Terapevt Arkh
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To clarify the mechanisms of the effect of osteoprotegerin (OPG) and sclerostin on vascular calcification and the state of the cardiovascular system in chronic kidney disease (CKD). ⋯ Changes in the regulation of bone-mineral metabolism, in which the proteins inhibitors of bone metabolism, OPG and sclerostin, as well as the interactive interaction between the vascular and skeletal systems, play a decisive role in the development of lesions of the cardiovascular system caused by vascular calcification in CKD.
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Lupus nephritis (LN) is the most common organ lesion in systemic lupus erythematosus (SLE), developing in 4050% of patients. Due to immunosuppressive therapy, the survival of patients with SLE has increased significantly over the past 50 years, and the proportion of severe kidney damage in the death structure has decreased. However, LN relapses and complications of immunosuppression, accelerated atherogenesis, concomitant diseases lead to the accumulation of organ damage and an increased risk of death. The article consideres the place of kidney damage in the SLE, the risk factors for LN development, the main renal histopathological changes, it identifies a number of issues that need to be addressed to optimize treatment and improve LN long-term outcomes, including, the revision of pathogenetic therapy regimens with restriction of glucocorticosteroids and prescribing drugs with steroid-sparing activity, the integration of new drugs for LN treatment, wider use of modern nephroprotection capabilities.
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The article presents an historical analysis of publications devoted lead intoxication to kidney damage developing during contact with lead. It is shown that one of the manifestations of occupational intoxication with this metal can be toxic nephropathy.
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Antiangiogenic drugs are widely used in oncological practice and are aimed at inhibiting angiogenesis. Despite the high antitumor efficacy, their use may be limited by nephrotoxicity, and therefore the search for early biomarkers of kidney damage remains relevant, which will preserve a favorable safety profile of therapy. ⋯ The predictors of renal damage in the treatment with antiangiogenic drugs were previously an increase in NGAL, KIM-1 and HIF-1 in urine during the first two weeks after the start of therapy.
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Membranous nephropathy (MN), an immune-mediated glomerular disease, is the most common cause of adult nephrotic syndrome. In MN, proteinuria is developed by podocyte damage due to the complement system activation in response to the subepithelial deposition of immune complexes containing various auto- and exogenous antigens. ⋯ Thus far, the main pathway of complement activation leading to the formation of MAC in MN has not been established. The review highlights current evidence of various complement pathways activation in the development of MN, as well as recently established new molecular mechanisms of complement-mediated podocyte damage.