Calcium urolithiasis,blood pressure and salt intake

OBJECTIVES: To determine whether stone-formers have higher BP than controls drawn from the general population and matched for age, sex and ethnic origin and to compare the relationship between sodium and calcium excretion in the two groups. PATIENTS AND METHODS: Thirty-six patients [mean (+/-standard deviation, SD) = 49.0 +/- 11.7 years; range 27-70 years] with kidney or ureteric stones and 108 controls (mean age of 49.6 +/- 6.8 years; range 39-61 years), matched for gender, ethnic origin and age group were studied. Patients and controls underwent physical measurements, a venous blood sample and they were asked to collect a 24-h urine sample for sodium, potassium, calcium and creatinine. RESULTS: Stone-formers were significantly heavier and had higher BP than age-, sex- and ethnic-matched population controls. Whilst the difference in systolic BP was independent of the difference in body mass index [16.8 mmHg (7.2-26.4 mmHg), p = 0.001), the difference in diastolic BP was attenuated after adjustment for body mass [1.8 (-3.4 to 7.1), p = 0.49]. Stone-formers passed less urine than controls [-438 ml/day (95% CI -852 to -25), p = 0.038]. They had higher urinary calcium than controls [+3.7 mmol/day (2.8-4.6 mmol/day), p < 0.001], even when expressed as ratio to creatinine [+0.20 (0.11-0.29), p < 0.001]. Sodium excretion was positively associated with urinary calcium in both stone-formers and in controls. The slopes were comparable (0.92 vs 0.98 mmol Ca/100 mmol Na) so that for any level of sodium excretion (or salt intake), stone-formers had a higher calcium excretion than controls. CONCLUSIONS: In stone-formers, the BP is higher than in controls. Stone-formers excrete more calcium than controls do. In stone-formers and controls, the relationship between urinary sodium and calcium is similar. Since this relationship results from an effect of sodium on calcium, a reduction in salt intake may be a useful method of reducing urinary calcium excretion in stone-formers. However, the "relative" hypercalciuria seen in stone-formers is independent of salt intake and may well reflect an underlying genetic predisposition.     

Body sodium/blood volume state in normotensive members of normotensive and hypertensive families

Exchangeable sodium is lower than normal in young male patients with essential hypertension. This may reflect a primary abnormality of sodium metabolism, or natriuresis caused by sodium-independent elevation of arterial pressure. To investigate this question, 31 normotensive men with positive and 31 normotensive men with negative family history of essential hypertension were studied. Blood pressure tended to be higher in the former (121/78 +/- 9/8 (s.d.) versus 113/74 +/- 11/9 mmHg; P less than 0.005); mean age, urinary sodium or potassium excretion, plasma sodium, potassium, renin activity or aldosterone levels and creatinine clearance were comparable. Exchangeable sodium and blood volume were also similar in the two groups, when expressed in absolute values (3113 +/- 306 versus 3044 +/- 242 mmol and 4902 +/- 581 versus 4769 +/- 579 ml, respectively) or in relation to body surface area (100.8 +/- 7.1 versus 100.2 +/- 6% and 103.8 +/- 12.2 versus 102 +/- 11.3%). In both groups, exchangeable sodium and blood volume were unrelated to arterial pressure. The body sodium/blood volume state is normal in normotensive subjects with positive family history. The low exchangeable sodium of young patients with essential hypertension does not appear to reflect a primary familial abnormality of body sodium metabolism.     

Controlled trial of long-term oral calcium supplementation in essential hypertension

A randomized, double-blind, placebo-controlled crossover trial of oral calcium supplementation was carried out in 18 patients with uncomplicated essential hypertension. After 15 weeks of oral calcium supplementation, 1 g/day, of the patients' habitual diet, the only blood pressure change (compared with the results of placebo treatment) was in the average standing systolic blood pressure, which was significantly reduced (-8.6 mm Hg; p less than 0.01). The 24-hour urinary calcium excretion and the total serum calcium concentration increased significantly during calcium supplementation (p less than 0.05), indicating good compliance with the treatment. The individual blood pressure changes with high calcium intake were found to be inversely related to basal 24-hour urinary calcium excretion (r = -0.69, p less than 0.001 for standing systolic pressure; r = -0.55, p less than 0.002 for standing diastolic pressure). This correlation was independent of age, basal blood pressure, serum calcium concentration, basal 24-hour urinary sodium excretion, and body weight changes during the trial. In particular, a subgroup of six patients, who had a basal 24-hour urinary calcium excretion higher than the mean + 2 SD of a reference healthy population previously described, showed a substantial average blood pressure fall at variance with the other patients in the study. These results do not support the usefulness of an oral calcium supplement in the majority of subjects with mild essential hypertension; however, they suggest that a group of patients with a previously reported abnormality of calcium metabolism may be responsive to this therapeutic measure.     

