Secondary Arterial Hypertension Research Articles

Egg white hydrolysate protects white adipose tissue against metabolic insult in deoxycorticosterone acetate-salt rats.

The purpose of this study was to investigate the effect of an egg white hydrolysate (EWH) to protect white adipose tissue damage from cardiometabolic changes induced by severe hypertension. Male Wistar rats were uninephrectomised and divided: SHAM (weekly subcutaneous vehicle (mineral oil + propylene glycol, 1:1)), SHAM + EWH (subcutaneous vehicle plus EWH via gavage, 1 g/kg per day), DOCA (deoxycorticosterone acetate diluted in vehicle subcutaneously weekly in subsequent doses of 20 mg/kg -1st week, 12 mg/kg - 2–3th week, and 6 mg/kg -4–8th week, respectively, plus 1 % NaCl and 0·2 % KCl in drinking water), and DOCA + EWH. Body weight gain, food and water intake, glucose and lipid metabolism were evaluated. Oxidative stress was assessed by biochemical assay and immunofluorescence for NOX-1, nuclear factor kappa B (NFκB), and caspase-3 in retroperitoneal white adipose tissue (rtWAT). Proinflammatory cytokines (IL-6 and 1β), CD163+ macrophage infiltration, and immunohistochemistry for TNFα and uncoupling protein-1 were evaluated, as well as histological analysis on rtWAT. Glutathione peroxidase and reductase were also determined in plasma. EWH showed hypocholesterolemic, antioxidant, anti-inflammatory, and anti-apoptotic properties in the arterial hypertension DOCA-salt model. The results demonstrated the presence of functional changes in adipose tissue function by a decrease in macrophage infiltration and in the fluorescence intensity of NFκB, NOX-1, and caspase-3. A reduction of proinflammatory cytokines and restoration of antioxidant enzymatic activity and mitochondrial oxidative damage by reducing uncoupling protein-1 fluorescence intensity were also observed. EWH could be used as a potential alternative therapeutic strategy in the treatment of cardiometabolic complications associated with malignant secondary arterial hypertension.

Occurrence of Arterial Hypertension in Patients with sleep Apnoea Syndrome

Introduction: Sleep apnoea syndrome (SAS) is a serious under-diagnosed chronic disease, which often coincides with arterial hypertension (AH). The U.S. Joint National Committee considers SAS to be the most common cause of secondary arterial hypertension. Objective: To determine the incidence of arterial hypertension in patients diagnosed with SAS in an accredited sleep laboratory (ASL) in Bratislava in the years 2013-2022. Methods: The monitored group consisted of 688 patients examined in an ASL in Bratislava who underwent an initial examination (anamnesis, anthropometry, sleep questionnaire) and a diagnosis of sleep-disordered breathing (nocturnal polysomnography) in order to confirm or refute the diagnosis of OSAS. Data collection also took place by using a copy of the patients’ medical records (presence of AH). We used Microsoft Excel and statistical software SPSS, version 21.0 to process the obtained data. We considered the result to be statistically significant if p ≤ 0.05. Results: We demonstrated a statistically significant difference in the incidence of AH in patients with SAS compared to patients without SAS, i.e., there was a statistically significantly higher incidence of AH in patients with SAS compared to patients without SAS (39% vs. 17.5%; OR=3.0; p<0.001). We also demonstrated that the higher the AHI value in patients with SAS, the higher the incidence of AH (p=0.002; 95% CI 1.4 – 4.4). In addition, there was a 1.9 times higher risk of developing AH in patients with a moderate degree of SAS compared to patients with a mild degree of SAS (p=0.014) and up to a 2.8 times higher risk of developing AH in patients with a severe degree of SAS compared to patients with moderate SAS (p<0.001) regardless of BMI. Conclusion: Due to the high coincidence (1/3) of arterial hypertension and sleep apnoea syndrome in the monitored group, it is necessary to focus on effective screening of SAS in high-risk persons as well as effective screening of SAS in persons with present AH.

Conn´s syndrome after kidney transplantation.

