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Сardiovascular disease (СVD) is the most common complication of chronic kidney disease (СKD). In patients with the earlier stages of CKD, the risk of death from CVD greatly exceeds the risk of progression to end-stage renal disease. In recent years, accumulated data suggest that chronic kidney disease — mineral and bone disorders (CKD-MBD) are strongly associated with cardiovascular events and mortality. Among cardiovascular damage in CKD, both, the progressive cardiac remodeling and vascular calcifi cation, contribute immensely, and lead to an urgently high cardiovascular mortality in patients with CKD. Clarifi cation of CKD progression mechanisms and possible early markers of CVD has led to interest in studying the identifi ed factors such as fi broblast growth factor-23 (FGF-23), Klotho and sclerostin in recent years. Results of studies show that disorders in the system of FGF-23–Klotho–sclerostin correlate with the frequency and severity of hypertension, cardiac remodeling, vascular calcifi cation, anaemia, malnutrition, infl ammation, and strongly aggravate cardiovascular risk in CKD. This review represents an analysis of the available data showing the potential association of СVD with established (phosphate, parathyroid hormone (PTH), Vitamin D) and newer (FGF-23, Klotho, sclerostin) СKD-MBD biomarkers. In addition, it has been shown that renoprotective therapy, including renin-angiotensin blockers, low-protein diet with amino/keto acid supplementation, phosphate binders, erythropoiesis stimulators, vitamin D metabolites used to reach the target levels of blood pressure, serum phosphorus, haemoglobin, PTH and nutritional status disorders, can aff ect CKD-MBD biomarkers and reduce the risk of cardiovascular events in CKD patients.

Aim. To evaluate the results of immunosuppressive and/or antiviral treatment of patients with hepatitis C virus (HCV)-induced mixed cryoglobulinemic (MC) vasculitis. Material and methods. This prospective study included 60 patients (m/f - 23/49, age - 45,9±11,1) with HCV-MC vasculitis. The Birmingham vasculitis activity score (BVAS) was used before the treatment and during follow-up (3,5±4,1 years). The rate of clinical and immunological responses to the treatment, the frequency of relapses and the influence of different treatment approaches on the prognosis of the disease were evaluated. Logistic regression analysis was used to assess factors influencing the effectiveness of treatment. Results. 23 (38%) patients had liver cirrhosis. BVAS scores before treatment ranged from 2 to 36. 25 (41,6%) patients had BVAS≥15. 6 (10%) patients presented with B-cell non-Hodgkin lymphomas. The antiviral treatment resulted in the elimination of the virus in 48.0% of the cases, complete clinical and immunological responses were achieved in 68,0% and 32,0% respectively. It had an advantage over immunosuppressive therapy in terms of long-term results of the treatment. We established the superiority of anti-CD monoclonal antibodies (rituximab) over conventional immunosuppressive drugs: complete clinical response 73% vs 13% (p=0,001). Combined therapy (rituximab and antiviral treatment) was more effective in patients with severe vasculitis (BVAS≥15). A case of successful treatment using direct-acting antivirals (DAAs) is reported. Causes of MC-vasculitis relapses after achieving sustained viral response are discussed. Conclusion. Antiviral therapy is the treatment of choice in all patients with HCV- HCV-MC vasculitis. Preference should be given to highly effective and safe modern therapy regimens with the use of DAAs. The antiviral treatment of severe forms of vasculitis must be combined with rituximab therapy.