Measurement Of Renin Research Articles

PP.27.23] GUIDELINES FOR PRIMARY ALDOSTERONISM

Objective: In 2008 the Endocrine Society published guidelines for the diagnosis and treatment of primary aldosteronism (PA), recommending screening testing in around 30% of the hypertensives. The present study was undertaken to establish the extent to which general practitioners (GPs) are aware of the guidelines and their familiarity with the management of PA. Design and method: The study took place in Italy and Germany. A questionnaire was administered to 250 physicians in Italy and 250 in Germany by the market research firm Stethos srl. The physicians chosen cared for at least 1000 monitored patients. Results: The median of patients seen by each physician resulted to be 1,500 in both countries, 18% of which were hypertensives in Italy and 25% in Germany. Among hypertensive patients, 11% were considered to be affected by secondary hypertension (in 34.4% of cases attributed to an endocrine disease) and 7.6% displayed resistant hypertension in Italy; prevalence of secondary and resistant hypertension resulted 20% and 7.9% in Germany, respectively. At diagnosis of hypertension 50.4% of Italian GPs and 42.9% of German GPs request diagnostic tests to the patient; potassium levels are only requested by 43% GPs in Italy and 58% in Germany; renin and aldosterone measurement are required by around 8% of the GPs in both countries. Only 3% of the patients had the renin and aldosterone levels measured before the beginning of pharmacological therapy in both countries. In Italy, each GP follows an average of 3 PA patients, which results in a prevalence of PA of 1% among hypertensive patients; in Germany, each GP follows an average of 7 PA patients which results in a prevalence of PA of 2%. Conclusions: In conclusion, there is a significant gap between theory, as laid down in guidelines, and practice. It is likely that a similar gap exists throughout the world.

New Advances in the Diagnostic Workup of Primary Aldosteronism.

Primary aldosteronism is an important and common cause of hypertension that carries a high burden of morbidity. Outcomes, however, are excellent if diagnosed and treated appropriately. The diagnostic workup for primary aldosteronism is complex and comprises three steps: (1) screening, (2) confirmatory testing, and (3) subtype differentiation. In this review, we discuss recent advances in the diagnostic workup for primary aldosteronism. The development of accurate mass spectroscopy–based assays for measuring aldosterone will lead to improved confidence in all diagnostic aspects involving measurement of aldosterone, and accurate measurement of angiotensin II may soon advance us beyond the measurement of renin. We now have a greater understanding of hormonal influences on the aldosterone/renin ratio, which are particularly important when screening premenopausal women or those taking estrogen-containing preparations. Confirmatory testing is important, but there are limitations to the commonly used methods that have recently become more apparent, with new approaches offering a way forward. Adrenal venous sampling (AVS) is a challenging procedure but is important for deciding on treatment options. Success rates may be improved by the use of Synacthen stimulation and of rapid intraprocedural measurement of cortisol. Better understanding of AVS interpretation criteria allows improved prognostication and aids treatment decisions. The use of labeled metomidate positron emission tomography computed tomography scanning may also offer an alternative to AVS in some units. Although the diagnostic approach to patients with primary aldosteronism remains a complex multistep process in which attention to detail is important, recent advances will improve patient care and outcomes.

Renin angiotensin aldosterone system altered in resistant hypertension in Sub-Saharan African diabetes patients without evidence of primary hyperaldosteronism.