Conn's syndrome, defined as unilateral aldosterone-producing adenoma, accounts for 35-40% of cases of primary hyperaldosteronism. Primary hyperaldosteronism typically occurs in younger patients with poorly controlled arterial hypertension due to extracellular fluid retention, in whom at least atriple combination of antihypertensives, including adiuretic, is needed to maintain normotension. The clinical picture of arterial hypertension may be complemented by symptoms associated with hypokalaemia, such as weakness, fatigue, palpitations, convulsions, polydipsia, or polyuria. In addition to arterial hypertension and hypokalaemia, the diagnosis of Conn's syndrome relies on examination of serum renin and aldosterone concentrations, plasma renin activity, exercise or furosemide stimulation tests, and imaging studies, preferably computed tomography. The method of treatment of Conn's syndrome is adrenalectomy. In patients with primary hyperaldosteronism with underlying bilateral adrenal cortical hyperplasia or patients contraindicated for surgery, mineralocorticoid receptor antagonists are administered in combination with antihypertensives targeted for optimal blood pressure control.In the group of patients after kidney transplantation, the exact incidence of primary hyperaldosteronism is unknown. Based on across-sectional study performed in 2020, it is estimated to be approximately 15% in the group of patients with unsatisfactorily compensated arterial hypertension; in the cohort of normotensive recipients, the incidence of primary hyperaldosteronism is not documented. Diagnosis of Conn's syndrome in patients in the early period after kidney transplantation is problematic, as the prevalence of arterial hypertension in transplanted patients is high (70-90%) according to the literature. Mineral abnormalities, including hypokalaemia, are also common in the early post-transplant period, mainly due to factors such as duration of cold ischaemia, onset of graft function, donor parameters, post-transplant tubulopathy, and diuretics, the effects of immunosuppressive drugs (especially calcineurin inhibitors and corticosteroids), and possibly potassium-restricted dietary habits that the patient brings from the pre-transplant period, which may mask the effect of hyperaldosteronism on potassium.We present the case of apatient who was diagnosed with Conn's syndrome 7 months after primary kidney transplantation from adeceased donor based on persistent hypokalaemia unresponsive to replacement therapy. At the time of the first manifestation of severe hypokalaemia, the patient was treated with adual combination of antihypertensives (amlodipine at adaily dose of 5 mg and carvedilol at adaily dose of 50 mg), without the need for adiuretics.We consider the case interesting because the spectrum of mineral and acid-base abnormalities in advanced renal failure and in the early post-transplant period, as well as acid-base and mineral imbalances, including hypokalaemia, and the high prevalence of arterial hypertension in the post-transplant period, may mask the picture of Conn's syndrome (Fig. 3, Ref. 19). Text in PDF www.elis.sk Keywords: kidney transplantation, primary hyperaldosteronism, hypokalaemia, metabolic alkalosis, secondary arterial hypertension.

Pediatric hypertension as an early manifestation of cardiovascular disease in children.

In adults, cardiovascular events associated with arterial hypertension (AH) have a major impact on morbidity and mortality. In light of recent findings, AH in children has been interpreted as early cardiovascular disease (CVD), while exposure to CV risk factors in children proves to be a predictor of subclinical CVD in adults. The American College of Cardiology/American Heart Association has recently updated the classifications for measuring blood pressure (BP) in adults and children. Primary AH in children is generally asymptomatic, and it is associated with a family history of AH, overweight/obesity, and normal morphofunctional characteristics of the urinary system. The younger the child and the higher the BP, the greater the likelihood of secondary AH. The investigation into the etiology of AH begins with a detailed anamnesis, which should include clinical information and details on the use of medication, smoking, and alcohol consumption from the perinatal period to the time of consultation. Modifying risk factors by reducing weight, decreasing alcohol consumption and increasing vegetable intake from childhood to adulthood has been associated with the resolution of AH in the childhood-adulthood transition, and with the reversal of cardiometabolic adverse effects in non-obese adult individuals. Pharmacological therapy should be initiated in cases of symptomatic AH, AH secondary to chronic kidney disease or diabetes mellitus, presence of target organ lesions, stage 2 AH with no modifiable cause and resistant AH unresponsive to lifestyle changes.

Primary hyperaldosteronism: the choice in favor of conservative surgery

Primary hyperaldosteronism (PHA) is the most common cause of secondary arterial hypertension among endocrine disorders. Given that patients with this pathology are at a higher risk of developing fatal and non-fatal cardiovascular events, early diagnosis and timely treatment are of great importance. Currently, the two main forms of PHA are aldosterone-producing adenoma and bilateral adrenal hyperplasia, which are treated with laparoscopic adrenalectomy or pharmacotherapy with mineralocorticoid receptor antagonists. Although most patients experience restoration of their functional and metabolic status after surgical intervention, some may develop postoperative adrenal insuffi ciency, which requires long-term hormone replacement therapy. This review examines the options for organ-preserving surgeries, such as partial adrenalectomy and selective embolization of the adrenal artery.