Estimation of salt intake by urinary sodium excretion in a Portuguese adult population and its relationship to arterial stiffness.

BACKGROUND: Portugal has one of the highest mortality rates from stroke, a high prevalence of hypertension and probably a high salt intake level. AIM: To evaluate Portuguese salt intake levels and their relationship to blood pressure and arterial stiffness in a sample of four different adult populations living in northern Portugal. METHODS: A cross-sectional study evaluating 24-hour urinary excretion of sodium (24 h UNa+), potassium and creatinine, blood pressure (BP), and pulse wave velocity (PWV) as an index of aortic stiffness in adult populations of sustained hypertensives (HT), relatives of patients with previous stroke (Fam), university students (US) and factory workers (FW), in the context of their usual dietary habits. RESULTS: We evaluated a total of 426 subjects, mean age 50 +/- 22 years, 56% female, BMI 27.9+/-5.1, BP 159/92 mmHg, PWV 10.4+/-2.2 m/s, who showed mean 24h UNa+ of 202 +/- 64 mmol/d, corresponding to a daily salt intake of 12.3 g (ranging from 5.2 to 24.8). The four groups were: HT: n = 245, 49 +/- 18 years, 92% of those selected, 69% treated, BP 163/94 mmHg, PWV 11.9 m/s, 24 h UNa+ 212 mmol/d, i.e. 12.4 g/d of salt); Fam: n = 38, 64 +/- 20 years, 57 % of those selected, BP 144/88 mmHg, PWV 10.5 m/s, 24 h UNa+ 194 mmol/d, i.e. 11.1 g/d of salt; US: n = 82, 22 +/- 3 years, 57% of those selected, BP 124/77 mmHg, PWV 8.7 m/s, 24h UNa+ 199 mmol/d, i.e. 11.3 g/d of salt; FW: n = 61, 39 9 years, 47% of those selected, BP 129/79 mmHg, PWV 9.5 m/s, 24 h UNa+ 221 mmol/d, i.e. 12.9 g/d of salt. The ratio of urinary sodium/potassium excretion (1.9 (0.4) was significantly higher in HT than the other three groups. In the 426 subjects, 24h UNa+ correlated significantly (p < 0.01) with systolic BP (r = 0.209) and with PWV (r=0.256) after adjustment for age and BP. Multivariate analysis showed that BP, age and 24h UNa+ correlated independently with PWV taken as a dependent variable. CONCLUSIONS: Four different Portuguese populations showed similarly high mean daily salt intake levels, almost double those recommended by the WHO. Overall, high urinary sodium excretion correlated consistently with high BP levels and appeared to be an independent determining factor of arterial stiffness. These findings suggest that Portugal in general has a high salt intake diet, and urgent measures are required to restrict salt consumption in order to prevent and treat hypertensive disease and to reduce overall cardiovascular risk and events.     

Plasma levels of atrial natriuretic factor in mild to moderate hypertensives without signs of left ventricular hypertrophy: correlation with the known duration of hypertension