BackgroundThe renin-angiotensin-aldosterone system may be altered in patients with resistant hypertension. This study aimed to evaluate the relation between renin-angiotensin-aldosterone system activity and resistant hypertension in Cameroonian diabetes patients with resistant hypertension.MethodsWe carried out a case-control study including 19 diabetes patients with resistant hypertension and 19 diabetes patients with controlled hypertension matched to cases according to age, sex and duration of hypertension since diagnosis. After collection of data, fasting blood was collected for measurement of sodium, potassium, chloride, active renin and plasma aldosterone of which the aldosterone-renin ratio was derived to assess the activity of renin-angiotensin-aldosterone system. Then, each participant received 2000 ml infusion of saline solution after which plasma aldosterone was re-assayed.ResultsPotassium levels were lower among cases compared to controls (mean: (4.10 ± 0.63 mmol/l vs. 4.47 ± 0.58 mmol/l), though nonsignificant (p = 0.065). Active renin, plasma aldosterone both before and after the dynamic test and aldosterone-renin ratio were comparable between cases and controls (all p values > 0.05). Plasma aldosterone significantly decreased after the dynamic test in both groups (p < 0.001), but no participant exhibited a post-test value>280 pmol/l. We found a significant negative correlation between potassium ion and plasma aldosterone (ρ = −0.324; p = 0.047), the other correlations being weak and unsignificant.ConclusionAlthough this study failed to show an association between RH and primary hyperaldosteronism in our context, there was a hyperactivity of renin-angiotensin-aldosterone system. Moreover, this study confirms the importance of potassium dosage when screening the renin-angiotensin-aldosterone system.

Metabolic Syndrome among Ischaemic Stroke Patients in Ghana: The Possible Role of Renin and Aldosterone

Background: Both metabolic syndrome (MetSyn) and the Renin Angiotensin Aldosterone System (RAAS) are predictors of adverse outcomes in stroke patients. This study aimed at evaluating the association between RAAS and MetSyn among ischaemic stroke subjects in a tertiary hospital of Ghana from September 2015 to June 2016. Methodology: The study purposively recruited 252 Ghanaians comprising 132 ischaemic stroke patients and 120 apparently healthy control subjects. The participants were subjected to measurements of plasma renin, serum aldosterone, lipid profile, anthropometries and blood pressure. Results: MetSyn prevalence among the stroke subjects compared to the controls were 50.0% vs 8.3% (NCEP/ATP III), 71.2% vs 9.2 (IDF) and 71.2% vs 6.7% (H_MS). Both renin and aldosterone were significantly (p 3) aldosterone (aOR = 2.7, p = 0.008), obesity (aOR = 11.7, p = 0.004) and high triglyceride (aOR = 5.3, p p = 0.742) were independently associated with increasing odds of metabolic syndrome. Moreover, there was a significant (p p

Hyponatraemia secondary to nivolumab-induced primary adrenal failure.

SummaryCheckpoint inhibitors, such as ipilimumab and pembrolizumab, have transformed the prognosis for patients with advanced malignant melanoma and squamous non-small-cell lung cancer, and their use will only expand as experience is gained in a variety of other malignancies, for instance, renal and lymphoma. As the use of checkpoint inhibitors increases, so too will the incidence of their unique side effects, termed immune-related adverse events (irAEs), which can affect dermatological, gastrointestinal, hepatic, endocrine and other systems. Nivolumab is a monoclonal antibody that blocks the human programmed death receptor-1 ligand (PD-L1) found on many cancer cells and is licensed for the treatment of advanced malignant melanoma. We describe the first case of nivolumab-induced adrenalitis resulting in primary adrenal failure presenting with hyponatraemia in a 43-year-old man with malignant melanoma. The case highlights the potentially life-threatening complications of checkpoint inhibitors and the need for patient education and awareness of irAEs among the wider clinical community because such side effects require prompt recognition and treatment.Learning points:Nivolumab can cause primary adrenal insufficiency.Not all cases of hyponatraemia in patients with malignancy are due to SIADH.Any patient on a checkpoint inhibitor becoming unwell should have serum cortisol urgently measured and if in doubt hydrocortisone therapy should be initiated.Although hyponatraemia can occur in patients with ACTH deficiency, the possibility of primary adrenal failure should also be considered and investigated by measurement of renin, aldosterone and ACTH.Patients receiving checkpoint inhibitors require education on the potential risks of hypocortisolaemia.PET imaging demonstrated bilateral increased activity consistent with an autoimmune adrenalitis.

Guidelines for primary aldosteronism: uptake by primary care physicians in Europe.