Clinical manifestations of damage to the cardiovascular system and predictors of poor prognosis of Takayasu arteritis in Kyrgyz patients

Damage to the cardiovascular system (CVS) in Takayasu arteritis (AT) is characterized by a wide range of clinical manifestations and an unfavorable prognosis of the disease. Objectives: determine the characteristics of clinical manifestations of damage to the CVS and predictors of unfavorable prognosis in Kyrgyz patients with АТ. Methods: The study included 135 patients with a reliable diagnosis of AT, verified according to the classification criteria of the American College of Rheumatology/The European Alliance of Rheumatology Associations (ACR/EULAR, American College of Rheumatology/European Alliance of Associations for Rheumatology). All patients underwent clinical and standard laboratory and instrumental examination. Results: CVC lesion was observed in 84.4% of patients with AT and was manifested mainly by secondary arterial hypertension (AH) and aortic regurgitation (AR) – 52.8% and 27.8% of cases, respectively. The main cause of secondary hypertension was renovascular hypertension (63.4%). Myocarditis (8.5%) and coronary syndrome (3.8%) were significantly less frequently diagnosed. Among the cardiovascular complications (CVc) that developed in 32.5% of patients, decompensated chronic heart failure (DCHF) (48.7%) and acute cerebrovascular accident (ACVA) were the most common (40,5%). The immediate cause of death in the observed cohort was DCHF (66.7%) due to severe AR (83.3%) and ischemic cardiomyopathy (16.7%). Predictors of the development of CVc were the V anatomical type of vascular lesion, high activity of the pathological process, severity of stenotic changes, serious clinical complications (CC) and severe AR (p<0.05). Conclusion: 1. CVS lesion was observed in 84.4% of Kyrgyz patients with AT. 2. The most frequent variant of cardiovascular pathology was secondary hypertension (52.8%) caused by vasorenal (63.4%), coarctation (33%) and aortic (3.6%) changes. The second most common was pathology of the aortic valve (27.8%) with a predominance of minor AR (45.8%). 3. CVc was observed in one third of patients (32.5%) and in most cases were presented with DCHF (48.7%) and ACVA (40.5%). 4. Unfavorable factors associated with an increased risk of CVc in the observed patients were V anatomical type of vascular lesion, high activity, pronounced stenotic changes, severe CC and severe AR (p<0.05).

The Dysfunction of Ca2+ Channels in Hereditary and Chronic Human Heart Diseases and Experimental Animal Models.

Chronic heart diseases, such as coronary heart disease, heart failure, secondary arterial hypertension, and dilated and hypertrophic cardiomyopathies, are widespread and have a fairly high incidence of mortality and disability. Most of these diseases are characterized by cardiac arrhythmias, conduction, and contractility disorders. Additionally, interruption of the electrical activity of the heart, the appearance of extensive ectopic foci, and heart failure are all symptoms of a number of severe hereditary diseases. The molecular mechanisms leading to the development of heart diseases are associated with impaired permeability and excitability of cell membranes and are mainly caused by the dysfunction of cardiac Ca2+ channels. Over the past 50 years, more than 100 varieties of ion channels have been found in the cardiovascular cells. The relationship between the activity of these channels and cardiac pathology, as well as the general cellular biological function, has been intensively studied on several cell types and experimental animal models in vivo and in situ. In this review, I discuss the origin of genetic Ca2+ channelopathies of L- and T-type voltage-gated calcium channels in humans and the role of the non-genetic dysfunctions of Ca2+ channels of various types: L-, R-, and T-type voltage-gated calcium channels, RyR2, including Ca2+ permeable nonselective cation hyperpolarization-activated cyclic nucleotide-gated (HCN), and transient receptor potential (TRP) channels, in the development of cardiac pathology in humans, as well as various aspects of promising experimental studies of the dysfunctions of these channels performed on animal models or in vitro.

Epidemiology and diagnosis of primary aldosteronism. What have we learned from the SPAIN-ALDO registry?