The relationship between plasma atrial natriuretic factor (ANF), blood pressure (BP), age, plasma renin activity (PRA) and urinary sodium excretion was studied in 64 normal subjects (mean age 48.7 +/- 2.1 yrs; BP: 126.5 +/- 1.6/79.5 +/- 0.9 mmHg) and in 104 untreated uncomplicated essential hypertensives (50.8 +/- 1.1 yrs; BP: 164.7 +/- 1.6/105.2 +/- 0.6 mmHg). ANF was measured by radioimmunoassay after extraction on C18 columns. ANF was significantly higher in the hypertensives than in the normal subjects (37.1 +/- 1.2 vs 29.7 +/- 1.5 pg/ml, P less than 0.01). In normals plasma ANF was significantly correlated with age (r = 0.72, P less than 0.001), Na excretion (r = 0.42, P less than 0.001) and PRA (r = -0.71, P less than 0.001) whereas in the hypertensives ANF plasma levels correlated only with systolic (r = 0.46, P less than 0.001) and diastolic (r = 0.51, P less than 0.001) BP. In addition in hypertensive patients, by multivariate linear regression analysis, a significant correlation was found between age, known duration of hypertension and plasma ANF. The partial correlation coefficient between duration of hypertension and plasma ANF was highly significant (r = 0.80, P less than 0.001). These findings suggest that in essential hypertension the level of arterial BP is a main determinant of the ANF plasma values offsetting the ability of other physiological factors to regulate plasma ANF levels.     

Hormonal profile and participation of nitric oxide in salt-sensitive and salt-resistant essential arterial hypertension

Recent studies have shown that cardiovascular events and end-organ damage occur more frequently in patients with salt-sensitive essential hypertension (SH) than in salt-resistant essential hypertension (RH). Nitric oxide (NO) plays an important role in regulating the pressure-natriuresis relationship. Therefore impaired NO synthesis may produce or aggravate salt-sensitive hypertension. This study was conducted to determine the hormonal levels and nitric oxide metabolites in hypertensive patients. 25 patients underwent salt sensitivity testing. 24 h ambulatory blood pressure was recorded after a 5-day period on low salt diet (20 mEq/d) and after a 5-day period on a high salt diet (200 mEq/d). Subjects showing > or = 10 mmHg increase in mean BP when changing from low to high dietary salt intake were classified as salt sensitive and as salt resistant when the BP changes were < 10 mmHg. Based on BP recordings 13 patients were characterised as white coat hypertension (WC), 13 patients as salt resistant (SR) and 12 as salt sensitive (SS). A significative relationship was seen between plasma glucose-insulin concentration and body mass index. The ventricular mass index was similar in SS and SR patients. The plasma uric acid, triglicerides and PAI-I were elevated in SS compared with SR, and control group (C). During low sodium intake, plasma renin and aldosterone were decreased in SS compared with SR, and C. No differences in plasma catecholamines or their changes with intake sodium modifications were seen among the patients. During high sodium intake urinary NO excretion increased in SR (38 +/- 9 vs 18 +/- 2 mg/g creat), and C (24 +/- 2 vs 16 +/- 3 mg/g creat) (p < 0.01) but not in SS patients (21 +/- 3 vs 26 +/- 4 mg/g creat). The NO excretion changes showed negative correlation with BP changes (r = 0.49, p < 0.01). During low sodium intake, SR and SS patients showed a normal nocturnal decrease of BP (dippers). During high sodium intake SS patients became non-dippers. Our results showed that patients with salt sensitive hypertension displayed a suppressed renin-aldosterone system, an attenuated nocturnal decline in blood pressure on high-salt diet and an impairment of endothelial function. The relationship between urinary nitrate excretion and arterial pressure suggest that the salt sensitivity of arterial pressure may be related bo blunted generation of endogenous nitric oxide.     

Sodium intake and cardiac sympatho-vagal balance in young men with high blood pressure.

We have previously reported that a high sodium intake increases sleep-time blood pressure (BP) in young men. However, there are cases in which this relation does not apply. To account for them, we investigated the relation between sodium intake and cardiac sympatho-vagal balance (SVB) in young men with high BP. Sodium intake was estimated from the amount of urinary sodium excretion over 1 week. Twenty-four-hour (24-h) urinary sodium excretion (Salt24), 24-h ambulatory BP and ECG were obtained on the last day of the observation period. As an index of sodium intake, the expression In(Salt24/Cr24) (Cr24, 24-h urinary creatinine excretion) was used. From power-spectral analysis of ECG-RR intervals during sleep, we obtained the LF/HF ratio between the low-frequency component (LF) and the high frequency component (HF) and used it as an index of SVB. The subjects were male medical students divided into a normal BP group (N-group; n=103) and a high BP group (H-group; n=26, 24-h BP>125/75 mmHg). Mean In(Salt24/Cr24) and LF/HF in the H-group were significantly higher than those in the N-group (LF/HF: 1.86+/-0.44 [SD] vs. 1.37+/-0.30, p<0.001). The calculated discriminant function (D) for the H-group and N-group was D=1.6x + 5y - 11, where x is In(Salt24/Cr24) and y is LF/HF. This formula (D) resulted in high discriminant predictive accuracy (82%) between the groups. If D=0 (the value of the cut-off line determining separation of the groups), the relation y=-0.32x + 2.2 (negative relation between y and x) was obtained. These results suggest that excessive sodium intake in combination with accentuated SVB (LF/HF) increases BP in young men.     