Primary aldosteronism is the most frequent form of secondary hypertension but is still markedly underdiagnosed. In 2008, the Endocrine Society released guidelines for primary aldosteronism diagnosis and management; current indications are that they are not being widely followed. To investigate the level of knowledge and application of the guidelines in a large representative cohort of general practitioners (GPs) in Italy and Germany. The study was carried out by web questionnaire on hypertension and primary aldosteronism management with 500 GPs (250 in Italy and 250 in Germany), stratified by geographical area and city size. The mean number of patients seen was 1747 (Germany) and 1388 (Italy). Of these, 18% were diagnosed as hypertensive in Italy and 25% in Germany. Renin and aldosterone measurements were ordered by 7% of GPs in Italy and 8% in Germany. GPs in Italy considered 8% of patients eligible for aldosterone and renin measurements compared with 13% of GPs in Germany. In Italy, primary aldosteronism prevalence was 1% among hypertensive patients; 36% of the GPs reported no primary aldosteronism patients under their care or diagnosed previously. In Germany, the prevalence of primary aldosteronism was 2% among hypertensive patients; 19% of GPs had no primary aldosteronism patients. In Germany and in Italy, primary aldosteronism is not widely recognized by GPs; Endocrine Society guidelines for primary aldosteronism diagnosis are not well known or applied, resulting in marked underdiagnosis of the disease.

LBPS 02-61 GUIDELINES FOR PRIMARY ALDOSTERONISM

Objective: In 2008 the Endocrine Society published guidelines for the diagnosis and treatment of primary aldosteronism (PA), recommending screening testing in around 30% of the hypertensives. The present study was undertaken to establish the extent to which general practitioners (GPs) are aware of the guidelines and their familiarity with the management of PA. Design and Method: The study took place in Italy and Germany. A questionnaire was administered to 250 physicians in Italy and 250 in Germany by the market research firm Stethos srl. The physicians chosen cared for at least 1000 monitored patients. Results: The median of patients seen by each physician resulted to be 1,500 in both countries, 18% of which were hypertensives in Italy and 25% in Germany. Among hypertensive patients, 11% were considered to be affected by secondary hypertension (in 34.4% of cases attributed to an endocrine disease) and 7.6% displayed resistant hypertension in Italy; prevalence of secondary and resistant hypertension resulted 20% and 7.9% in Germany, respectively. At diagnosis of hypertension 50.4% of Italian GPs and 42.9% of German GPs request diagnostic tests to the patient; potassium levels are only requested by 43% GPs in Italy and 58% in Germany; renin and aldosterone measurement are required by around 8% of the GPs in both countries. Only 3% of the patients had the renin and aldosterone levels measured before the beginning of pharmacological therapy in both countries. In Italy, each GP follows an average of 3 PA patients, which results in a prevalence of PA of 1% among hypertensive patients; in Germany, each GP follows an average of 7 PA patients which results in a prevalence of PA of 2%. Conclusions: In conclusion, there is a significant gap between theory, as laid down in guidelines, and practice. It is likely that a similar gap exists throughout the world.

Dose-effect relationship of perindopril 10, 14 and 20 mg assessed by urine and plasma AcSDKP levels in mildly sodium-depleted healthy volunteers