To summarize the available data on the prevalence, clinical repercussion, and diagnosis of primary aldosteronism (PA) and to discuss the SPAIN-ALDO registry's findings, which is the largest PA patient registry in Spain. A comprehensive review of the literature focused on the prevalence, clinical presentation and diagnosis of PA was performed. PA is the most common cause of secondary arterial hypertension. In addition, PA patients have a higher cardio-metabolic risk than patients with essential arterial hypertension matched by age, sex, and blood pressure levels. However, despite its high prevalence and associated metabolic and cardiovascular complications, PA remains largely under-recognized, with less than 2% of people in at-risk populations ever tested. The diagnostic investigation is a multistep process, including screening, confirmatory testing, and subtype differentiation of unilateral from bilateral PA forms. Data from the SPAIN-ALDO registry have shed light on the cardiometabolic impact of PA and about the limitations in the PA diagnosis of these patients in Spain. The most common cause of secondary hypertension is PA. One of the most challenging aspects of the diagnosis is the differentiation between unilateral and bilateral PA because adrenal venous sampling is a difficult procedure that should be performed in experienced centers. Data from the SPAIN-ALDO registry have provided important information on the nationwide management of this pathology.

Problems in the diagnosis of secondary arterial hypertension of adrenal origin

Primary hyperaldosteronism is the leading cause of secondary arterial hypertension of adrenal origin. Its prevalence is underestimated. This leads to late diagnosis, although a timely diagnosis can achieve a complete cure for the patient, ensure control of blood pressure and avoid the development of complications. The article discusses the prevalence of primary hyperaldosteronism, its etiology and pathogenesis, the mechanisms of formation of autonomous secretion of aldosterone, including with the combined production of cortisol. The main clinical effects of aldosterone hypersecretion, its role in the formation of complications in the cardiovascular system and metabolic control are discussed. The assessment of the main clinical effects of aldosterone hypersecretion and its role in the formation of complications from the cardiovascular system and metabolic control is given. The authors remind about risk groups in which screening should be carried out, about the stages of a diagnostic search for suspected primary hyperaldosteronism. For the primary test, a preliminary assessment of the level of plasma potassium is necessary, and if hypokalemia is detected, its correction. If the result of the primary test is false negative, retesting will be carried out with the transfer of patients to antihypertensive drugs with minimal effect on the renin-angiotensinaldosterone system. It is important to remember that confirmatory sodium loading tests are contraindicated in some patients. Computed tomography with contrast in combination with selective venous blood sampling in patients are the most significant methods for the topical diagnosis of primary hyperaldosteronism. The choice of treatment method and its effectiveness depend on their results.

Интраренальная и центральная гемодинамики после травмы почки Grade I‑III: существует ли прямая причинно-следственная связь с посттравматической артериальной гипертензией?

Introduction. Mechanical kidney injuries lead to renal dysfunction and vasospastic reaction, resulting in adaptive reactions of the organism, with the possibility of formation of secondary arterial hypertension. Purpose of the study: to determine the types of central gemodynamics, intrarenal blood flow characteristics, correlation interrelations of indices and to estimate the risks of secondary posttraumatic arterial hypertension development after Grade I-III kidney injury. Material and methods. Systemic hemodynamic parameters with identification of blood circulation type and intrarenal hemodynamic parameters were studied in 196 male victims in the posttraumatic period, the control group consisted of 30 men. During statistical processing Pearson correlation coefficients (r) and linear regression coefficient of determination (r2) were additionally calculated. Results. After kidney injury, the organ blood flow velocity was increased from 12,5% to 31,2%, resistance index (RI) increased from 4,7% to 44,8%, and pulsation index (PI) decreased from 9,2% to 41,2%. The indices of intrarenal vascular resistance were in negative from very strong to medium strength correlation with the parameters of systemic hemodynamics in the following gradation structure by decreasing strength: total peripheral resistance → diastolic blood pressure → systolic blood pressure → mean arterial pressure → stroke volume → cardiac index → minute volume of blood. Hypokinetic type steadily prevailed in central hemodynamics, the share of eukinetic type increased, and hyper-kinetic type of hemodynamics remained at a constant level. Conclusion. After kidney injury of non-critical severity the ascertained parameters of systemic and organ hemodynamics do not possess predictive power for realization of direct causal relationship in the development of secondary renoparenchymatous arterial hypertension.

