Hyperaldosteronism among black and white subjects with resistant hypertension

Recent reports suggesting that the prevalence of primary hyperaldosteronism may be higher than historically thought have relied on an elevated plasma aldosterone concentration/plasma renin activity ratio to either diagnose or identify subjects at high risk of having primary hyperaldosteronism and have not included suppression testing of all evaluated subjects. In this prospective study of 88 consecutive patients referred to a university clinic for resistant hypertension, we determined the 24-hour urinary aldosterone excretion during high dietary salt ingestion, baseline plasma renin activity, and plasma aldosterone in all subjects. Primary hyperaldosteronism was confirmed if plasma renin activity was <1.0 ng/mL per hour and urinary aldosterone was >12 microg/24-hour during high urinary sodium excretion (>200 mEq/24-hour). Eighteen subjects (20%) were confirmed to have primary hyperaldosteronism. The prevalence of hyperaldosteronism was similar in black and white subjects. Of the 14 subjects with confirmed hyperaldosteronism who have been treated with spironolactone, all have manifested a significant reduction in blood pressure. In this population, an elevated plasma aldosterone/plasma renin activity ratio (>20) had a sensitivity of 89% and a specificity of 71% with a corresponding positive predictive value of 44% and a negative predictive value of 96%. These data provide strong evidence that hyperaldosteronism is a common cause of resistant hypertension in black and white subjects. The accuracy of these results is strengthened by having done suppression testing of all evaluated subjects.     

Influence of spironolactone on urinary prostaglandin E2 and kinin excretions in spontaneously hypertensive rats

Spironolactone was administered to spontaneously hypertensive rats (SHRs) in order to examine the urinary excretions of prostaglandin E2 (PGE2) and kinin. Thirteen SHRs were divided into 2 groups, and 0.1 ml of sesame oil was administered to one of 2 groups (spironolactone-untreated group) (n = 6) and 20 mg of spironolactone in 0.1 ml of sesame oil was administered to the other group (spironolactone-treated group) (n = 7) by the subcutaneous route for 10 days in succession, followed by the determination of body weight, blood pressure, urine volume, excretion levels of Na, K, kinin and PGE2 in 24-hour urine. Blood samples were drawn after these animals were killed by decapitation for determining plasma renin activity (PRA). In consequence, decreased blood pressure and increased urinary Na excretion were observed in the spironolactone-treated group. On the other hand, PGE2 excretion level in 24-hour urine markedly decreased immediately after administration of spironolactone (p less than 0.05) and was maintained at lower levels up to the end of experiment. However, 24-hour urinary kinin levels showed similar changes in the spironolactone-treated group and the untreated group with no significant difference between the two groups. These results indicate that spironolactone has a suppressive effect on urinary PGE2 excretion, the activity of which is not mediated by kinin production in the kidneys but produced by a direct action of spironolactone itself.     

IS THE ‘SODIUM INDEX’ A USEFUL WAY OF EXPRESSING CLINICAL PLASMA RENIN,ANGIOTENSIN AND ALDOSTERONE VALUES?

In normal subjects taking variously high, normal or low sodium diets, while potassium intake was maintained within the normal range, highly significant inverse relationships were demonstrated between 24 h urinary sodium output and the concurrent plasma concentrations of renin, angiotensin II and aldosterone. With linear coordinates, these relationships were described by rectangular hyperbolae. With logarithmic plots the relationships became rectilinear. When 24 h urinary sodium output was 75 mmol or higher, there was no worthwhile advantage in relating renin to sodium excretion; plasma angiotensin II and aldosterone, however, were significantly related inversely to urinary sodium in this range. When 24 h urinary sodium output was below 10 mmol, plasma renin, angjotensin II and aldosterone all varied over wide but elevated ranges and were not significantly related to urinary sodium excretion rates. We conclude that whereas estimations of urinary sodium may be of value in revealing latent aberrations of sodium intake, there is no distinct advantage in relating measurements of renin or angiotensin II to urinary sodium output if the diet is known to be within broad ‘normal’ limits. This should simplify the relevant blood sampling procedure under both ward and outpatient conditions. If plasma renin, angiotensin II and aldosterone are to be related to concurrent urinary sodium output, logarithmic, rather than linear, co-ordinates, are appropriate.     

Dipyridamole decreases circulating renin-angiotensin system activity in hypertensive patients.

