Abstract
Chronic Kidney Disease (CKD) is an injury that causes progressive impairment of exocrine and endocrine renal functions. A very common complication is anemia, caused by reduced erythropoietin production, iron deficiency and inflammation. Evidence demonstrates that vitamin D has effects on anemia of inflammation, through the increase in erythrocytes and decrease in pro-inflammatory cytokines. This study aims to review the effects of vitamin D supplementation on 25(OH)D2 concentrations, on anemia markers and on PTH levels. This is an integrative review carried out through the search and selection of original publications, in english and portuguese, indexed in PubMed, Web of Science and Science Direct databases belonging to the 2010-2020 range. The results pointed to 25(OH)D2 concentrations compatible with normality after vitamin D supplementation. In five studies, there was no change in hemoglobin and PTH levels, and in four studies there was a reduction in the dose of EPO or erythroid stimulating agent, attributing such effect on the role of calcitriol as a substrate for bone marrow erythropoietic cells. The study concluded that vitamin D supplementation had beneficial effects for correction of 25(OH)D2 deficiency, however, it reinforces the controversy about the behavior of vitamin D on the improvement of anemia markers and PTH levels in patients with DRC. Therefore, it is suggested that the beneficial effect of vitamin D on anemia in renal patients may be independent of PTH suppression.
Highlights
Chronic Kidney Disease (CKD) is a global health problem (Daimon et al, 2020)
Vitamin D can have a favorable impact on anemia control, anemia of inflammation, by increasing erythroid progenitor proliferation and decreasing hepcidin-stimulating pro-inflammatory cytokines, reducing their concentrations, as well as acting directly on the hepcidin, down-regulating the transcription of messenger RNA of the antimicrobial peptide hepcidin (Sim et al, 2010; Smith & Tangpricha, 2015; Naini et al, 2015; Masoud et al, 2018)
Considering that vitamin D supplementation can have a favorable impact on the control of anemia, in anemia of inflammation and/or reduction in EPO requirements, this study aimed to review the effects of vitamin D supplementation on concentrations of 25(OH)D2, anemia markers (EPO, hemoglobin, ferritin and transferrin saturation) and parathyroid hormone (PTH) levels, considering possible ways of interaction, based on the literature
Summary
Chronic Kidney Disease (CKD) is a global health problem (Daimon et al, 2020). In recent years, with increasing longevity, there has been a trend towards an increase in the number of patients on dialysis, as attested by the Brazilian ChronicDialysis Survey conducted in 2019, where 139.691 patients were on dialysis in the country (Neves et al, 2021).Anemia secondary to CKD is a complication that is often not treated, which occurs early in the course of the disease and can become intractable with the decline in kidney function resulting in high morbidity, increased hospitalizations, impaired cognition and mortality (Begum & Latunde-Dada, 2019).The main causes of anemia are: reduced production of erythropoietin (EPO), which stimulates the production of erythrocytes (Bueno & Frizzo, 2014; Naini et al, 2015; Oliveira et al, 2019; Agarwal, 2021), deficiency of iron, inflammation, and vitamin D axis deficiencies (Zughaier et al, 2014; Bacchetta et al, 2014; Lima, 2017; Al-shaer et al, 2020).Attempts to improve the prevention and treatment of anemia or the use of potential therapies can help to reduce the burden of the disease (Arabi et al, 2020). Chronic Kidney Disease (CKD) is a global health problem (Daimon et al, 2020). Anemia secondary to CKD is a complication that is often not treated, which occurs early in the course of the disease and can become intractable with the decline in kidney function resulting in high morbidity, increased hospitalizations, impaired cognition and mortality (Begum & Latunde-Dada, 2019). Vitamin D can have a favorable impact on anemia control, anemia of inflammation, by increasing erythroid progenitor proliferation and decreasing hepcidin-stimulating pro-inflammatory cytokines, reducing their concentrations, as well as acting directly on the hepcidin, down-regulating the transcription of messenger RNA (mRNA) of the antimicrobial peptide hepcidin (Sim et al, 2010; Smith & Tangpricha, 2015; Naini et al., 2015; Masoud et al, 2018)
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