatic, unsolved problem in uraemic patients treated with peritoneal dialysis, and casts doubts on the effectiveness of our current peritoneal dialysis strategies and pharmacological management of hypertension.

The aim of this work was to evaluate the intracellular Na concentration, the passive Na permeability and the activity of Na, K pump, Na, K cotransport, Na, Li countertransport in the red cells of patients with autosomal dominant polycystic kidney disease (ADPKD) in relationship with their blood pressure status. Sixteen patients with ADPKD and normal renal function (6 males, 10 females, median age 31.5 years, range 20-42 years) and twenty healthy controls (10 males, 10 females, median age 30 years, range 23-47 years) were studied. Eight ADPKD were hypertensive. The rate constant of ouabain-sensitive Na efflux was lower in hypertensive than in normotensive ADPKD patients. The activity of Na,Li countertransport was significantly higher in hypertensive ADPKD patients than in both normotensive patients and control subjects. A significant inverse correlation was found between Na,Li countertransport activity and the rate constant of ouabain-sensitive Na efflux in fresh red cells (rho = 0.62; p = 0.016). Hypertension in patients with ADPKD and normal renal function is associated with abnormalities of red cell sodium transport: an increase of Na,Li countertransport, possibly primitive, and a reduction of Na,K pump in fresh cells, possibly secondary to a circulating inhibitor.

It has been suggested that an increased erythrocyte Na-Li countertransport (Na-Li CNT) rate in patients with IDDM is associated to the risk of developing diabetic nephropathy. Little is known, however, about the possible influence of metabolic control on Na-Li activity. Aims of the study were to evaluate Na-Li CNT at the onset of IDDM and during the remission phase and its relationship with some clinical and metabolic parameters. Twelve insulin-dependent diabetic children (6 males, 6 females; mean age 10 +/- 0.6 years) were studied at the onset and 1, 4, 12 months after the diagnosis; 6 of them had a family history of hypertension. Twelve healthy children (6 males, 6 females; mean age 12 +/- 0.3 years) served as controls. As compared to control subjects (212 +/- 24 mumol/l RBC/h), red cell Na-Li countertransport activity of diabetic children was significantly higher at the onset (354 +/- 31 mumol/l RBC/h) of IDDM and at the first month (348 +/- 36 mumol/l RBC/h). Red cell Na-Li countertransport activity returned toward normal range at the fourth (239 +/- 33 mumol/l RBC/h) and twelfth month (162 +/- 34 mumol/l RBC/h). No correlation was found between the values of red cell Na-Li countertransport activity and those of clinical and biochemical parameters at any time. Patients with hypertensive relatives showed at baseline evaluation a significantly higher red cell Na-Li countertransport activity than those without (436 +/- 28 vs 273 +/- 34 mumol/l RBC/h; p < 0.002). This difference, although not statistically significant, was still evident at the late follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Arterial hypertension is a common side effect of cyclosporine A (CyA). Aim of the study was to evaluate the activity of erythrocyte (RBC) Na transport in two groups of patients with a well functioning renal graft (Crs less than 1.7 mg/dl) treated by prednisone+azathioprine (10 pts), or prednisone+CyA (21 pts), in relationship with blood pressure status. Twenty-one age matched healthy subjects were studied as a control group. Na,K pump and Na,K cotransport were significantly lower in CyA than in AZA patients (2,184 +/- 106 vs 3,089 +/- 162 and 58 +/- 8 vs 187 +/- 28 mumol/l RBC/h: p less than 0.01), without differences between normotensive and hypertensive patients. Na,K pump efflux in normal subjects was 2334 +/- 66 mumol/l RBC/h (p less than 0.01 vs AZA), NA,K cotransport was 205 +/- 18 mumol/l RBC/h (p less than 0.01 vs CyA). Significant correlations were found between RBC Na,K pump activity and trough plasma CyA levels (p less than 0.02) and between systolic pressure and plasma creatinine in CyA patients (p less than 0.01). Trough plasma CyA levels were higher in hypertensive than in normotensive CyA patients (64 +/- 5 vs 46 +/- 4 ng/ml; p less than 0.01).

The effects of a 2 litre isotonic saline infusion on erythrocyte Na,K pump activity and urinary sodium excretion (UNaV) were evaluated in 20 patients with essential hypertension and 15 normotensive subjects. The effect of preincubation of normal erythrocytes in plasma from hypertensive patients on erythrocyte Na,K pump was also studied. Before saline infusion no significant differences were found between normotensive and hypertensive subjects in the mean values of intracellular sodium and potassium concentration, ouabain-sensitive Na efflux in erythrocytes and urinary sodium excretion. Erythrocyte Na,K pump activity decreased significantly (p less than 0.01) after saline infusion in both groups of subjects. The reduction was significantly lower in hypertensives than in normotensive. delta UNaV was significantly higher in hypertensive patients than in normotensive subjects (25 +/- 4 vs 14 +/- 2 mmol/h; p = 0.04). Only in normal subjects a significant correlation was found between the difference in Na,K pump activity pre and post saline infusion and delta UNaV (r = 0.52; p less than 0.05). Plasma from hypertensive patients obtained before saline infusion significantly (p less than 0.01) inhibited Na,K pump of erythrocytes from normal subjects; plasma taken after saline infusion produced a marked increase of this inhibition, significantly (p less than 0.01) higher than serum taken before the infusion.