Effects of amlodipine on urinary sodium excretion, renin-angiotensin-aldosterone system, atrial natriuretic peptide and blood pressure in essential hypertension.

We studied the effect of amlodipine, a long-acting dihydropyridine calcium antagonist, on blood pressure, urinary sodium excretion, plasma renin activity, aldosterone and atrial natriuretic peptide in six patients (aged 47-63 yrs) with essential hypertension. Patients were placed on a fixed sodium intake of 150 mmol/day. After a control period, amlodipine 10 mg/day was given for two weeks. There was a gradual reduction in supine BP over the first two days of treatment, from 165/103 +/- 5/4 mmHg to 137/92 +/- 6/4 mmHg (P less than 0.001) and BP remained at this level during treatment. Three days after amlodipine was stopped the BP was still reduced at 136/87 +/- 5/4 mmHg but was back to pretreatment levels two weeks later. Plasma amlodipine rose after two weeks of treatment to 29.7 +/- 4.7 ng/ml but had only decreased to 15.0 +/- 3.4 ng/ml three days after the treatment was withdrawn. During the first two days of treatment there was no evidence of an increase in urinary sodium excretion and when amlodipine was withdrawn there was no evidence of sodium retention. Plasma renin activity increased from 1.26 +/- 0.30 to 2.99 +/- 0.68 ng/ml/h (P less than 0.001) and plasma atrial natriuretic peptide fell from 19.3 +/- 7.0 to 11.4 +/- 3.8 pg/ml (P less than 0.03) with two weeks of treatment. This study demonstrates that amlodipine is a long-acting calcium antagonist with a slow onset of action and a slow end of action after withdrawal. This makes it difficult to detect alterations in sodium balance when assessed by changes in urinary sodium excretion. However, one explanation for the increase in plasma renin activity and fall in atrial natriuretic peptide is a small reduction in total body sodium.     

Normal vitamin D and mineral metabolism in essential hypertension

The effects of dietary sodium upon serum and urinary calcium and selected vitamin D metabolites were studied in two groups (n = 10 each) of age and gender matched, white normotensive subjects and patients with normal-renin hypertension. Isocaloric diets were consumed on a metabolic ward with sequential daily sodium intake of 109 meq for 5 days and 9 meq and 259 meq for 6 days each. Values for serum and urinary calcium, phosphorus, magnesium and electrolytes, creatinine clearance, plasma immunoreactive parathyroid hormone, and serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were similar in both study groups on each diet. Measurements of plasma renin activity and serum aldosterone levels were higher in the hypertensive than in the normotensive group on each diet (p less than .05-.01). Serum 1,25-dihydroxyvitamin D and urinary calcium increased on the high sodium diet in the normotensive (p less than .05) and the hypertensive groups (p less than .01). When the data for normotensive subjects and hypertensive patients were pooled by gender, males had a 1 1/2 to 3 times the urinary calcium excretion than females, regardless of diet. The present study indicates that there are no differences in the selected components of calcium and vitamin D metabolism in response to sodium intake in patients with essential hypertension and normal plasma renin activity as compared to normal controls.     

