Background: Meningococcal infection (MI) is one of the most significant bacterial infections in children, it is characterized by a life-threatening and unpredictable fulminant course in the structure of infectious diseases. MI in Ukraine represents an important cause of mortality. The Transcarpathian region is located on the western boundary of Ukraine with 4 European countries. Such location of the district and its geopolitical issues related to immigration plays a crucial role in disease transmission and serve as a gate to infectious diseases to and from European Union. Methods: This was a retrospective study that included 32 patients with a confirmed diagnosis of meningococcaemias. The data were obtained from patients’ electronic medical records (EMR). Data collected included demographic, clinical, and laboratory. Continuous variables were expressed as means with standard deviations. Categorical variables were summarized as counts and percentages. Results: Meningococcal morbidity in the Transcarpathian region was higher than in the whole of Ukraine in all researched years. Primarily, the highest incidence was recorded in the Perechyn district and in Uzhhorod city. 53% of all cases of MI occur in the period from December to February. The main constant clinical manifestation of the disease was skin symptoms. Conclusions: The incidence rate of MI is an important problem for public health and may pose a threat to neighboring countries. The methods for the prevention of meningococcal infection include antimicrobial chemoprophylaxis following identification of an index case, use of droplet precautions, vaccination prior to exposure, and avoidance of exposure.

Acute decompensated heart failure has an increasing incidence and poor prognosis, being a major cause of death and hospital readmission and requiring urgent optimized therapy[1]. Under the influence of some decompensation risk factor, such as infections, arrhythmias, decompensation of some comorbidities, lack of adherence to the treatment, patients with a history of heart failure may suffer a progressive symptomatology worsening
therefore, more than 70% of cases of acute heart failure represent the clinical worsening of chronic heart failure - ADHF[2]. [...]

The link between kidney damage and HT remains a challenge in medical research from a century when HT concept was defined, taking in consideration than HT is a major risk factor for cardiovascular disease morta-lity worldwide, due to the increasing prevalence, poor compliance to treatment and many complications[1-3]. The hypertensive nephrosclerosis is currently diagnosed in the latest stages of the disease because, for a long period of time, the injuries are compensated by kidney and therefore the clinical presentation is not specific[4]. The current diagnostic methods are non-specific, especially for early diagnosis of hypertensive nephrosclerosis, except the renal biopsy which is considered the gold standard but is rarely indicated in clinical routine due to its invasiveness and possible severe complications[5]. The pathogenic mechanism is complex and not very well understood but renal microcirculation impairment seems to be responsible for the onset and progression of this disease[6]. Therefore, any method that can accurately assess the early microvasculature changes of renal cortex, easy to use, simple and safe, with no invasiveness, could be an important diagnostic tool in hypertensive nephrosclerosis approach. [...]

Cystic renal masses represents a pathology that may rise diagnosis and management difficulties. The differential diagnosis of large renal cystic masses should be made with normal renal cysts, hydronephrosis, renal abscess, renal hematoma, morpho-functional demaged kidney or with a renal tumor with necrosis and abscess. [...]

Despite the constant technological advances achieved during the past decades, large size benign prostatic hyperplasia (BPH) pathology continues to raise questions concerning the most appropriate therapeutic approach. Interestingly enough, the classical open prostatectomy still represents the standard option for this type of cases despite the substantial perioperative morbidity [1]. [...]

There is increased evidence that the prevalence of peripheral artery disease (PAD) in hemodialysed patients is higher than in general population [1,2]. According to ACC/AHA (American College of Cardiology / American Heart Association) guidelines, the following risk factors are associated with PAD [3,4]

Related to the rehabilitation of patients with osteoarthritis, kinesiotherapy addresses the methods, procedures and methodology that will be used depending on the anatomic, functional and clinical stage of the disease and its location after setting treatment goals. Furthermore, priorities of the rehabilitation program are established considering both medical issues and also paramedical and social aspects [1].
The kinesiotherapeutic opera tional strategy in rehabilitating patients with osteoarthritis is planned according to the characteristic comorbidities of elderly patients [2]. Clinical trials highlight that cardiovascular mortality is reduced when sedentary individuals become moderately active [3,4].

Osteoarthritis, as a major cause of disability and due to the high prevalence among chronic diseases, represents one of the most important public health problems worldwide [1]. The limitation of physical function and the restriction of independence produce negative effects on the mental status of patients suffering from osteoarthritis, namely the emergence of depression and decreased self-confidence [2,3].
Developing a kinesiotherapeutic strategy based on the clinical, anatomical and functional stage of the disease and other comorbidities, as well as exploiting psychological and psychopedagogical resources will improve the physical performance and increase the independence of these patients [4,5].