To study the effect of adenosine on renin release, n = 6 hypertensive patients, while on a constant 80 to 100 mEq/24 h Na+ diet, received oral 150 mg dipyridamole (an adenosine uptake inhibitor) three times daily for 3 days while upright plasma renin activity (PRA) and plasma aldosterone, urinary aldosterone, plasma and urinary Na+,K+, and creatinine clearance were monitored the day before (basal) the first and third day of the treatment and the day after the withdrawal (recovery). As compared to basal and to recovery, dipyridamole significantly decreased PRA, and plasma and urinary aldosterone without affecting plasma and urinary Na+ and K+, creatinine clearance, blood pressure, and heart rate. These data, showing that dipyridamole decreases PRA and aldosterone, confirm also in hypertensives that endogenous adenosine inhibits the circulating renin-angiotensin-aldosterone system.     

Lipid metabolism, atherogenesis, and haemostasis in Eskimos: the role of the prostaglandin-3 family

In Eskimos coronary heart disease is a rarity. This can partly be explained by their favorable plasma lipid levels. An additional factor seems, however, to be that in Eskimo food polyunsaturated fatty acids of the omega-3 series replace those of the omega-6 series. C20:5, omega-3 can be converted by the vessel wall to an antiaggregatory substance, whereas it has no proaggregatory effect on platelets. Consistent with these findings Eskimos were found to have a nearly 2-fold longer bleeding time than Danes. Platelet aggregability, too, was markedly depressed when exposing platelets from Eskimos to ADP and collagen.     

Active and Inactive Renin and Kidney Function in Young Subjects with Different Predisposition to Develop Essential Hypertension

Renal and cardiac function were measured in 65 offspring of hypertensive parents (OHP) and in 56 offspring of normotensive parents (ONP). in two additional groups of 24 OHP and 42 ONP plasma renin activity (PRA) and plasma active (PRAC), inactive (PRIC) and total (PRTC) concentration were measured. OHP had significantly higher renal plasma flow (p < 0.01), glomerular filtration rate (p < 0.02) and 24-hour urinary output than ONP, while PRA was lower (p < 0.01). The measurements of the different forms of renin gave the following results:

PRIC and PRTC were lower in OHP than in ONP, but the only statistically significant difference concerns PRIC (p < 0.025). A possible interpretation of these findings is that a primary increased tubular ion and water reabsorption might be the cause of the kidne function pattern seen in OHP.     

Sodium excretion and racial differences in ambulatory blood pressure patterns.

The influence of Na+ excretion and race on casual blood pressure and ambulatory blood pressure patterns was examined in a biracial sample of healthy, normotensive children and adolescents (10-18 years; n = 140). The slopes relating 24-hour urinary Na+ excretion to systolic blood pressure were different for both black and white subjects for casual blood pressure (p less than 0.001) and blood pressure during sleep (p less than 0.03). For casual blood pressure, the slope was significant for black subjects (beta = 0.17; p less than 0.001) but not for white subjects. For blood pressure during sleep, the slope was again significant for black subjects (beta = 0.08; p less than 0.01) but not for white subjects. Na+ excretion was also related to awake levels of systolic blood pressure for black subjects (beta = 0.08, r = 0.36; p less than 0.01), although the slopes for both black and white subjects were not significantly different. Further analyses indicated the results were not due to racial differences in 24-hour urinary K+ excretion. However, plasma renin activity was marginally related to Na+ excretion in white subjects (r = 0.22; p less than 0.06) but not black subjects, a finding that is consistent with previous studies. Na+ excretion was not associated with diastolic blood pressure or heart rate in either group under any condition. The results of this study support research that has demonstrated a stronger relation between Na+ handling and casual blood pressure in black subjects and extend these findings to blood pressure while the subject is both awake and asleep.     