Four thousand hemofiltrations have been performed in 22 patients with low tolerance to conventional hemodialysis (20 cases), and severe arterial hypertension (2 cases). In comparison with hemodialysis, hemofiltration had a low incidence of intradialytic collapses, vomit and cramps, and allowed a better state of well-being during interdialytic periods. In hypertensive patients hemofiltration has accomplished a better control of arterial pressure and pharmacotherapy has been reduced. In this study, we report the data concerning metabolism, electrolytes, acid-base balance during our experience utilizing bicarbonate in the replacement fluid. Our experience further supports the impression that hemofiltration may have some advantages in patients with low tolerance to conventional dialysis and/or severe dislipemia and hypertension. The possibility to reduce dialysis duration to 3 hrs, stimulates further application of this new treatment in a wider number of patients on RDT.

The effects of a 2-litre isotonic saline infusion, with and without prior oral canrenone (150 mg) administration, on erythrocyte Na+, K+ pump, urinary sodium excretion and arterial pressure were evaluated in nine patients with essential hypertension. Ouabain-sensitive Na+ efflux in fresh erythrocytes was used as an index of Na+, K+ pump activity, and the inhibitory effect on this ion efflux of preincubation of erythrocytes in plasma was used to test the presence of a circulating ouabain-like substance. Erythrocyte Na+, K+ pump activity decreased significantly (P less than 0.01) after saline infusion; canrenone administration was able to prevent this inhibition. Plasma from hypertensive patients obtained before saline infusion significantly (P less than 0.01) inhibited the Na+, K+ pump of erythrocytes from normal subjects, while plasma taken after the saline infusion plus canrenone was unable to produce any significant inhibition. Both systolic and diastolic arterial pressure fell significantly (P less than 0.05) only at the end of saline infusion with prior canrenone administration. This study supports the hypothesis that protection of Na+, K+ pump against endogenous inhibitors, other than exogenous, seems to be a pharmacological effect of canrenone, and may partly explain its antihypertensive activity.

In 38 uraemic dialysed patients (17 normotensive, 21 hypertensive) we measured (1) erythrocyte sodium concentration [Nai] and ouabain-sensitive sodium efflux, and (2) arterial pressure, cardiac index and total peripheral resistance. Erythrocyte Na-K pump activity was lower in hypertensive than in normotensive patients (P less than 0.02). Hypertensive patients had significantly higher peripheral resistance than normotensive patients (P less than 0.05), while the cardiac index was similar in both groups. Inverse correlations were found between the rate constant for ouabain-sensitive sodium efflux in erythrocytes and both systolic and diastolic pressure (r = -0.43 and r = -0.45, respectively; P less than 0.01) and total peripheral resistance (r = -0.76; P less than 0.0001). Our data suggest that reduced sodium transport by the Na-K pump plays a role in the pathogenesis of arterial hypertension in patients with chronic uraemia.

The aim of this work was to review evidence on the role of the sympathetic nervous system (SNS) in chronic renal failure (CRF). Three main points are discussed: 1) SNS and pathogenesis of arterial hypertension; 2) SNS and cardiovascular risk; 3) implication of SNS in arterial hypotension during hemodialysis. Several lines of evidence indicate the presence of a sympathetic hyperactivity in CRF, and its relationship with arterial hypertension. It is suggested that diseased kidneys send afferent nervous signals to central integrative sympathetic nuclei, thus contributing to the development and maintenance of arterial hypertension. The elimination of these impulses with nephrectomy could explain the concomitant reduction of blood pressure. Several experiments confirmed this hypothesis. Regarding SNS and cardiovascular risk, some data suggest that reduced heart rate variability identifies an increased risk for both all causes and sudden death, independently from other recognized risk factors. Symptomatic hypotension is a common problem during hemodialysis treatment, occurring in approximately 20-30% of all hemodialysis sessions and is accompanied by acute withdrawal of sympathetic activity, vasodilation and relative bradicardia. This reflex is thought to be evoked by vigorous contraction of a progressively empty left ventricle, activating cardiac mechanoceptors. This inhibits cardiovascular centers through vagal afferents, and overrides the stimulation by baroreceptor deactivation. Alternative explanations include cerebral ischemia and increased production of nitric oxide, which inhibit central sympathetic activity. It is hoped that therapies aimed at modulating sympathetic nerve activity in patients with CRF will ameliorate their prognosis and quality of life. [ABSTRACT FROM AUTHOR]