Native arteriovenous fistulae (AVF) are the best options for chronic hemodialysis (HD) access. Unfortunately, not every patient fulfils the requirements necessary for this type of vascular access: the artery and the vein implicated in dialysis fistula creation must accomplish some criteria which makes them suitable for this procedure. If these criteria are not fully met, the chances to a successfully intervention and a quick and qualitative maturation of the fistula are dropping [1-5]. An artery that is suitable for AVF creation has an inner diameter > 2 mm, optimal initial flow and elastic walls allowing dilatation to accommodate a supplementary 10 - 20 fold blood flow increase after the AVF is performed [1,2,5-11]. The participating vein must be superficial enough (less than 5 mm from the skin surface), wide enough (a caliber bigger than 2.5 mm) and its walls must allow important dilatation (without fibrosis, injuries, and thickenings). In elderly, diabetics or patients with late initiation of HD some of these demands are frequently absent we need to adapt surgical procedures, taking advantage of any oppor tunity to overcame shortcomings and create a native dialysis access [1,2,5,9].

Epstein-Barr virus (EBV) is a member of the Herpes Virus family and is also known as Human Herpes Virus 4. The virus was first isolated in 1964 by the British virologists Michael Anthony Epstein and Yvonne Barr, on a cell line derived from a Burkitt lymphoma. EBV infection is especially common in young individuals with low hygiene standards and also low social and economic status. Thereby it is considered that until the third decade of life, around 80 - 100% individuals have become carriers of infection [1,2]. Although EBV is considered to be a lymphotropic B virus, it can also infect T and NK lymphocytes or some epithelial cells, as it has beenfound in T cell lymphomas, stomach, nose, andthroat carcinomas [2]. The most common host cellfor EBV is B lymphocyte, although in some cases the virus can also be detected in epithelial cells. The role of epithelial cells is likely to permit the replication and amplification of EBV persistence than that of the latent infection [3].

The prevalence of end stage renal disease (ESRD) is constantly increasing in worldwide population, as is the necessity of renal replacement therapy [1-3]. The improvements in dialysis techniques determined increasing quality and lifetime of dialysis patients and the need for a reliable vascular access that sustains the procedure for long periods of time. On the other hand, the progressive aging of dialyzed population and the emerging complications, as well as the rising prevalence of diabetes as a cause for chronic kidney disease (CKD), hampers the processes of obtaining and maintaining an adequate vascular access [1,4,5].

Angiodysplasia (AD), gastric antral vascular ectasia (GAVE or watermelon stomach), radiation-induced vascular ectasia and Dieulafoy's lesions are considered sporadic lesions and they can induce gastrointestinal bleeding (1). AD is the most common vascular abnormality of the gastrointestinal tract, probably the most common cause of recurrent gastrointestinal hemorrhage in patients with renal failure (2) and an important cause of erythropoiet-inresistant anaemia in dialyzed patients. Angiodysplasia injuries developed in the gastric antrum were first described in 1953 and named GAVE, being characterized as submucosal capillary dilatation and fibromuscular hyperplasia (3).

Chronic kidney disease (CKD) is a worldwide health problem [1,2] affecting between 7 - 10% of young individuals (30 - 64 years old) in Europe [2] and approximately 10 - 18% of the population in the USA [3]. In 2013, in Romania, the prevalence of CKD was approximately 13.1%, meaning about 1,900,000 persons, and 13,899 patients were on chronic dialysis [4].
CKD is associated with increased cardiovascular morbidity, even from early stages [5-8]. Decreased glomerular filtration rate (GFR) is a strong predictor of cardiovascular events, even in the absence of other cardiac risk factors [9]. Risk for cardiovascular disease in CKD patients is 10 - 30 times higher than in non-CKD individuals and mortality from cardiovascular diseases (CVD) accounts for approximately 50% from all causes of death in dialysis population [6,10,11,12]. Predisposing features for developing CVD in CKD patients include both traditional and nontraditional - uremia associated - factors [11,12].

Protein-energy malnutrition is a frequent clinical condition in chronic hemodialysis patients (1). The causes of protein-energy malnutrition are: interaction between blood and dialyzer with subsequent activation of the complement, amino acids and peptides losses when undergoing hemodialysis, metabolic acidosis, chronic inflammation and anorexia (2). There are two types of protein-energy malnutrition. Type 1 protein-energy malnutrition is characterized by patients’ poor food intake. This occurs along with slow decrease of serum albumin and loss of muscle mass, the presence of normal levels of C-reactive protein and response to nutritional interventions. The second type of protein-energy malnutrition is characterized by an increased serum level of C-reactive protein and lower serum albumin level than in type 1, even with an optimal food intake. This type of protein-caloric malnutrition is strongly associated with chronic inflammation and does not respond to nutritional intervention (3).

