Mortality from diseases of the circulatory system is a challenge for the modern health care. Arterial hypertension (AH) mostly contributes to development of cardiovascular complications. It often proceeds against the background of metabolic disorders. Pathogenesis of hypertension is currently being considered a multifactorial disease. Pathogenesis of hypertension certainly has distinct features in presence of metabolic disorders,. Therefore, it is relevant to summarize current literature on the role of immunological disorders, endothelial dysfunction and hemostatic disorders in AH genesis during metabolic syndrome (MS). Most authors agree with existence of several mechanisms that determine relationships between AH and insulin resistance. Development of hypertension in MS patients with is a consequence of immunometabolic processes. Abdominal obesity is an important component of MS. It is associated with chronic inflammation of visceral adipose tissue, its excessive infiltration by immune cells, and increased production of adipokines and cytokines (TNFα, IL-6) with hypertension. AH is associated with a significant increase in T cells, that mediate endothelial dysfunction (ED) and provide a link between hypertension and subsequent atherosclerosis. T lymphocytes trigger a cascade of reactions. IL-17 is the end product of these events It is involved not only in increasing blood pressure, but also contributes to the development of vascular wall stiffness in АН patients. Thus, the relationship between several types of immune cells leads to inflammatory reactions, including those of vascular wall, initiating endothelial dysfunction. Chronic non-specific inflammation in MS, supported by the cytokine system, is a triggering mechanism for ED progression. Excessive production of endothelin-1 and inhibition of nitric oxide production are the classic markers of ED. Immune damage leads to imbalance in the production of vasoconstrictor and vasodilating substances, proliferative and antiproliferative factors in endothelium. It was shown that ED is an integral aspect of the insulin resistance syndrome in pathogenesis of arterial hypertension associated with metabolic disorders, and contributes to its worsening, increased vascular reactivity and further AH development. According to modern studies, it has been shown that excessive synthesis of pro-inflammatory cytokines introduces disturbances in the system of vascular hemostasis. When studying the effects of metabolic disorders upon hemostatic system, we may conclude that activation of fibrinolytic and plasma chains occurs in the same way for both men and women, with small gender characteristics of individual components. The rheological properties of the blood are also changed with developing MS. Systematization of the available literature data on the issue under study can serve as a basis for determining prognostic criteria of hypertension progression and risk of thrombotic complications.

The clinical study enrolled 120 patients, who were hospitalized to the Therapeutic Department of Republican Clinical Hospital No.  5 of Saransk. The patients were divided into 2 groups: Group I (n = 60) included patients with metabolic syndrome; Group II (n = 60)  included patients with arterial hypertension. The paper presents data on the assessment of the functional state of kidneys in the  analysed groups, defines the role of metabolic disorders in the progression of renal dysfunction in patients with metabolic syndrome  and arterial hypertension. It is noted that more pronounced functional changes in the kidneys (microalbuminuria, increased cystatin  C levels, decreased glomerular filtration rate) are detected in patients with arterial hypertension and metabolic syndrome, as compared with patients without metabolic disorders. Cystatin C and microalbuminuria have been shown to be one of the earliest markers of kidney damage in hypertension, especially in combination with metabolic disorders. Cystatin C and microalbuminuria level is  significantly higher in patients with arterial hypertension and metabolic syndrome, as compared with patients with arterial hypertension, who have no metabolic disorders. Significant correlations were found between cystatin C, microalbuminuria levels and lipid  and carbohydrate metabolism in patients with arterial hypertension in combination with metabolic disorders.

Our study was aimed at assessing a relationship between immune system alterations, hypoxia and inflammation in arterial hypertension (AH) coupled to metabolic disturbances. A total of 117 patients were enrolled into clinical study, having been randomized into groups in accordance with study protocol, aged 30 to 62 years. They sought care in outpatient setting or underwent periodic health examination at the Republican Clinical Hospital №5, Saransk, Mordovia, Russia. A control group contained 25 apparently healthy subjects lacking signs of metabolic syndrome (MS) and elevated arterial pressure. A comparison group contained 47 patients with AH grade I-II featured with damaged target organs, but lacking associated relevant clinical manifestations, as based on the assay data. The main group contained 45 patients receiving antihypertensive therapy with overt AH grade I-II verified upon medical consultation coupled to damaged target organs and MS signs with its randomly combined components, but lacking associated clinical manifestations. The patients from main and comparison groups received antihypertensive therapy in accordance with approved guidelines and clinical recommendations for management of AH patients consisting of one of renin-angiotensin-aldosterone system blockers, diuretic and/or dihydropyridine calcium channel blocker. Cytokine profile, level of hypoxia and non-specific inflammation were measured in blood serum. The data obtained demonstrated that AH patients with/without metabolic syndrome were noted to display cytokine profile shifted towards elevated proand anti-inflammatory immune arm pointing at imbalanced immune regulation. Hypoxic changes were also found in blood serum that was confirmed by elevated level of lactic and pyruvic acid in these groups. Moreover, development of such pathology was coupled to hypoxia which served as a modulator of immune-related and non-specific inflammation. Rise of non-specific low-grade inflammation correlates developing irreversible AH-associated changes in organs, progression of atherosclerosis and accelerated cardio-metabolic continuum. Altogether, such alterations underlie pathogenetic mechanisms of tissue damage emerging upon AH and MS being mutually aggravating factor along with activated renin-angiotensin-aldosterone system.

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The widespread prevalence of comorbid pathology determines the relevance of this problem. Comorbid pathology due to the interaction of diseases, drug pathomorphism, age characteristics of the patient, significantly changes clinical picture and course of the main nosology, affects severity of complications and their nature, significantly affects quality of life and prognosis of patients. Diagnosis and treatment of many diseases is complicated in the conditions of comorbidity. The article presents a clinical case of a comorbid patient with arterial hypertension from the moment of exposure to risk factors and ending with the formation of many concomitant diseases, as an example of trans-nosological comorbidity.