Impaired sodium excretion during mental stress in mild essential hypertension

In hypertensive rats, environmental stress causes sodium retention by an exaggerated increase in renal sympathetic nerve activity, which is modulated by angiotensin II. We tested whether similar effects can be observed in humans. In 66 normotensive subjects (half of them with a family history of hypertension) and 36 subjects with mild essential hypertension, urinary sodium excretion and renal hemodynamics were examined at rest and during mental stress treated either with placebo or ACE inhibition in a double-blind, randomized, cross-over design. Despite a marked increase in glomerular filtration rate in response to mental stress (Deltaglomerular filtration rate, 4.3+/-7.7 mL/min in normotensives without versus 5.6+/-8.4 mL/min in normotensives with a family history versus 10.1+/-5.7 mL/min in patients with mild essential hypertension; P:<0.002), the increase in urinary sodium excretion was blunted in patients with mild essential hypertension (Deltaurinary sodium excretion, 0.12+/-0.17 mmol/min versus 0.10+/-0.14 mmol/min versus 0.05+/-0.14 mmol/min; P:<0.05). ACE inhibition corrected the natriuretic response to mental stress in subjects with mild essential hypertension (Deltaurinary sodium excretion, 0.05+/-0.14 mmol/min with placebo versus 0.13+/-0.19 mmol/min with ACE inhibition; P:<0.01); thus, after ACE inhibition, urinary sodium excretion increased similarly in all 3 groups. In conclusion, impaired sodium excretion occurs during mental stress in human essential hypertension but not in subjects with positive family history of hypertension. This abnormality in sodium handling during activation of the sympathetic nervous system appears to be mediated by angiotensin II.     

Anti-proteinuric effect of an N-type calcium channel blocker, cilnidipine

The objective of the present study was to determine anti-proteinuric effect of an N-type calcium channel blocker-cilnidipine. Subjects were 43 essential or renal hypertensive subjects who had been taking calcium channel blockers other than cilnidipine for at least 6 months. All patients had proteinuria greater than 0.2 g/day in spite of fair blood pressure control (<150/90 mmHg). Calcium channel blockers in 25 patients (62+/-3 years) were switched to cilnidipine (cilnidipine group), whereas other 18 patients (58+/-3 years) continued to take originally prescribed calcium channel blockers (control group). The 24-hr urine collections were done at baseline and after 6 months of the follow-up period. Baseline characteristics including age, blood pressure levels, body mass index and creatinine clearance were similar between cilnidipine and control groups. Urinary protein excretion also was comparable between cilnidipine (0.61+/-0.10 g/day) and control (0.86+/-0.17 g/day) groups. Urinary protein significantly decreased after 6 months in cilnidipine group (- 0.21+/- 0.11 g/day, - 36%, p< 0.01), whereas it did not change in control group (+ 0.01+/- 0.15 g/day, 0.4%, ns). There were no significant changes in blood pressure, serum creatinine, creatinine clearance, estimated protein intake, and urinary salt excretion during the follow-up period in either group. The reduction of urinary protein by cilnidipine was evident in essential hypertensives (- 54+/-9%, n=18, p<0.01) but not in renal hypertensives (+10+/-35%, n=7, ns). Results suggest that cilnidipine has an anti-proteinuric effect especially in patients with essential hypertension.     

Effects of the selective aldosterone blocker eplerenone versus the calcium antagonist amlodipine in systolic hypertension

Eplerenone is a highly selective aldosterone blocker, which is under development for the treatment of hypertension and heart failure. To assess its usefulness in older patients with systolic hypertension and widened pulse pressure, we compared the effects of eplerenone with amlodipine, on clinic blood pressure (BP) and pulse pressure and in a subset of the patients, ambulatory BP, vascular compliance, and urinary albumin excretion. The study involved 269 patients > or =50 years of age who were randomly assigned to either eplerenone (50 to 200 mg daily) or amlodipine (2.5 to 10 mg daily) in a double-blind titration to effect design. After 24 weeks of therapy, reductions in clinic systolic BP were similar for both treatments (eplerenone, -20.5+/-1.1 mm Hg; amlodipine, -20.1+/-1.1 mm Hg). Reductions in clinic diastolic BP were modestly larger on amlodipine (-6.9+/-0.7 mm Hg) compared with eplerenone (-4.5+/-0.7 mm Hg) (P=0.014). Pulse pressure was also reduced similarly from baseline by the 2 treatment groups (eplerenone, -15.9 mm Hg versus amlodipine, -13.4 mm Hg, P=0.07). Changes from baseline in pulse wave velocity after 24 weeks of therapy were statistically similar for eplerenone and amlodipine. In patients with microalbuminuria at baseline (>30 mg albumin/g creatinine), eplerenone reduced the urinary albumin/creatinine ratio by 52% compared with a reduction of 10% by amlodipine (P=0.04). Thus, eplerenone was as effective as amlodipine in lowering systolic BP and pulse pressure as well as pulse wave velocity in older patients with widened pulse pressure hypertension. Furthermore, eplerenone reduced microalbuminuria to a greater extent than amlodipine in this older patient group.     