Contribution of circulating angiotensinogen concentrations to variations in aldosterone and blood pressure in a group of African ancestry depends on salt intake

In high-Na(+), low-K(+) diets, which suppress renin release in salt-sensitive groups, the mechanisms maintaining increases in renin-angiotensin-aldosterone system activation downstream from renin and renin-angiotensin-aldosterone system-induced effects on blood pressure (BP) are uncertain. Whether circulating angiotensinogen concentrations (AGT) or its determinants may contribute to maintaining serum aldosterone concentrations (aldosterone) and increases in BP on high-Na(+), low-K(+) diets was evaluated in 579 participants of a community sample of African ancestry. Plasma renin concentrations were inversely related to BP (P<0.0001) and an index of salt intake (24-hour urinary Na(+)/K(+), P<0.0001). An interaction between AGT and urinary Na(+)/K(+) was independently associated with aldosterone (P<0.001) and systolic BP (SBP; P<0.05). Independent of confounders, in participants with urinary Na(+)/K(+) at or more than the median for the sample, AGT was positively associated with aldosterone (P<0.0001) and SBP (P<0.005). No independent AGT-aldosterone or AGT-SBP relationships were noted in participants with urinary Na(+)/K(+) less than the median for the sample. Standardized β-coefficients (slopes) of AGT-aldosterone and AGT-SBP relationships were greater in participants with urinary Na(+)/K(+) at or more than the median (AGT-aldosterone=0.30±0.06, AGT-SBP=0.16±0.05) compared with those with urinary Na(+)/K(+) less than the median (AGT-aldosterone=-0.04±0.06; AGT-SBP=-0.03±0.05; P<0.01-0.0001 for comparison of slopes). The AGT-SBP relationship in participants with urinary Na(+)/K(+) at or more than the median for the sample was equivalent to the relationship between body mass index and BP. In conclusion, in participants of African ancestry, in the presence of high-Na(+), low-K(+) diets, which suppress renin release, renin-angiotensin-aldosterone system activation and its impact on BP are maintained in part by AGT.     

The Diagnostic Value of the 24 Hour Integrated Concentration of Plasma Aldosterone

The 24-hour urinary excretion rate of aldosterone, the 24-hour integrated concentration of plasma aldosterone (IC-ALDO) and the morning plasma aldosterone levels from a single, discrete venipuncture of 92 subjects (30 normal subjects, 62 patients with mild, essential hypertension) were compared, using the variance ratio method, to 12 patients with primary aldosteronism.

The variance of the IC-ALDO was significantly lower than the respective variances of the 24-hour urinary excretion of aldosterone (P < 0.01) and of the discrete, morning plasma levels of aldosterone (P < 0.01).

The clinical usefulness of this diagnostic procedure depends on its ability to discriminate between healthy subjects and various hypertensive patients. Because of its narrower variance and enhanced discriminatory ability, the 24-hour IC-ALDO may have useful application in diagnosis of various disorders of aldosterone secretion. We have found the IC-ALDO completely separated 11 of 12 primary aldosteronism patients (mean 36±17) from essential hypertensive controls (mean 9.6±4.1)(P < 0.01). When IC-ALDO was combined with integrated concentration of plasma renin activity in an ALDO/RENIN ratio, all 12 primary aldosteronism patients were diagnosed.     

Renal underexcretion of uric acid is present in patients with apparent high urinary uric acid output

OBJECTIVE: To compare renal handling of uric acid in patients with primary gout with that of a control group. METHODS: A case-control study of 100 patients with primary gout and 72 healthy controls was undertaken. Creatinine clearance, uric acid clearance, 24-hour uric acid urinary excretion, fractional excretion of uric acid, excretion of uric acid per volume of glomerular filtration, urinary uric acid to creatinine ratio, and glomerular uric acid filtered load were calculated using 24-hour urine samples. After treatment with allopurinol to achieve similar glomerular filtered load of uric acid, patients were again compared with controls. RESULTS: Patients with gout showed lower uric acid clearance, fractional excretion of uric acid, excretion of uric acid per volume of glomerular filtration, and urinary uric acid to creatinine ratio than controls at baseline, when patients showed hyperuricemia. Although the glomerular uric acid filtered load was much higher in patients with gout than controls, 24-hour uric acid excretion was not statistically different. After treatment with allopurinol, and achieving similar uric acid filtered loads, patients still showed lower figures than controls. When patients with 24-hour urinary uric acids levels >700 mg/day were compared with controls, they had lower uric acid clearance and fractional excretion of uric acid than controls, both at baseline and after achieving similar filtered loads with allopurinol therapy. CONCLUSIONS: Renal underexcretion is the main mechanism for the development of primary hyperuricemia in gout, but even patients showing apparent high 24-hour uric acid output show lower uric acid clearance than controls, indicating that relative, low-grade underexcretion of uric acid is at work.     