Adrenal incidentalomas: unresolved diagnostic issues

In this review paper, we present data on the prevalence, etiology, and diagnostic methods of adrenal incidentalomas (AIs). AIs are tumors larger than 1 cm in size that are accidentally detected using various imaging tests. AIs are known to be responsible for secondary arterial hypertension associated with the risk of cardiovascular complications. Dual-energy CT and radiomics are promising diagnostic technologies for AIs. The conducted literature review points to the problems of verifying the hormonal profile of these tumors, which is particularly relevant in cases of bilateral adrenal lesions. We discuss the diagnostic value of comparative selective adrenal venous sampling (AVS) for determining the site of hormone hyperproduction. Despite technical challenges, AVS remains the most informative diagnostic tool for pathological process lateralization.

End-Organ Damage in Hypertension: An Insight on a Differentiated Outpatient Consultation.

The objective of this study was to determine the prevalence of end-organ damage in hypertensive patients attending an outpatient consultation. Patients were selected from an outpatient consultation at a tertiary hospital care center. All patients who consulted between July 2022 and March 2023 were included. Data on demographic characteristics, blood pressure records, hypertension etiology, medication use, and the presence of target organ damage were collected. A total of 73 patients were included in the study, with 34 patients being male (46.6%) and 39 patients being female (53.4%). The mean age of the patients was 49.8 years. Among the cases of hypertension, 14 (19.2%) were classified as secondary arterial hypertension (AH). The most common cause of secondary AH was obstructive sleep apnea (OSA) (42.9%). Approximately 23.2% of patients had documented end-organ damage potentially related to hypertension, with kidney disease being the most frequent (n = 10, 13.7%). The most commonly prescribed pharmacological classes were angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists (n = 46, 63%). Despite numerous studies and trials on arterial hypertension, it remains a significant contributor to morbidity and mortality, necessitating the continued awareness of its long-term implications.

Assess the pulmonary arterial pressure in patients with group 1 pulmonary arterial hypertension by echocardiography

Objective: We assess the right ventricular in patients with group 1 pulmonary arterial hypertension by echocardiography.
 Method and Results: 45 patients with group 1 pulmonary arterial hypertension was measured the right ventricular by echocardiography between September 2021 and October 2022. Right ventricular diameter and Right ventricular area in patients with idiopathic pulmonary arterial hypertension were not significantly different in patients with secondary pulmonary arterial hypertension (35.7 ± 10.1 mm versus 30.8 ± 9 mm; p=0,12) và (24.1 ± 11.6 cm2 versus 19.7 ± 7 cm2; p=0,12). However, right ventricular function in patients with idiopathic pulmonary arterial hypertension were significantly lower than in patients with secondary pulmonary arterial hypertension via %FAC (28.3 ± 8.5 versus 38.8 ± 8.3; p<0,001), TAPSE (14.2 ± 3.1 mm versus 19.4 ± 3.5 mm; p<0,001), S’tricuspid (9.6 ± 2.2 cm/s versus 11.7 ± 1.9;p=0,002).[1]
 Conclusion: Right ventricular function in patients with idiopathic pulmonary arterial hypertension was significantly lower than in patients with secondary arterial pulmonary hypertension.

Arterial hypertension as manifestation of endocrine pathology

Primary hyperaldosteronism, Cushing’s syndrome, pheochromocytoma, thyroid disease, and hyperparathyroidism can lead to secondary arterial hypertension. A physician in real clinical practice should keep in mind a possible endocrine genesis of the disease, especially in young patients, because the therapy should be aimed not only at the correction of arterial pressure, but also at the treatment of endocrine pathology.

MULTIPLE RENAL ARTERIES AS A RISK FACTOR FOR SEVERE HYPERTENSION IN YOUNG ADULTS?