Aldosterone excretion rates in children and adults during sleep

The present study undertook to examine aldosterone excretion during sleep as an integrated measurement of aldosterone production. A 24-hour urine collection was divided into awake and sleep fractions. Urinary aldosterone and electrolyte excretion were measured in 26 healthy children (mean age, 8.9 +/- 1.9 [SD] years) and 28 adults (mean age, 29.9 +/- 9.5 years). Aldosterone excretion in children was 5.6 +/- 3.9 (SD) micrograms/g creatinine during the awake period, which was significantly different from the 3.9 +/- 4.1 micrograms/g creatinine value recorded during sleep (p less than 0.002). In adults, awake aldosterone excretion was significantly greater than that during sleep; 4.9 +/- 2.7 versus 3.2 +/- 1.6 micrograms/g creatinine (p less than 0.001). Sleep aldosterone excretion values were highly correlated with the corresponding 24-hour aldosterone excretion values (r = 0.85, p less than 0.001) in children and in adults (r = 0.64, p less than 0.001). Sleep aldosterone excretion was correlated with 24-hour potassium excretion (p less than 0.02) only in children. Sleep aldosterone excretion correlated with neither sleep nor 24-hour sodium excretion in children or adults. Sleep electrolyte excretion rates were highly correlated with 24-hour excretion rates in both children and adults. Dexamethasone, 1 mg, administered the night before to suppress the normally high morning levels of endogenous adrenocorticotropic hormone, had no discernible effect on sleep aldosterone excretion. These results indicate that measurement of aldosterone excretion in an easily collected sleep urine sample provides a reliable index of aldosterone production in children and adults.     

Urinary excretion of cyclic adenosine 3',5'-monophosphate in children of different ages.

The urinary excretion of cyclic AMP was investigated in 97 healthy children, 3 months to 16 years old. When the excretion was expressed as mumol/24 h an increase with age (r = 0.693, P less than 0.001) and an increase with body weight (r = 0.700, P less than 0.001) were found to be quite similar. In relation to surface area, the average excretion for children up to 91/2 years old was 4.45 +/- 1.71 mumol/m2 in constrast with 2.22 +/- 0.66 mumol/m2 in older children (P less than 0.001). The decline appears to be associated with approaching puberty. When cAMP excretion was related to urinary creatinine, an inverse correlation with age was found (r = -0.772, P less than 0.001). In the youngest category, 3 months to 4 years old, the ratio was 9.26 +/- 1.49 mumol/g creatinine vs 4.67 +/- 1.05 mumol/g creatinine in the age group 12 to 16 years old (P less than 0.001), which compares closely with the normal adult average of 4.34 +/- 1.25 mumol/g creatinine found in our previous study. Throughout there was no evidence of sex differentiation.     

Environmental and physiological characteristics in adolescents genetically predisposed to hypertension

To clarify the possible risk factors for the development of hypertension, we examined the influences of heredity and environment on blood pressure regulation and whether or not the physiological condition differed in high school students with different levels of blood pressure. A borderline hypertensive (BH) group, consisting of 75 male students with systolic blood pressure (SBP) consistently above 140 mmHg on two separate occasions, was compared to a normotensive (N) group of 84 male students with SBP below 130 mmHg. In the BH group, 43% of students had a family history of hypertension within two generations of relatives, while 18% had one in the N group (p less than 0.05). The BH group was characterized by a gain in weight, a slight increase in 24-hour urinary sodium excretion, a higher heart rate, elevated values of plasma renin and urinary aldosterone, and an elevated sodium concentration in erythrocytes. Nevertheless, urinary excretion of potassium and kallikrein did not differ between the two groups. In each group, students with familial hypertension had a significantly (p less than 0.05) lower 24-hour urinary kallikrein excretion than those without it. Although kallikrein excretion correlated fairly well with aldosterone excretion (r = 0.47, p less than 0.01) or creatinine clearance (r = 0.59, p less than 0.01) in the BH students without familial hypertension, no such correlations were found in those with familial hypertension. These results indicate that the abnormal relationships of aldosterone to kallikrein metabolism and of kallikrein to renal function control may be involved as hereditary factors in the development of hypertension.     

