Patients with End-Stage Renal Disease (ESRD) are at high risk of death as a result of the cardiovascular disease (CVD), which cannot be explained by the conventional risk factors only. Haemodialysis patients frequently have elevated serum concentrations of the cardiac troponins T, specific markers of myocardial injury. Plasma levels of brain natriuretic peptide (BNP) are elevated in fluid volume overload and heart failure, and decreased during dialysis. Currently, LV hypertrophy and LV dysfunction are considered the strongest predictors of cardiovascular mortality in dialysis population, and the synthesis of cardiac natriuretic peptides is high in the presence of alterations in the left ventricular (LV) mass and function. The aim of this study was to investigate the factors associated with the increased serum levels of BNP and CTN in haemodialysis patients, and their impact on cardiovascular morbidity. In this cross-sectional study we included 30 patients with ESRD, without coronary symptoms, who were subjected to regular dialysis treatment three times a week for the duration of four hours. Heart failure was defined as an ejection fraction (EF) of < 35%, and dyspnoea associated with either elevated jugular pressure or interstitial oedema evidenced in chest X-ray. All patients were in sinus rhythm at the time of the study. Twenty-five patients were on erythropoietin treatment. Blood samples were taken before and after the dialysis session. Our study included 30 patients (17 males, 13 females). The average age was 53,8 years (total range 31-74) divided into two groups: euvolemic and hypervolemic. The average dialysis time was 70,3+/-46,95 months. All haemodialysis patients had excessively high levels of BNP 2196,66+/-4553,86 ng/cm3. Plasma cTnT was found to be increased in 33,3% of patients. Patients with hypervolemia had significantly higher cTnT levels (0,0577+/-0,0436), as compared to the euvolemic patients 0,0184+/-0,0259 p<0,05. The elevated cTnT significantly correlated with the level of BNP (p<0,01), while average post-dialysis BNP was not significantly lower (1698,06+/-3499,15; R=0,191; p-ns.) as compared to the pre-dialysis BNP (1839,13+/-3691,55; R=432; p<0,01). The pre-dialysis cTnT was lower (0,0315+/-0,0372) as compared to the post-dialysis cTnT (average 0,0399). Euvolemic patients had BMI 24,28+/-3,15, as compared to the hypervolemic patients BMI 25,71+/-4,20 (p-n.s.). Increased BNP was not in correlation with older age (R-0,271 p-ns.) and duration of dialysis (R-0,198). The hematocrit level increases significantly during haemodialysis (39,9%; p<0,05). Patients with higher BNP and cTnT have significantly higher indexed left ventricular mass, as compared to the patients with normal ventricular function. Our study shows that 33,3% of asymptomatic patients on haemodialysis have elevated cTnT while all patients have elevated BNP. Measuring the plasma concentration of brain natriuretic hormones may be useful for identification of the dialysis patients with LVH.

It has been recognized that some people have a genetic variant which leads to elevated levels of homocysteine and impairs ability to process folate. This condition was recognized as independent risk factor of coronary heart disease. Recently, connection between this termolabile mutation of the methylenetetrahydrofolate reductase and numerous conditions and diseases has been established. Aim of this review is to draw attention to this interesting area in medicine. Additionally, well defined study about presence and frequency of gene polymorphism in our region will provide proper diagnosis and achieve possible delay of development of diseases with vitamin supplementation.

Neuropathic pain is result of damage or dysfunction of periphery or central nervous system. There is no adequate adaptation and produce suffering without biological helpfulness. The aim of treatment of patient with neuropathic pain is soothing of pain and suffering and prevention of further development of pathological process. Periphery mechanisms of neuropathic pain include hyperexcitability of cell membrane and periphery sensibilization. Central mechanism includes central sensibilization, central reorganization of alphabeta fibers and loss of inhibition mechanisms. The main symptoms of neuropathic pain are described as lancinating, stabbing, or shooting pain. Hyperalgesia and allodynia are special kind of neuropathic pain that is provoked by mechanic or thermal stimuli. Mononeuropathy, plexopathy, radiculopathy, and myelopathy, lesions of thymus, cortex or brain stem are real cause of neuropathic pain. In the treatment of neuropathic pain drug such as opioid, nonsteroid antirheumatics, analgetics, tricyclic antidepressant and antiepileptic are used. The most successful treatment is with antiepileptic drugs of second generation. Carbamazepin was the drug of choice till ten years ago. Since then the leader position in treatment has belong to gabapentin in dose from 900-2400 mg daily. Currently the new drug is tested, antiepileptic pregabaline. The first experiences are promising.