Objective: The significance of multiple renal arteries (MRAs) in arterial hypertension (AH) is not fully understood. Lower perfusion pressure due to longer length and narrower caliber of MRAs could cause segmental hyperreninemia sufficient to result in renin-dependent systemic hypertension. Sympathetic renal nerve activity might be affected by hyperreninema as well. The aim of the study was to examine the characteristics of young adult hypertensives in relation to the existence of MRAs that were diagnosed during evaluation for secondary arterial hypertension. Design and method: 32 patients underwent routine evaluation for secondary hypertension and target organ damage. Patients were divided into two groups, one with MRAs and the other without MRAs. Data were presented as mean +standard deviation and compared by the Indipendent-Sample t-test. Results: The mean age was 38 years, and 13 patients were diagnosed with MRAs. There were more men in the MRAs group, otherwise, there were no significant differences in baseline characteristics between the groups (BMI, smoking, family history). None of them were diagnosed with secondary endocrine hypertension or renal artery stenosis. MRAs group showed significantly higher values of office SBP/DBP (p < 0,012) and 24-hour SBP/DBP (p < 0,001), and nonsignificantly higher values of heart rate. Although nonsignificant, direct renin concentrations were slightly higher in the MRAs group, while insulin levels were higher in the non-MRAs group. Dyslipidemia was diagnosed in most patients, without significant differences between groups. Electrocardiographic and echocardiographic changes suggesting hypertensive heart remodeling were found in 55% of patients in MRAs compared to 32% in non-MRAs, there were no significant differences in NTproBNP levels. A nonsignificant reduction in glomerular filtration rate was noticed in the MRAs group, while there were no significant differences in 24-hour albuminuria (p 0,308; p 0,614). Conclusions: The significance of MRAs in arterial hypertension is a matter of debate. In our study of young patients with arterial hypertension and MRAs, we observed features of more severe hypertension with already existing hypertensive target organ damages. Proper medical treatment with antihypertensive agents is crucial. Future studies will answer the question about interventional therapeutic procedures’ role in preventing cardiovascular complications.

The role of baroreflex activation therapy in patients with resistant hypertension

Resistant hypertension has become an interesting and controversial topic in the last decade. According to the European Guidelines for the management and treatment of hypertension, resistant hypertension is defined as the lack of blood pressure control despite the control of risk factors and good compliance with a treatment with at least three antihypertensives in the maximum tolerated doses, one of which is a diuretic, at patients in whom possible causes of secondary arterial hypertension were excluded. In the official position of the AHA (American Heart Association) on this subject, resistant HTN is considered as HTN uncontrolled with three antihypertensive drugs or HTN controlled but requiring at least four drugs. Although the medical world has a complex arsenal of antihypertensive preparations, with them it is not possible to correct the values in a good part of the patients. A solution would be the development and study of the effectiveness of baroreflex activation therapy.

Diagnostics, monitoring and treatment of arterial hypertension in children

The review presents material on the current relevance of AH in children. The prevalence of AH in overweight and obese children aged 6-18 years is 27–47 %, while secondary arterial hypertension remains dominant, especially in children younger than 5 years. AH is a major risk factor for atherosclerosis and cardiovascular disease in adults. The onset of these diseases may occur in childhood or adolescence. The use of modern methods to monitor and control BP is crucial for improving the management of AH and preventing damage to target organs. Twenty-four-hour BP measurements are an important tool in determining the prognosis and treatment of children with AH. AH in children can be classified as primary or essential if there is no identifiable cause, or as secondary AH when it arises from a specific cause. The incidence of primary arterial hypertension increases with age, whereas secondary arterial hypertension predominates in early childhood. The secondary causes of AH also depend on the age of the patient. Thus 34-79 % of patients with secondary forms of arterial hypertension have renal parenchymal disease and impaired renal structure. Signs of AH include headache, visual disturbances, dizziness and nosebleeds. Dyspnoea on exercise, facial paralysis and seizures indicate target organ damage. In children with obesity, diabetes, renal insufficiency, aortic coarctation/repaired coarctation and those receiving medication causing AH, BP should be measured at every visit to the physician. Therapeutic lifestyle changes are an early therapy in the treatment of AH in children. IAPs, BCAAs, BRAs and thiazide diuretics are the most effective drugs for AH in children.

Hypertensive retinopathy: a literature review

Enrika Mačiulaitytė1, Raminta Oleškevičiūtė1, Daiva Emilija Rekienė2 1Lithuanian University of Health Sciences, Faculty of Medicine, Kaunas, Lithuania 2Lithuanian University of Health Sciences, Department of Internal Medicine, Kaunas, Lithuania Abstract Introduction: Hypertensive retinopathy is a disease that is described as a disorder of the retinal blood vessels, caused by poorly controlled primary or secondary arterial hypertension. People who are diagnosed with this condition tend to have prolonged hypertension, have relatives with the same diagnosis and are smokers. A third of the population in Lithuania has hypertension, so it is important to be aware of the complications. Aim: to review diagnostics, treatment, and prognosis of hypertensive retinopathy. Methodology: the literature used for this review was selected using “Google Scholar” and “Pubmed” databases. Following dates from 2012 to 2022, using keywords “hypertensive retinopathy”, “hypertension”, and “eye diseases”. More than 20 publications on hypertensive retinopathy were analysed. Results. Fundoscopic exam along with previously diagnosed arterial hypertension remains the most important method for diagnosing hypertensive retinopathy. Clinical findings are not significant for diagnosis, whereas optical coherence tomography has the potential to detect and diagnose the disease. The aim of treating hypertensive retinopathy is to lower blood pressure to achieve blood pressure values below 120 – 130/80. Angiotensin – converting enzyme (ACE) inhibitors are the first – line medications for treating this disease. Conclusions. Hypertensive retinopathy is usually diagnosed during fundoscopic examination when the patient has already been diagnosed with hypertension. Mitchell–Wong classification is used to evaluate the severity of the disease. The main method of management of hypertensive retinopathy is achieving targeted blood pressure with medications. In most cases the prognosis of hypertensive retinopathy is good if blood pressure is well controlled. Keywords: hypertensive retinopathy, hypertension, eye diseases. Full article https://doi.org/10.53453/ms.2023.2.11