The relationship between obesity and transforming growth factor beta on renal damage in essential hypertension

The aim of this study was to evaluate the effect of obesity on renal functions and the possible relationship between TGF-beta1 and obesity in hypertensive patients. Seventy newly diagnosed, hypertensive patients (male/female 36/34, aged 45.0 +/- 8.0 years) and 30 (male/female 17/13, aged 41.8 +/- 7.7 years) normotensive controls were included. Patients in both groups were analyzed for serum levels of glucose, creatinine, uric acid, lipids, and TGF-beta1. A 24-hour urine sample was also obtained; creatinine clearance rate and urinary albumin excretion (UEA) were investigated. TGF-beta1 levels were significantly higher (40.7 +/- 13.6 versus 34.2 +/- 12.1 pg/mL, P = 0.02), and creatinine clearance was significantly lower in patients compared with controls (98.9 +/- 25.5 versus 124.5 +/- 23.1 mL/min. per. 1.73 m(2), P = 0.001). Serum TGF-beta1 levels (45.2 +/- 14 versis 38.0 +/- 12.8 pg/mL, P = 0.03), creatinine clearance rates (109.8 29.9 versus 93.0 +/- 20.8 mL/min. per. 1.73 m(2), P = 0.001), and urinary albumin excretion (55.7 +/- 62.0 versus 12.7 +/- 12.6 mg/24 h, P = 0.002) were higher in obese hypertensive patients than in nonobese patients. In hypertensive patients, TGF-beta1 levels correlated with body mass index (r = 0.296, P = 0.01) and creatinine clearance (r = 0.238, P = 0.04). The results suggest that increased body mass index is associated with increased creatinine clearance, urinary albumin excretion, and TGF-beta1 levels in essential hypertension. In addition, TGF-beta1 is positively correlated with body mass index and creatinine clearance in patients with essential hypertension.     

OESTROGEN-PROGESTOGEN ORAL CONTRACEPTIVES AND URINARY CALCIUM EXCRETION

To examine the effects of age and use of oestrogen-progestogen oral contraceptive agents (OCA) on urinary calcium excretion, 24 h urine collections were obtained from 525 women aged 16-69 years during a health survey, and measurements made of the amounts of calcium, creatinine, sodium, potassium and magnesium excreted. Younger women using OCA excreted more potassium and creatinine but less calcium, and less calcium and magnesium relative to creatinine, than corresponding controls using no OCA. Older women excreted less creatinine, but significantly greater amounts of calcium, sodium, potassium and magnesium relative to creatinine than younger women. It is postulated that the diminished urinary calcium excretion observed in women using OCA resulted from suppression of bone resorption by oestrogens in OCA.     

Sodium and potassium in children with hypertension

On a baseline survey of 4936 school children, age ranged from 6 to 16 years, 199 children with the systolic blood pressure (SBP) value equal or greater than 95-th percentiles for age and sex were chosen as the hypertensive group (HBP), and the same number of children with the SBP lower than 50-th percentiles were matched as the normotensive group (NBP). For both groups the intra-RBC and plasma Na and K content, three sequential nights 8-hour urinary Na, K and creatinine excretion, and an oral saline-load test were performed. The results show that: (1) The intra-RBC K in the HBP was lower than in NBP, 259 +/- 57 vs 291 +/- 78 mumol/g-protein, P less than 0.01. That in those with positive hypertensive family history (FH+) was lower than in those of negatives (FH-). The intra-RBC K content was correlated inversely with diastolic BP, r = -0.43, P less than 0.001. No correlation between intra-RBC Na and BP was found; (2) Plasma Na concentration in HBP was much lower than in NBP, 137.5 +/- 7.9 vs 142.6 +/- 6.9 mmol/L, P less than 0.001. No difference was found between FH+ and FH-; (3) Mean 8-hour urinary K excretion at night was lower in HBP than in NBP, 23.9 +/- 11.5 vs. 28.2 +/- 14.7 mmol/g-creatinine, P less than 0.01; (4) After a load of oral saline the 4-hour urinary Na excretion was significantly higher in HBP than in NBP, 39.5 +/- 29.1 vs 30.8 +/- 23.2 mmol, P less than 0.01. Of those children with FH-, the 4-hour Na excretion in HBP was higher than in NBP, 39.8 +/- 29.4 vs 29.3 +/- 21.5 mmol, P less than 0.001, but no significant difference was found between HBP and NBP in children with FH+. We believed that the above changes in electrolytes in the children with their BP at higher-level percentiles represent an abnormal relation between potassium and arterial BP in the early stage of hypertension, as well as the early compensatory natriuresis of the kidneys.     

