Background and objectives: Chronic kidney disease (CKD) in children is a complex medical and social issue around the world. One of the serious complications is mineral-bone disorder (CKD-MBD) which might determine the prognosis of patients and their quality of life. Fibroblast growth factor 23 (FGF-23) is a phosphaturic hormone which is involved in the pathogenesis of CKD-MBD. The purpose of the study was to determine what comes first in children with CKD: FGF-23 or phosphate. Materials and Methods: This cross-sectional study included 73 children aged 2–18 years with CKD stages 1–5. We measured FGF-23 and other bone markers in blood samples and studied their associations. Results: Early elevations of FGF-23 were identified in children with CKD stage 2 compared with stage 1 (1.6 (1.5–1.8) pmol/L versus 0.65 (0.22–1.08), p = 0.029). There were significant differences between the advanced stages of the disease. FGF-23 correlated with PTH (r = 0.807, p = 0.000) and phosphate (r = 0.473, p = 0.000). Our study revealed that the elevated level of FGF-23 went ahead hyperphosphatemia and elevated PTH. Thus, more than 50% of children with CKD stage 2 had the elevating level of serum FGF-23, and that index became increasing with the disease progression and it achieved 100% at the dialysis stage. The serum phosphate increased more slowly and only 70.6% of children with CKD stage 5 had the increased values. The PTH increase was more dynamic. Conclusions: FGF-23 is an essential biomarker, elevates long before other markers of bone metabolism (phosphate), and might represent a clinical course of disease.

Background and Objectives: Nowadays, every tenth adult in the world suffers from diabetes mellitus (DM). Diabetic retinopathy (DR) is the most common microvascular complication of type 2 DM (T2DM) and a leading cause of acquired blindness in middle-aged individuals in many countries. Previous studies have identified associations of several gene polymorphisms with susceptibility to microvascular complications of DM in various worldwide populations. In our study, we aimed to test the hypothesis of the associations of single nucleotide polymorphisms (SNP) of the VEGF (−2549I/D), RAGE (−429T/C and −374T/A), TCF7L2 (rs7903146), and ITGA2 (BglII) genes with a predisposition to DR among T2DM patients in the Kazakhstan population. Materials and Methods: We conducted a case–control study comparing the genotype distribution and allele frequencies between groups of DR patients (N = 94), diabetic patients without DR (N = 94), and healthy controls (N = 51). Genotypes were identified using the PCR-RFLP method. Results: In all cases, the genotype distribution corresponded to the Hardy–Weinberg equilibrium. The groups of diabetic patients with and without DR did not significantly differ in the genotype distribution of the SNPs studied. Differences between both groups of diabetic patients and healthy controls in four out of five SNPs were also not significant. At the same time, both groups of diabetic patients differed significantly from healthy controls in genotype distribution (p = 0.042 and 0.005, respectively) and allele frequencies (p = 0.021 and 0.002, respectively) of the BglII polymorphism in the ITGA2 gene. After adjusting for multiple comparisons, the differences between the group of diabetic patients without DR and the control group remained significant (p_Bonf = 0.027 for genotypes and p_Bonf = 0.009 for alleles). The BglII− allele was associated with diabetes: OR = 1.81 [1.09–2.99] for DR patients, and OR = 2.24 [1.34–3.75] for diabetic patients without DR. The association was also observed in the subset of Kazakhs. Conclusions: This study shows that the BglII polymorphism in the ITGA2 gene can be associated with T2DM but not with DR. According to our data, the risk allele for diabetes is the wild BglII− allele, and not the minor BglII+, which is considered as risky for DR.

Nowadays chronic kidney disease (CKD) is one of the leading chronic non-communicable diseases in terms of morbidity and mortality. One of the most serious complications is mineral-bone disorder, which worsen the clinical course and prognosis of patients. Fibroblast growth factor 23 (FGF-23) is a new biomarker that regulates phosphate metabolism and plays an important role in the pathogenesis of many complications in CKD. Purpose. To study the physiological role of FGF-23, as well as its potential clinical significance in the progression of CKD and its complications. Material and methods. A 20-year-deep literature search was conducted in the international scientific databases PubMed / Medline, Web of Science and Google Scholar for the following keywords: "Fibroblast growth factor 23", "FGF-23", "phosphate homeostasis", "chronic kidney disease", "Mineral and bone disorders", "left ventricular hypertrophy". Results and discussion. FGF-23 is a protein secreted by bone cells and its primary physiological role is to regulate urinary excretion of phosphate to maintain a stable level in serum. Moreover, FGF-23 decreases calcitriol levels and inhibits parathyroid hormone secretion. In CKD, there is a gradual increase in FGF-23 levels as renal function declines, which can be regarded as physiological compensation to stabilize serum phosphate levels. According to the several studies, FGF-23 might be associated with cardiovascular complications, such as left ventricular hypertrophy and heart failure. Conclusion. Thus, FGF-23 is not only a marker of mineral-bone disorders in CKD, but also a key link in the pathogenesis of the development of secondary hyperparathyroidism and cardiovascular complications. With this in mind, FGF-23 may represent a multifunctional therapeutic target that may improve the prognosis of patients with CKD. Keywords: fibroblast growth factor-23, phosphate, parathyroid hormone, left ventricular hypertrophy, mineral-bone disorder.

IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide and is a major contributor to the global burden of chronic kidney disease. Strong evidence highlights complement activation as a key driver of the disease pathogenesis and its progression. In this regard, the emergence of new therapies targeting the complement system has further increased interest in specific biomarkers that can help in diagnosis, prognosis, and assessment of response to therapy in patients with IgAN. Although complement biomarkers show promising associations with disease severity and prognosis, most remain exploratory and lack adequate validation for routine clinical application. Further research should focus on standardization and prospective multicenter validation of putative biomarkers to facilitate a biomarker-driven approach to the use of complement inhibitors in IgAN. Therefore, this review summarizes a growing body of evidence on the role of complement-related biomarkers in IgAN and discusses their diagnostic and prognostic potential, as well as several limitations for implementation in clinical practice.

INTRODUCTION: Hypertension (HTN), otherwise known as high blood pressure (BP), is a leading cause of cardiovascular diseases. According to the Barker hypothesis, low birth weight (LBW) has a causal relationship to the origins of HTN. It’s now well established that the kidney does have a key role in pathogenesis of essential HTN: probably due to defect of sodium excretion (high salt diets cause an estimated 150 000 premature deaths in the U.S. each year). The aim of study: early detection of risk factors for arterial hypertension among young adults.