Effects of long-term treatment with indomethacin on renal function

The prolonged effects (42 days) of indomethacin treatment on the renin-angiotensin-aldosterone axis, renal hemodynamics, and renal excretory function in humans were studied. Indomethacin produced a 41% sustained depression in the 24-hour excretion of prostaglandin E2 and a mild (7%) decrease in inulin clearance but did not affect the clearance of p-aminohippurate, the 24-hour excretion of sodium and potassium, or the basal values of plasma aldosterone; however, it decreased the basal values of renin and prevented the stimulated (3 hours of walking) responses of plasma renin activity and plasma aldosterone. Indomethacin also produced a decrease in both the diuretic and saluretic response to furosemide and in the renal ability to concentrate urine. The indomethacin-induced hyporeninism and hypoaldosteronism were more pronounced when the subjects were receiving a sodium-restricted diet. This finding indicates that prolonged administration of anti-inflammatory drugs induces chronic hyporeninism and hypoaldosteronism. Prolonged treatment with indomethacin also produced some of the symptoms of a syndrome of hypoprostaglandinism, such as decreased plasma renin activity, plasma aldosterone, and urinary prostaglandin E2 in association with increases in plasma potassium levels and diastolic pressure.     

Physiologic roles of 11beta-hydroxysteroid dehydrogenase type 2 in kidney

We developed enzyme-linked immunosorbent assays to measure urinary free cortisone (E) and cortisol (F) and analyzed correlations between clinical measures reflecting mineralocorticoid action and 24-hour urinary excretion of E and F or their ratio, uE/F, which has been considered as the most sensitive index of renal 11beta-hydroxysteroid dehydrogenase type 2 activity. Two hundred nineteen healthy men were enrolled in this study. The uE/F ratio was 1.10 +/- 0.41 (mean +/- SD), and a strong linear correlation between uE and uF was observed in a double reciprocal plot. Urinary acid-labile aldosterone excretion had a negative correlation with 24-hour urinary Na excretion and Na/K ratio, but uE/F ratio had a weak positive correlation with the Na/K ratio and no significant correlation with 24-hour urinary Na excretion. In contrast, uE and uF had positive correlations with 24-hour urinary excretions of Na and K, raising the possibility of separate renal effects mediated by the glucocorticoid receptor. Furthermore, uE and uE/F ratio had strong negative correlations with urinary concentrations of Na and K. These results suggest that renal 11beta-hydroxysteroid dehydrogenase type 2 is an important regulatory factor of renal Na and K handlings independently of and/or complementary to the mineralocorticoid action of aldosterone.     

Effects of the renin inhibitor MK-8141 (ACT-077825) in patients with hypertension

The renin inhibitor MK-8141 (ACT-077825) demonstrates substantial immunoreactive active renin (ir-AR) increase (sevenfold) without a persistent plasma renin activity (PRA) decrease. The present study assessed the antihypertensive efficacy of MK-8141 in hypertensive patients. In this double-blind, placebo- and active comparator-controlled study, 195 patients with hypertension (trough sitting diastolic blood pressure ≥92 to <105 mm Hg, trough sitting systolic blood pressure <170 mm Hg, and 24-hour mean diastolic blood pressure [DBP] ≥80 mm Hg) were randomized to one of four treatments (stratified by race, black versus others): MK-8141 250 mg, MK-8141 500 mg, enalapril 20 mg, or placebo. Blood pressure was measured at trough and as 24-hour ambulatory blood pressure monitoring. The primary end point was change from baseline in 24-hour mean ambulatory DBP measured after 4 weeks. At week 4, the change from baseline in 24-hour mean (95% CI) ambulatory DBP compared with placebo was ?1.6 mm Hg (?4.2, 1.1), ?1.1 mm Hg (?3.9, 1.6), and ?4.9 (?7.5, ?2.2) for MK-8141 250 mg, MK-8141 500 mg, and enalapril 20 mg, respectively. Only mean ambulatory DBP-lowering with enalapril 20 mg was statistically significant. Enalapril, but not MK-8141, also significantly lowered 24-hour mean ambulatory systolic blood pressure (SBP) compared with placebo (?6.7 mm Hg [?10.5, ?2.8]). Neither enalapril nor MK-8141 significantly lowered trough DBP and SBP compared with placebo. MK-8141 was generally well tolerated. In patients with hypertension, MK-8141 (ACT-077825) did not produce significant blood pressure–lowering efficacy despite a demonstrated effect of the drug on ir-AR, in the absence of durable PRA suppression.     