Urinary sodium excretion and blood pressure in chronic psychiatric in-patients.

Studies of populations or communities with no rise in blood pressure (BP) with advancing age and low prevalence of hypertension, may provide aetiological clues on the cause of hypertension. Within westernised societies, low blood pressures have been reported amongst chronic psychiatric in-patients and closed order secluded nuns. To investigate factors associated with BP in chronic psychiatric in-patients, we surveyed the BP and lifestyle factors in 89 such subjects in low security wards in three psychiatric hospitals. The average age of examines was 48.1 years (s.d. 15.8) and the patients had been in hospital for a mean of 8.6 years (range 1.1 to 51.7 years). The mean systolic and diastolic blood pressures of this group were 122.0 mm Hg (s.d. 14.2) and 76.9 mm Hg (s.d. 8.5) respectively. This was lower than pressures obtained when they were admitted to hospital (mean systolic BP change -17.1 mm Hg (s.d. 14), paired t-test P < 0.001; mean diastolic BP change -3.7 mm Hg (s.d. 12.2), paired t-test P < 0.001). BP at examination was significantly correlated with the urinary sodium to creatinine ratio (r = 0.302, P = 0.027), but not with the urinary sodium or potassium concentrations or potassium/creatinine ratio. The change in mean systolic BP (that is, the difference in BP between admission and examination) was significantly correlated with sodium/creatinine ratio (r = 0.62, P < 0.0001), urinary sodium concentration (r = 0.27, P = 0.045) and urinary sodium/potassium ratio (r = 0.36, P = 0.008). No relationship was found between BP and the nature of the psychiatric diagnosis or the type of psychotropic medication that was being prescribed. Stepwise multiple regression demonstrated that urinary sodium creatinine ratio and age were predictive of the change in systolic BP since admission to hospital. Our study confirms previous observations of lower mean systolic and diastolic blood pressures in chronic psychiatric subjects after a long in-patient stay. This fall is related to a low urine sodium excretion and suggests that a low dietary sodium intake may, in part, account for the low BP, or the difference between BP in the stressed and relaxed state, seen in these patients.     

Effect of dietary electrolytes upon calcium excretion: the Yi People Study.

OBJECTIVE: To investigate the relations of dietary sodium, potassium, calcium and magnesium with urinary calcium excretion. DESIGN: Cross-sectional epidemiologic study of 417 Chinese men with a wide variation of electrolyte intakes. METHODS: Three consecutive 24-h dietary recall data and three 24-h urinary samples were obtained on the same days. Urinary analyses included calcium, sodium, potassium, magnesium and creatinine. A fasting blood sample was obtained on the first morning, and serum analyses included electrolytes, creatinine and urea nitrogen. Correlation and regression analyses were used to examine the relation between electrolyte intake and calcium excretion. RESULTS: Whilst urinary calcium was not related to dietary calcium, it was significantly correlated with dietary sodium and potassium. A linear relationship was seen between dietary sodium, potassium and urinary calcium. After adjustment for age, body mass index, serum creatinine, dietary calcium intake and other electrolytes, urinary calcium was positively related to dietary sodium and negatively related to dietary potassium. This relation was seen at different levels of dietary calcium intake. The relation between magnesium intake and calcium excretion was inconsistent. CONCLUSION: These results suggest that sodium and potassium intake influence urinary calcium excretion in normotensive men.