Terapevt Arkh
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Chronic kidney disease (CKD) is a supra - nosological term that reflects the progressive nature of chronic kidney diseases, which are based on the mechanisms of nephrosclerosis. Diagnosis of CKD at the earliest stages is of great importance, because it allows, by using therapeutic agents, to slow the progression of renal dysfunction and the development of cardiovascular complications. However, the currently available methods for diagnosing renal function impairment, including the determination of endogenous creatinine clearance, can detect renal dysfunction too late, when around 40-50% of the renal parenchyma is already reversibly or irreversibly damaged. ⋯ In particular, it has been shown that their expression profile in blood or urine can reflect changes in cells involved in a particular pathological process, since these cells can secrete a specific population of microRNAs, for example, through secretion of microRNA-containing exosomes. This gave grounds for considering increased or decreased expression of individual microRNAs in renal tissue or biological fluids (including urine) as new biomarkers for the diagnosis and monitoring of CKD. This review presents the results of recent experimental and clinical studies on these issues.
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Polycystic kidney disease (PKD) is a genetically determined pathological process associated with the formation and growth of cysts originating from the epithelial cells of the tubules and/or collecting tubes. PBP is represented by two main types - autosomal dominant (ADPKD) and autosomal recessive PKD (ARPKD), which are different diseases. The main causes of ADPKD are mutations of the PKD1 and PKD2 genes, which encode the formation of polycystin-1 and polycystin-2 proteins. ⋯ Mechanisms of cysts formation and growth include a) mutations of polycystines genes located on the cilia; b) increased activity of renal intracellular cAMP; c) vasopressin V2 receptors activation; d) violation of the tubular epithelium polarity (translocation of Na,K-ATPasa from basolateral to apical membrane); e) increased mTOR activity in epithelial cells lining renal cyst. The most promising directions of ADPKD therapy are blockade of vasopressin V2 receptors activation, inhibition of mTOR signaling pathways and reduction of intracellular cAMP level. The review presents clinical studies that assessed the effectiveness of named drugs in ADPKD.
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Protein restriction diet (PRD) with ketoanalagues of essential amino acids (KA) combination can improve of chronic kidney disease (CKD) course while, the precise mechanisms of PRD + KAA action in CKD are not known yet. We have conducted a prospective, randomized, controlled study of PRD and KAA patient's group in compare with PRD without KAA group in regarding to serum Klotho and FGF-23 levels in patients with CKD. ⋯ Use of PRD + KAA provides adequate nutrition status and more efficient correction of FGF-23 and Klotho imbalance in CKD progression that may contribute to alleviation of both cardiovascular calcification and cardiac remodeling in CKD. Importantly, a prolonged PRD use without supplementation of KAA may lead to malnutrition signs.
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To determine the frequency, clinical and morphological features of a nephropathy with C1q deposits in chronic glomerulonephritis adult patients. ⋯ Deposits of C1q in kidney were revealed in 4.05% of biopsy specimens in CGN. The most frequent morphological form was the membranous nephropathy. The clinical course was characterized by a nephrotic syndrome, more than at a half of patients - with renal dysfunction.