Hyponatraemia as a marker for high renin heart failure.

The factors that might activate the renin-angiotensin system in treated heart failure were explored. Serum Na+ correlated inversely with plasma renin activity. The degree of congestive heart failure measured by right atrial pressure, pulmonary capillary wedge pressure, cardiac index, and systemic vascular resistance did not correlate with plasma renin activity. Similarly, renal function as measured by blood urea nitrogen, creatinine, and urinary Na+ excretion did not correlate with plasma renin activity. In a prospectively screened group, seven patients with congestive heart failure who were found to be hyponatraemic had plasma renin activities greater than 15 ng/ml per h. Serial determinations in one patient showed plasma renin activity to vary inversely with the serum Na+. It is concluded that serum sodium can be used to identify those patients with congestive heart failure who have a high plasma renin activity. The value of identifying these high renin heart failure patients was seen in their response in four cases to specific therapy with a converting enzyme inhibitor.     

Serum Magnesium in Greenland Eskimos

ABSTRACT Serum magnesium in Greenland Eskimos living in Greenland is significantly higher (p<0.001) than in Greenlanders and Danes living in Denmark. Danes living in Greenland show intermediate values. The higher serum magnesium may be due to a high intake of nutrients from fish and sea mammals. A more complete intestinal absorption of magnesium caused by a low dietary calcium should also be considered. The high serum magnesium may contribute to the rare occurrence of urinary calculi in Grenlanders.     

Ethnic, geographic and dietary influences upon vasoactive hormones and blood pressure among Greenland Inuit and Danes

AIM: To study levels of vasoactive hormones and urinary excretion of sodium and potassium between groups of Greenland Inuit and Danes, and to analyse the relationship between these hormones and 24-h blood pressure, including nightly blood pressure dips and pulse pressure. METHODS: 145 Greenlandic participants were categorized in three groups according to degree of westernization, based on dietary habits and current place of residence; 41 Danes were included as controls. Twenty-four-hour blood pressure was measured. Venous plasma concentrations of vasoactive hormones were measured. Urine was collected for 24 hours for analysis of excretion of sodium and potassium. RESULTS: The Inuit population of Greenland had a lower diastolic blood pressure, a higher pulse pressure and lower nocturnal blood pressure dip than Danes had. Angiotensin II in plasma and urine excretion of potassium were higher among Greenlanders compared with Danes, irrespective of diet and place of residence. Aldosterone and urine excretion of sodium were significantly higher among participants in Denmark compared with participants in Greenland. Brain natriuretic peptide and atrial natriuretic peptide were independently and negatively associated with diastolic blood pressure, and vasopressin was positively associated with systolic blood pressure and pulse pressure. Ethnic differences in the effect of vasoactive hormones or urinary sodium and potassium excretion could not explain the difference in blood pressure. CONCLUSION: It is suggested that a high dietary intake of potassium and low sodium intake among Greenlanders may affect blood pressure. Further attention should be drawn to the occurrence of high pulse pressure and high activity in the renin-angiotensin system in Inuit populations.     

Detection of primary aldosteronism by the 6-hour integrated aldosterone/renin ratio

An outpatient diagnostic procedure measuring the 6-hour integrated plasma concentration of aldosterone and plasma renin activity was used to detect primary aldosteronism in 12 patients with low renin hypertension, including six with mild hypertension and normal urinary excretion and spot plasma levels of aldosterone. The ratio of integrated plasma concentration of aldosterone to plasma renin activity in the 12 patients (mean, 339; range, 116-700; p less than 0.0001) did not overlap with that measured in 105 normotensive controls (mean, 27.8; range, 5-97) or in 87 subjects with essential hypertension (mean, 29.2; range, 4-67). Eight patients had surgically proven adenomas (3 of which measured less than 5 mm) with normalization of blood pressure following adrenalectomy. The four remaining patients had bilateral hyperplasia. The 6-hour integrated plasma concentration of aldosterone to plasma renin activity ratio was found to be a useful new outpatient diagnostic tool for evaluation of primary hyperaldosteronism.     