BackgroundWe describe a pharmacodynamic study of the dose-effect relationship of perindopril arginine at 10, 14, and 20mg with in vivo angiotensin-converting enzyme (ACE) activity, assessed by urine and plasma AcSDKP levels, as well as the effect on plasma active renin concentrations and blood pressure. MethodsThis randomized, double-blind, four-period, crossover study involved single-dose administration of perindopril arginine (10, 14, and 20mg or placebo) to 32 healthy male normotensive mildly sodium-depleted volunteers. Blood and urine were collected over 48h for AcSDKP, ACE activity, and plasma active renin measurements. ResultsThere were dose-related increases in urinary AcSDKP excretion and plasma AcSDKP concentration after administration of perindopril, with significant between-period differences (estimate of the median difference in urinary excretion over 48h of AcSDKP, 49.1 [95% CI: 15.3–82.0] nmol for 14 versus 10mg, and 73.2 [95% CI: 44.9–106.3] nmol for 20 versus 14mg). Consequently, a dose-dependent increase in plasma active renin concentration was observed. Even though each dose of perindopril 10 to 20mg was associated with a significant 24-h ambulatory blood pressure reduction versus placebo, no dose-dependency was detected in these normotensive subjects. ConclusionsAdministration of perindopril arginine 10, 14, or 20mg to mildly sodium-depleted healthy volunteers is associated with a dose-dependent inhibition of in vivo ACE activity with significant between-dose differences. This effect was associated with a dose-dependent increase in plasma active renin concentration, indicating a dose-dependent blockade of the renin angiotensin system.

Hiperaldosteronismo e hipoaldosteronismo

IntroductionAldosterone is a mineralocorticoid hormone which regulates the sodium homeostasis, the plasma volume and the blood pressure. EtiopathogeniaHypoaldosteronisms are a group of syndromes characterized by decreased levels of aldosterone (or resistance to its action). Primary hyperaldosteronisms have elevated levels of aldosterone and decreased of levels of renin, mainly due to primary adrenal hyperplasia (60%) or an aldosteronoma (30%). Clinical ManifestationsHypoaldosteronisms present with hyponatremia, natriuresis, hypovolemia and hyperkalemia/metabolic acidosis. Hyperaldosteronisms produce hypertension, sometimes with hypokalemia and metabolic alkalosis. DiagnosisThe association with a deficit of glucocorticoid should be discarded. The measurement of aldosterone and renin (basal / after stimulus) is necessary to guide the hypoaldosteronism diagnosis. The diagnosis of hyperaldosteronism requires a positive screening test and also a confirmation test; for differential diagnosis we should use adrenal CT and catheterization. TreatmentIn hypoaldosteronisms it is necessary to treat the precipitating cause and to administrate fludrocortisone. In hyperaldosteronisms the patient must be referred for surgery or treated with aldosterone antagonists according to the localization exams.

Establishment of reference intervals for aldosterone and renin in a Caucasian population using the newly developed Immunodiagnostic Systems specialty immunoassay automated system.

Measurement of aldosterone and/or renin is essential to aid the differential diagnosis of secondary hypertension, guide strategy for therapeutic management of hypertension and assess adequacy of mineralocorticoid replacement. The objective was to establish normative data for aldosterone and renin using the Immunodiagnostic Systems specialty immunoassay system platform in a Caucasian population. Following informed consent, 365 subjects were recruited to this study. Subjects were ambulatory and attended clinic for blood pressure measurement and phlebotomy between the hours of 7:00 and 11:00. Blood pressure was measured according to the 2013 European Society of Hypertension/Cardiology guidelines. The inclusion criteria: age ≥18 years, BMI <30 kg/m(2), non-pregnant, blood pressure <140/90, normal electrolytes and kidney function and not taking prescribed/over the counter medications. Ninety-four subjects were excluded based on these criteria. A total of 271 volunteers (females n = 145), aged 18-65 years formed the reference cohort. Blood for aldosterone/renin was collected into ethylenediaminetetraacetic acid specimen tubes. Samples were kept at room temperature and transported within 30 min of blood draw to the laboratory for immediate processing (centrifugation, separation and freezing of plasma). Plasma was stored at -20℃ prior to analysis on the Immunodiagnostic Systems specialty immunoassay system instrument. The established reference intervals in an Irish Caucasian population for renin: females: 6.1-62.7 mIU/L, males: 9.0-103 mIU/L, for aldosterone: females: <138-1179 pmol/L, males: <138-670 pmol/L, respectively. This study demonstrates that reference intervals for aldosterone and renin should be gender specific. These automated immunoassays offer rapid stratification of patients with refractory hypertension and will better facilitate the optimization of therapeutic management.

