Introduction. Tertiary hyperparathyroidism (THPT) and vitamin D deficiency are commonly seen in kidney transplant recipients, which may result in persistently elevated fibroblast growth factor 23 (FGF23) level after transplantation and decrease graft survival. The aim of this study is to evaluate the effect of vitamin D supplementation on THPT, FGF23-αKlotho axis and cardiovascular complications after transplantation. Materials and Methods. 209 kidney transplant recipients were included and further divided into treated and untreated groups depending on whether receiving vitamin D supplementation. We tracked the state of THPT, bone metabolism, FGF23-αKlotho axis within 12 months posttransplant and explored the predictors and risk factors for intact FGF23 levels, αKlotho levels, THPT and cardiovascular complications in recipients. Results. Vitamin D supplementation significantly improved FGF23 resistance, THPT and high bone turnover status, preserved better graft function and prevented coronary calcification in treated group comparing with untreated group at month 12. The absence of vitamin D supplementation was an independent risk factor for THPT and a predictor for iFGF23 and αKlotho levels at month 12. Age and vitamin D deficiency were independent risk factors for coronary calcification in recipients at month 12. Conclusion. Vitamin D supplementation effectively improved THPT, FGF23 resistance and bone metabolism, preserved graft function and prevented coronary calcification after transplantation.
Background: Although posttransplant anemia (PTA) is a common complication after kidney transplant, it has not been thoroughly evaluated for appropriate treatment. Roxadustat can stimulate erythropoiesis by increasing erythropoietin (EPO) production and improving the utilization of iron. However, there are currently a few case reports describing its effect on PTA in kidney transplant recipients (KTRs). Our purpose was to evaluate the efficacy and safety of roxadustat in KTRs with PTA.Methods: In this retrospective study, KTRs with early PTA were divided into a roxadustat group, erythropoiesis-stimulating agent (ESA) group, and untreated group (neither roxadustat nor ESA) according to the treatment prescribed by their physicians. We compared the levels of hemoglobin (Hb), creatinine, lipids, hepcidin, intact fibroblast growth factor 23 (iFGF23) and iron-related indices, at baseline and different time points posttransplant. Outcome was assessed at both month 3 and month 12 posttransplant. Adverse events during the treatment course were also recorded.Results: A total of 57 KTRs were included (n=22 roxadustat group, n=13 ESA group, n=22 untreated group). There was no difference in age, sex, body mass index, dialysis method and duration, donor type among three groups at baseline. The mean Hb levels at month 3 posttransplant (128.00±19.62 vs. 118.59±11.60 g/L, P=0.048) and the average change in Hb levels from week 2 to month 3 (48.05±22.53 vs. 31.45±12.96 g/L, P=0.005) in the roxadustat group were significantly higher than those in the untreated group. However, there was no significant difference in the above indices between the roxadustat and ESA groups. At month 3, the total iron binding capacity (TIBC) and levels of transferrin were significantly higher while levels of ferritin, hepcidin and iFGF23 were significantly lower in the roxadustat group than in other groups (P<0.05). No significant difference was found in creatinine or estimated glomerular filtration rate (eGFR) levels among the three groups at month 3. During the follow-up, no adverse events related to roxadustat were reported.Conclusions: Administration of roxadustat in KTRs with early PTA could elevate Hb levels effectively and safely by enhancing endogenous EPO production and improving iron utilization. Further randomized studies with larger sample size are necessary to verify our results.
BackgroundChronic allograft dysfunction(CAD) is the leading cause of graft loss in kidney transplant recipients (KTRs). Inflammatory process is believed to be one of the major contributors to CAD. The aim of this study is to explore the anti-inflammatory effect of vitamin D (VD) supplementation in KTRs and its role in the graft function improvement(protection).MethodsA retrospective cohort of 39 KTRs with chronic antibody mediated rejection(CAMR)or stable renal function and a prospective cohort of 42 KTRs treated or untreated with VD were enrolled. Serum levels of vitamin D metabolism and serum inflammatory cytokines, renal graft function, and routine blood biomarkers were tested and dynamically tracked within 12 months post-transplant.ResultsCompared with the stable group, the CAMR group exhibited significantly elevated serum levels of inflammatory cytokines IL-1β, IFN-γ, IL-2, IL-10, IP-10, and HMGB1 (P <0.05). The supplementation of vitamin D effectively increased the serum concentration of vitamin D in kidney transplant recipients (KTRs) in the treated group. During the course of treatment, the treated group exhibited a gradual increase in eGFR levels, which were significantly higher than those observed in the untreated group at 12 months post-transplant (p<0.05). Notably, as eGFR improved, there was a significant decrease in levels of IL-1β, IFN-γ, IL-2, IL-10, IP-10 and HMGB1 in the treated group compared to the untreated group (P<0.05).ConclusionThis study confirmed that immune-inflammation is a crucial factor in the development of CAD in KTRs.VD deficiency impairs its anti-inflammatory activity. By assisting in the regulation of excessive immune inflammation and restoration of immune homeostasis, effective VD supplementation contributes to protection and maintenance of graft function in KTRs.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.