Digestive manifestations due to uremia and uremic toxins are multiple in patients with chronic kidney disease (CKD) on hemodialysis (HD). As much as 79 percent of these patients report gastrointestinal symptoms manifested as nausea, vomiting, dry mouth, dysgeusia, halitosis, pyrosis, abdominal pain, bloating, diarrhea (1,2). Due to many pathogenic mechanisms, the prevalence of gastro-duodenal peptic ulcer disease is higher in HD subjects than in general population, but comparable in frequency with nondialyzed CKD patients (3-5). A recent published 10 years-study presented that the incidence of peptic ulcer disease is 4 times higher in patients with CKD and 9.4 times higher in individuals on chronic HD compared to the general population (6). Regarding localization, gastric ulcers are twice more frequent documented than duodenal ulcers (6-8). An imbalance between protective and aggressive mucosal factors in favor of the last ones is noticed in HD patients. Chronic dialysis stress, intradialysis hypotension (causing mucosal hypo-perfusion), anemia, intra-dialysis anticoagulant, metabolic acidosis, potentially ulcerogenic medication (steroids, non-steroid anti-inflammatory and antiplatelet drugs) lead to high frequencies of peptic ulcer disease (9). Since the appearance of ulcerous lesions, the risk of their complications (e.g.: hemorrhages, perforations, penetrating injuries) is much higher than in general population. One recent cohort study in Taiwan showed that the incidence of gastro-duodenal bleedings is double in CKD patients and 5 times higher in HD ones (2). Subsequently, common comorbidities such as diabetes, liver cirrhosis and ischemic heart disease participate as pathogens in digestive bleedings (10).
An adequate diagnosis and monitoring of peptic ulcer disease in dialysis patients represent a constant concern of our clinical practice, because of the high prevalence of this kind of pathology, the life-threatening potential complications and the complexity of the treatment. Therefore, further on we discuss the case of an atypical peptic ulcer disease in a chronic HD patient.

Patients with chronic renal disease frequently display eso-gastro-duodenal associated pathology: anorexia, heartburn, nausea, vomiting, abdominal pain, gastric motility disorder so far as gastroparesis
some of these symptoms decline once the substitution therapy of the renal function is initiated through hemodialysis, and some persist because of the interdialytic metabolic acidosis, used anticoagulant in dialysis or complementary therapies.
The most severe clinical manifestation is superior digestive hemorrhage, with multiple intricate causes (mucosal lesions induced by gastrin, angiodysplasia including GAVE - gastric antral vascular ectasia, treatments with lesion potential - NSAIDs, corticoids, oral iron drugs, mucosa inflammation under uremic toxins or oxygen radicals, gastric and intestinal wall edema due to interdialytic hypervolemia, malnutrition). The gastric hyperacidity induced injuries in renal patients are often esophagitis, gastritis, duodenitis and gastro-duodenal ulcer.

Hyponatremia, with an incidence of 15 - 22%, is considered when serum sodium levels are < 135 mEq/L (in institutionalized geriatric patients, in 1 - 4% to 7 - 53% cases there have been reported values below 130 mEq/L) [1-3]. Additionally, according to expert panel recommendations the frequency of hyponatremia in hospitalized patients depends on the detected level of hyponatremia [2]. This special condition is highly important to be detected on time because it represents a recognized risk factor of morbidity and mortality, even in asymptomatic patients [1]. Furthermore, it was noticed that a swift correction can induce severe neurological disorders and even death [1]. Therefore, for an adequate treatment management (prophylaxis and therapy) is vital for understanding hyponatremia main causes and the incriminated pathophysiological mechanisms [1].

Hypertension, diabetes mellitus, dyslipidaemia are frequently encountered in patients with chronic kidney disease (CKD) (1). They are the major risk factors for the development and progression of the endothelial dysfunction and atherosclerosis and contribute to the progression of renal failure (1). Microalbuminuria increases to two- to four-fold the cardiovascular risk (1). It is also a quantitative association between glomerular filtration rate (GFR) and cardiovascular risk (1). The risk increase to two to four-fold in stage 3 of CKD (GFR 30-59 mL/min/1.73 m²), four- to 10-fold in stage 4 (GFR 15-29 mL/min/1.73 m²) and 10- to 50-fold in stage 5 renal failure (GFR <15 mL/min/1.73 m² OR dialysis) in comparison with persons free of CKD (1). Atherosclerosis with intimal involvement and Moenckeberg’s media sclerosis are the main cardiovascular determinations in CKD. Coronary artery calcifications attain the highest levels in young adults patients with renal failure and dialysis, as has been shown in angiographic studies (2). These patients have many coronary risk factors leading to intimal calcifications and these are coexisting with medial calcification founded only in CKD (2). The degree of coronary artery calcifications seems to be related to the estimated GFR in a multivariate analysis (2). KDIGO guidelines recommend that patients with CKD stages 3-5D with known vascular/valvular calcification be considered at highest cardiovascular risk (class 2A recommendations) (3).