Primena magnetne angiografije kod dece sa arterijskom hipertenzijom - iskustvo jednog centra

Introduction: Renal blood vessel (RBV) stenosis is the cause of secondary arterial hypertension (AH) in 10% of children. Digital subtraction angiography (DSA) is the gold standard in diagnosing RBV stenosis. Many authors suggest Mr angiography (MRA), a non-invasive method without radiation, as an adequate diagnostic method. Our aim was to analyze the experience of our center in using MRA in children with AH. Method: This retrospective study included 148 patients hospitalized at the University Children's Hospital in Belgrade, due to AH. After initial examination, patients underwent DSA and/or MRA. Results: According to the current guidelines, DSA was performed in patients with highly suspected RBV stenosis, and the diagnosis was confirmed in 13/29 (45%). Diagnostic MRA was done in 116/119 (97.5%) patients, and control MRA was done after therapeutic revascularization in 3/119 (2.5%). In 4/116 (3.5%) patients, the findings indicated RBV stenosis, and in 44/116 (38%) it indicated some other abnormality of the kidney parenchyma and the urinary tract or RBV varieties. After MRA, DSA was performed in 7/116 (6%) patients (4 with RBV stenosis on MRA and 3 with clinical suspicion of RBV stenosis), but all findings were normal. Conclusion: According to the results, it is justified to perform a diagnostic MRA before DSA in children with highly suspected RBV stenosis, in order to avoid DSA which is an invasive procedure with radiation, in some patients with normal findings. Also, over time, we would have a clearer view of the sensitivity and specificity of MRA as a diagnostic method in RBV stenosis in children.

S-22-1: GENETIC MECHANISMS OF HYPERTENSION IN DIFFERENT FORMS OF PRIMARY ALDOSTERONISM

Primary aldosteronism is the most common form of secondary arterial hypertension, affecting up to 10% of hypertensive patients. It is responsible for treatment resistance and increased risk of cardiovascular complications. Due to the difficulty of its diagnosis, PA is frequently missed, and as a result, treatment of the condition is either delayed by many years after the onset of hypertension, or is not initiated at all. Over the past 10 years, important discoveries have been made regarding the genetic basis of aldosterone producing adenoma and familial forms of primary aldosteronism. In most cases, genetic abnormalities are found in genes coding for ion channels (KCNJ5, CACNA1D, CACNA1H, CLCN2) as well as ion pumps (ATP1A1, ATP2B3). They occur as somatic mutations in aldosterone producing adenoma and as germline mutations in familial forms of the disease. Mutations in these genes affect intracellular ion homeostasis and/or cell membrane potential, leading to increased intracellular calcium concentrations and activation of calcium signalling, which is the main regulator of aldosterone biosynthesis. In addition, double mutations in CTNNB1 and GNAQ/GNA11 have been identified in aldosterone producing adenoma presenting in puberty, pregnancy and menopause. Genetic studies have opened interesting diagnostic and treatment opportunities. While surrogate biomarkers of the mutation status may facilitate diagnosis and subtype identification in primary aldosteronism, innovative therapies are currently studied targeting mutated proteins. Finally, recent evidence suggests a continuum between unilateral and bilateral forms of primary aldosteronism, with somatic mutations being found in aldosterone producing cell clusters and aldosterone producing adenoma in patients with bilateral forms. We have recently identified genetic risk loci for primary aldosteronism through genome wide association studies, which may explain shared susceptibility and reveal new mechanisms involved in adrenal gland function and the development of aldosterone producing adenoma and bilateral adrenal hyperplasia.