Correlation of Serum FGF23 and Chronic Kidney Disease-Mineral and Bone Abnormality Markers With Cardiac Structure Changes in Maintenance Hemodialysis Patients.

Background: CKD-MBD is a mineral and bone metabolism syndrome caused by chronic kidney disease. FGF23 is an important factor regulating phosphorus and is the main influencer in the CKD-MBD process. In this study, we observed the correlation among serum FGF23 and calcium, phosphorus and parathyroid hormone, and the correlation between FGF23 levels and cardiac structural changes in MHD patients. Methods: We examined serum FGF23 concentrations in 107 cases of MHD patients using the ELISA method, recorded demographic information and biochemical data, and analyzed the correlation between serum FGF23 levels and blood calcium and blood phosphorus and PTH levels. All patients were evaluated by cardiac color ultrasound, and we finally analyzed the association between the FGF23 level and cardiac structural changes. Results: In 107 cases of MHD patients, serum FGF23 levels were linearly associated with serum calcium (r = 0.27 P < 0.01) and parathyroid hormone levels (r = 0.25, P < 0.05). FGF 23 was negatively correlated with age (r = -0.44, P < 0.01).Serum FGF23 levels were correlated with right atrial hypertrophy in HD patients (P < 0.05). No correlation was found among FGF23, left ventricular hypertrophy/enlargement, and valve calcification stenosis (P > 0.05). Conclusion: Serum FGF23 showed a positive correlation among blood calcium levels and PTH levels in hemodialysis patients, and FGF23 levels can affect the incidence of right atrial hypertrophy in MHD patients.

NFE2L3 as a Potential Functional Gene Regulating Immune Microenvironment in Human Kidney Cancer.

With the increasing incidence and mortality of renal cancer, it is pressing to find new biomarkers and drug targets for diagnosis and treatment. However, as one negative upstream regulator of p53, the prognostic and immunological role of NFE2L3 in renal cancer is still barely known. We investigated the expression, prognostic value, and relevant pathways of NFE2L3 using the datasets from public databases, including The Cancer Genome Atlas Program (TCGA), Genotype-Tissue Expression (GTEx), Cancer Cell Line Encyclopedia (CCLE), and UALCAN. Furthermore, we analyzed the relationship between NFE2L3 expression and the immune microenvironment using distinct methods. We found that NFE2L3 was higher expressed in kidney renal clear cell carcinoma (KIRC) and kidney renal papillary cell carcinoma (KIRP) tissues than adjacent normal tissues. Additionally, we identified NFE2L3 as one survival-related factor for KIRC and KIRP. The enrichment analyses revealed that NFE2L3 was associated with a variety of immune-relevant pathways in KIRC and related to the infiltration ratios of 17 types of immune cells in KIRC patients. Ultimately, we demonstrated nine significantly enriched mutations, such as TP53 and MET, in NFE2L3-expression-changing groups. The elevated expression of NFE2L3 in renal cancerous tissues versus normal tissues is associated with poor outcomes in patients. Besides, NFE2L3 has a role in the regulation of the immune microenvironment in renal cancer patients. The findings of our study provide a potential prognostic biomarker and a new drug target for renal cancer.