Circulating and intrarenal renin-angiotensin systems in healthy men and nonpregnant women.

The urinary excretion of renin–angiotensin system (RAS) proteins could reflect the activity of the intrarenal RAS. We hypothesized that the rates of excretion of RAS components into human urine are independent of circulating levels of these proteins and reflect the intrarenal RAS. There are no reports of the simultaneous measurement of prorenin, active renin, angiotensinogen (AGT), and angiotensin-converting enzyme (ACE) excretion in healthy individuals. Therefore, we measured plasma prorenin, ACE, and AGT and urinary renin (uRenin), prorenin (uProrenin), ACE (uACE), and AGT (uAGT) in men and nonpregnant women. Plasma (p) AGT was higher in women then men. Women who were taking estrogen had significantly higher pAGT. In women, pProrenin was negatively correlated with pAGT. There were no correlations between pProrenin, pAGT, and pACE and their urinary counterparts in either men or women. In men, uProrenin/creatinine ratios were lower than in women. There was no effect of estrogen use on urinary excretion of pProrenin, renin, AGT, and ACE. In men, there were significant correlations between uACE/creat and uRen/creat and uAGT/creat; uProrenin/creat and plasma cystatin C levels; and uRenin/creat and uNa/K were also positively correlated. No associations were found in women. In conclusion, urinary excretion of prorenin is sexually dimorphic and is not affected by estrogen use in women. Our data also suggest that the relationship between renal handling of sodium and urinary renin is sexually dimorphic. Since we found no associations between plasma RAS proteins and their urinary counterparts, and the ratio of uProrenin:pProrenin was strikingly different between men and women, levels of urinary RAS proteins in individuals with normal kidney function are most likely the result of tubular secretion, rather than ultrafiltration.

The utility of renal venous renin studies in selection of patients with renal artery stenosis for angioplasty: a retrospective study.

Recent studies of renal artery stenosis (RAS) failed to demonstrate greater benefit from angioplasty in terms of blood pressure (BP) lowering than medical treatment. Not all RAS are haemodynamically significant and identification of patients likely to benefit from angioplasty remains essential. We examined whether performing renal venous renin studies under stringent conditions might predict BP improvement. Patients with at least 60% RAS who underwent renal venous renin measurements in 2008-2013 were identified. Renal venous renin lateralization ratios (RVRRs) were calculated by dividing venous renin from the stenotic kidney with contralateral levels before and after stimulation with enalaprilat or captopril. Benefit was defined as BP less than 140/90 mmHg without medication, 10% decreased mean BP without increased daily defined doses (DDDs) or decreased DDD without a significant increase of mean BP. Twenty-eight patients were treated medically and 42 with angioplasty (median age 60.1 years, 41% male, 29% chronic kidney disease, 50% resistant hypertension). At 11.4 ± 3.3 months, 69% of patients treated with angioplasty had BP benefit compared with 25% with medical treatment (P < 0.001). Logistic regression identified resistant hypertension [odds ratio (OR) 0.18, 95% confidence interval (95% CI) 0.04-0.82, P = 0.03] and baseline DDD (OR 0.69, 95% CI 0.48-0.98, P = 0.04) as being negatively associated, and positive stimulated RVRR (OR 21.6, 95% CI 3.50-133.3, P = 0.001) positively associated with benefit from angioplasty. On multivariate logistic regression, only stimulated RVRR positivity predicted BP benefit (OR 20.5, 95% CI 2.9-145.0, P = 0.003). These findings suggest that a positive stimulated RVRR measured under optimal conditions may help to identify patients with RAS likely to improve from angioplasty.

Association of Post-Saline Load Plasma Aldosterone Levels With Left Ventricular Hypertrophy in Primary Hypertension.

Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular morbidity in hypertension. Current evidence suggests a contribution to LVH of plasma aldosterone levels that are inappropriately elevated for the salt status. The aim of this study was to investigate whether inappropriate modulation of aldosterone production by a saline load is associated with left ventricular (LV) mass in hypertensive patients. In 90 hypertensive patients free of clinically relevant cardiovascular complications in whom secondary forms of hypertension were ruled out, we performed a standard intravenous saline load (0.9% NaCl, 2 l in 4 hours) with measurement of plasma aldosterone and active renin at baseline and end of infusion. Bi-dimensional echocardiography was performed for the assessment of cardiac morphology and function. LVH was present in 19% of patients who had significantly worse renal function and higher body mass, blood pressure, and plasma aldosterone levels measured both at baseline and after the saline load than patients without LVH. LV mass was directly related to age, body mass, systolic blood pressure, duration of hypertension, baseline, and post-saline load plasma aldosterone levels and inversely to glomerular filtration. Multivariate regression analysis showed independent correlation of LV mass with body mass, systolic blood pressure, and plasma aldosterone levels measured after intravenous saline load, but not at baseline. In patients with hypertension, aldosterone levels measured after intravenous saline load are related to LV mass independent of age, body mass, and blood pressure, suggesting that limited ability of salt to modulate aldosterone production could contribute to LVH.

9B.06

Objective: Primary aldosteronism (PA) is the most frequent cause of secondary hypertension responsible for an increased rate of cardiovascular events. According to the Endocrine Society Guidelines, up to 50% of hypertensive patients should be screened for PA, using the aldosterone to renin (or plasma renin activity, PRA) ratio (AARR and ARR, respectively). The automated Diasorin LIAISON® chemiluminescent immunoassay for renin and aldosterone measurement became available and in many laboratories is currently used instead of the classical radioimmunometric PRA and aldosterone assay. Aim of the study was to prospectively compare the diagnostic accuracy of AARR and ARR as screening test for PA and the two aldosterone assays also during confirmatory test in patients with a positive screening test. Design and method: One hundred patients were screened for PA and 44 patients underwent confirmatory test (either by intravenous saline load or by captopril challenge test). We considered as cut off for the AARR 2.7 (ng/dL/mU/L) and for the ARR 30 (ng/dL/ng/mL/h). All patients positive to one of the two screening test underwent confirmatory test; patients with positive confirmatory test underwent subtype diagnosis by CT scanning and adrenal vein sampling. Results: Seventy three patients were diagnosed as essential hypertensives, 22 had bilateral adrenal hyperplasia and 5 had an aldosterone producing adenomas (APA). The AARR displayed a sensitivity of 78% and a specificity of 100%, whereas the ARR had a sensitivity of 96% and a specificity of 90%. Of the 6/27 PA patients missed by AARR, none resulted to be affected by APA. All PA patients were correctly diagnosed by chemiluminescence at confirmatory test. In the overall sample of 181 measurements available both the correlation for the PRA with renin and for aldosterone in chemiluminescence and radioimmunoassay were highly significant (Rho = 0.66, p < 0.0001 and Rho = 0.80, p < 0.0001, respectively). On ROC curves, the AUC for AARR was 0.905 (95% CI 0.821-0.988) and for ARR 0.947 (95% CI 0.903–0.991) and they were not significantly different. Conclusions: The automated aldosterone and renin chemiluminescent assay is a reliable alternative to the well-established radioimmunometric method, especially for the detection of APA.

Renin and Aldosterone Measurements in the Management of Arterial Hypertension

Renin-angiotensin-aldosterone system (RAAS) is recognized as the main regulatory system of hemodynamics in man, and its derangements have a key role in the development and maintenance of arterial hypertension. Classification of the hypertensive states according to different patterns of renin and aldosterone levels ("RAAS profiling") allows the diagnosis of specific forms of secondary hypertension and may identify distinct hemodynamic subsets in essential hypertension. In this review, we summarize the application of RAAS profiling for the diagnostic assessment of hypertensive patients and discuss how the pathophysiological framework provided by RAAS profiling may guide therapeutic decision-making, especially in the context of uncontrolled hypertension not responding to multi-therapy.