Roles of kidney and submandibular gland in the release of rat plasma inactive renin

In this study we outlined the development of an enzymatic technique to activate plasma inactive renin by trypsin in rat plasma. Using this method, we reported the releasing mechanism of the trypsin-activable inactive renin which has not yet been clarified. Adult male Wistar rats (260-300 g) were kept on regular diet (Na: 260 mg/100g) unless explained and underwent operation under pentobarbital anesthesia (50 mg/kg). Blood samples were obtained from conscious rats through the cannulae, which had been inserted into the left femoral arteries 24h before the experiments. After addition of excessive renin substrate which had been obtained from the 24 h-nephrectomized rat plasma, renin was measured by the commercial RIA-kit (Dainabot). Trypsin (Worthington) treatment (20 mg/ml plasma for 10 min at 4 degrees C) was followed by addition of SBTI (Sigma) (20 mg/ml plasma). This condition maximally increased the rate of angiotensin I generation and did not alter the Km or optimum pH of the renin reaction. In this condition, trypsin reaction was completely inhibited by adding these concentrations of SBTI. The molecular weight of inactive renin (51,000) in the normal rat plasma estimated by Sephadex G-100 column (Pharmacia) was the same as that in the nephrectomized rat plasma. In conclusion, trypsin treatment of plasma (20 mg/ml plasma for 10 min at 4 degrees C) followed by SBTI (20 mg/ml plasma) was justified for trypsin activation of rat plasma. Using this method, we investigated the changes in active and inactive renin after bilateral nephrectomy in the salt-depleted rat. Active renin decreased rapidly after bilateral nephrectomy with a half life of 23.6 +/- 4.0 min. Inactive renin, on the other hand, increased gradually and reached to a plateau 24 h after bilateral nephrectomy, and was kept unchanged during the following 24 h. The infusion of mouse submandibular gland active renin or angiotensin II could not prevent the increase of plasma inactive renin in the nephrectomized rat. These suggest that there may be no feedback mechanisms between plasma inactive and active renin or angiotensin II. Furthermore, we investigated the organ-related sources of plasma inactive renin which markedly increased after total nephrectomy. Simultaneous removals of submandibular glands but not of adrenal glands completely prevented the postnephrectomy increases of plasma inactive renin. But, removals of submandibular glands or adrenal glands alone were followed by no changes in the basal levels of plasma inactive renin.(ABSTRACT TRUNCATED AT 400 WORDS)     

Furosemide and plasma renin activity in essential hypertension.

Changes in arterial blood pressure, renal electrolyte excretion, and plasma renin activity in response to repeated doses of furosemide were measured in 12 patients with essential hypertension admitted to the medical service for electrolyte balance studies. Eighty and 120 mg/day furosemide in divided doses for 5 to 10 days produced a prompt increase in renal sodium excretion. Urinary Na/K concentration ratios, which were elevated during peak natriuresis, returned to control levels following the initial diuretic response. In 2 patients with high initial levels of plasma renin activity, arterial blood pressure was not reduced by furosemide, and more potent antihypertensive agents were required to control the blood pressure. In the remaining patients, furosemide produced a significant decrease in systolic and diastolic blood pressure. There was a general upward shift of plasma renin levels in terms of 24-hour renal sodium excretion in those who demonstrated an antihypertensive response to the drug. However, the average increase in plasma renin activity after repeated doses of furosemide was not statistically significant and no correlation was demonstrated between the level of plasma renin activity after furosemide and the blood pressure lowering effect of the drug.     

Characteristics of the course of hypertension in relation to on plasma renin activity

In 94 patients with hypertension the plasma renin activity was determined by the Yu. A. Serebrovskaya and I.A. Uchitel technique, the glomerular filtration--after Rehberg, potassium and sodium content in blood serum and 24-hour urine samples--by flame photometry. Hypertensive disease was found to be accompanied by an elevated plasma renin activity in 47.9% of the patients, by a normal level--in 26.9%, and by a reduced--in 25.6%, as compared with control group data. Cardiovascular complicatins were found in 1/5 of those with an elevated plasma renin activity, and no such complications were observed in those with a normal or reduced renin activity. An elevated plasma renin activity is a risk factor. The highest mean age and the longest duration of the disease history are typical for patients with low plasma renin activity. To choose the most rational therapy regimen it may be useful to calculate the renin-sodium index that reflects the relationship between the plasma renin activity and the urine excretion of sodium.