Comparison between aldosterone and renin measurement by chemiluminescent immunoassay and RIA for the diagnosis of primary aldosteronism

Comparison between aldosterone and renin measurement by chemiluminescent immunoassay and RIA for the diagnosis of primary aldosteronism

Long‐term L‐Triiodothyronine (T3) treatment in stable systolic heart failure patients: a randomised, double‐blind, cross‐over, placebo‐controlled intervention study

Chronic heart failure (HF) is characterized by reduced serum T3 levels and increased activity of the T3 degrading enzyme deiodinase D3. This may result in an intracellular composition of the cardiomyocyte mimicking that of hypothyroidism. Short-term T3-administration to systolic HF patients might be beneficial. Does long-term treatment with T3 have a beneficial effect on cardiac function and neurohormonal activation in chronic systolic HF patients with serum T3 levels below 1·6 nmol/l? A randomized, double-blind, cross-over, placebo-controlled intervention study with oral T3 treatment twice daily for 3 months. The T3 dose was uptitrated to a final dose avoiding reduced TSH levels. Left-ventricular ejection fraction (LVEF). Cardiac imaging was performed using multiple gated tomographic radionuclide ventriculography (MUGA-SPECT). Neurohormonal stimulation was evaluated by plasma measurements of natriuretic peptides, aldosterone, renin, noradrenalin and copeptin levels. The patients were monitored for potential cardiac arrhythmias at the start of each treatment period. Thirteen patients completed the protocol. Mean LVEF was 43%, range: 37-52 and serum T3 levels 1·4 nmol/l (0·9-1·6). The T3 dose was 20 μg per day (10-40). TSH levels did not change between groups, whereas serum T3 levels increased in the active arm. Cardiac function as measured by LVEF, end-diastolic and end-systolic volumes and cardiac output did not change during T3-treatment and neither did the neurohormonal profile. There were no side-effects in terms of cardiac arrhythmias and no change in resting heart rate. This study does not support the hypothesis that oral T3 treatment might be beneficial to patients with chronic, stable systolic HF with a modest degree of reduced LVEF and low-normal serum T3 concentrations. The study included both functional studies of heart contractility as well as measures of the neurohormonal activation.

Plasma renin levels and renin–blood pressure relationship in normal-weight and overweight children with obstructive sleep apnea and matched controls

BackgroundObstructive sleep apnea (OSA) has been increasingly linked to elevated blood pressure (BP) and hypertension. Repeated night-time hypoxia in OSA is associated with activation of two critical mechanisms of BP control: the autonomic nervous system and the renin–angiotensin system (RAS). The effects of OSA on the RAS are not well understood, especially in children. We hypothesized that children with OSA have elevated renin levels and abnormal relationships between BP and renin. MethodsPolysomnography was conducted in 173 children to diagnose OSA (apnea–hypopnea index [AHI] >1 event/h) and control (AHI ≤1 event/h) groups. Age- and gender-specific z-scores for body mass index (BMI) were calculated to divide subjects into obese (BMI ≥95%), overweight (BMI ≥85% and <95%) and normal-weight (BMI <85%) groups. Morning BP was measured with an automatic sphygmomanometer and venous blood samples were collected for measurements of plasma renin, after overnight polysomnography. ResultsPlasma renin levels were not significantly different in all four groups after adjustment of age, gender, and race. Significantly negative associations between renin and BP were present only in the normal-weight control group and were absent in the other three groups. ConclusionPlasma renin levels were not significantly increased in children with OSA compared to controls for both normal-weight and overweight subjects. The absence of normal, negative renin–BP relationships in both overweight and OSA children suggests a dysfunction of the RAS, which could be a mechanism for increased BP and the development of hypertension.

Automated chemiluminescent immunoassays for measurement of plasma renin: A method comparison versus radioimmunoassay

Automated chemiluminescent immunoassays for measurement of plasma renin: A method comparison versus radioimmunoassay

Sorafenib use in hepatocellular carcinoma: More questions than answers

Sorafenib use in hepatocellular carcinoma: More questions than answers