Native Hypovitaminosis D in CKD Patients: From Experimental Evidence to Clinical Practice

Alfieri, Carlo; Ruzhytska, Oksana; Vettoretti, Simone; Caldiroli, Lara; Cozzolino, Mario

doi:10.3390/nu11081918

Cited by 19 publications

(15 citation statements)

References 80 publications

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“…In the clinical setting, chronic kidney disease is an illness of particular interest with respect to vitamin D and CVD: primarily, because both low circulating 25(OH)D and low 1,25(OH) 2 D concentrations are frequent findings in CKD patients [ 93 , 94 ]; secondly, because the risk of vascular calcification and CVD is substantially higher in patients with CKD than in individuals with preserved kidney function [ 95 ]; and thirdly, because impaired kidney function is considered to contribute to the loss of homeostatic control of serum calcium concentrations and may thus influence the cut-off point defining the toxicity of vitamin D and calcium [ 15 ]. There is evidence that vitamin D administration of >2000 IU/d vitamin D or activated vitamin D significantly increased concentrations of the cardiovascular risk marker FGF-23, especially in patients with end-stage kidney/heart failure [ 96 ].…”

Section: Cardiovascular Events In Patients With Chronic Kidney Dismentioning

confidence: 99%

Vitamin D and Cardiovascular Disease: An Updated Narrative Review

Zittermann

Trummer

Theiler‐Schwetz

et al. 2021

IJMS

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During the last two decades, the potential impact of vitamin D on the risk of cardiovascular disease (CVD) has been rigorously studied. Data regarding the effect of vitamin D on CVD risk are puzzling: observational data indicate an inverse nonlinear association between vitamin D status and CVD events, with the highest CVD risk at severe vitamin D deficiency; however, preclinical data and randomized controlled trials (RCTs) show several beneficial effects of vitamin D on the surrogate parameters of vascular and cardiac function. By contrast, Mendelian randomization studies and large RCTs in the general population and in patients with chronic kidney disease, a high-risk group for CVD events, largely report no significant beneficial effect of vitamin D treatment on CVD events. In patients with rickets and osteomalacia, cardiovascular complications are infrequently reported, except for an increased risk of heart failure. In conclusion, there is no strong evidence for beneficial vitamin D effects on CVD risk, either in the general population or in high-risk groups. Whether some subgroups such as individuals with severe vitamin D deficiency or a combination of low vitamin D status with specific gene variants and/or certain nutrition/lifestyle factors would benefit from vitamin D (metabolite) administration, remains to be studied.

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Section: Cardiovascular Events In Patients With Chronic Kidney Dismentioning

confidence: 99%

Vitamin D and Cardiovascular Disease: An Updated Narrative Review

Zittermann

Trummer

Theiler‐Schwetz

et al. 2021

IJMS

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“…Also, "the fibroblast growth factor 23 (FGF23), as well as its co-receptor α-Klotho, may favourably affect CYP24A1 activity in response to hypercalcemia and hyperphosphatemia. Because of its critical involvement in regulating the levels of 1,25(OH)2D3 in the circulation, the extent of research into CYP24A1's significance in this regard has been widespread [21][22] . Mice lacking the CYP24A1 gene showed a much greater degree of impairment in 1,25(OH)2D3 and 25(OH-D3) pharmacokinetics than did mice that were heterozygous for the CYP24A1 gene.…”

Section: Role Of Cyp24a1 In Vitamin D Catabolismmentioning

confidence: 99%

CYP24A1 Polymorphism Effect on Chronic Drugs Administration and Development of Osteomalacia: A Review Article

Hammadi¹,

Ali

2021

Int. j. res. appl. sci. biotechnol.

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Osteomalacia is a condition that causes bone thinning, which is frequently caused by a vitamin D deficiency. Vitamin D aids in the formation of the body's bones, therefore when levels are low, the bones are not as strong as they should be. Muscle weakness, bone discomfort, and a waddling stride are some of the symptoms of osteomalacia. The lower back hips, and legs are particularly vulnerable to pain. The weakening of the bones may make them more susceptible to fracture. Osetomalacia may be induced by a lack of sun exposure or a lack of vitamin D in the diet. Bone metabolic problems, cancers, cardiovascular illnesses, and diabetes are all linked to a lack of 25OHD. Also linked to autoimmune illnesses and mental problems. Vitamin D is one of the most important minerals for human health.

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Section: H 2 S As a Signaling Mediator In The Kmentioning

confidence: 99%

“…On the other hand, glutathione peroxidase deficiency in kidney diseases contributed to the development of cardiac diseases risk due to an increase in ROS generation and inflammatory pathways [152]. Furthermore, CKD patients also display hypovitaminosis D [153] as well as hypoalbuminemia [154] and zinc deficiency [155]. Fascinatingly evidence demonstrated that NaHS suppresses the expression of the ROS-generating enzyme, NADPH oxidase (NOX) and its essential subunit, Rac-1, in cultured vascular smooth muscle cells [156].…”

Section: Antioxidant Role Of H 2 Smentioning

confidence: 99%

Hydrogen Sulfide and Carnosine: Modulation of Oxidative Stress and Inflammation in Kidney and Brain Axis

et al. 2020

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Emerging evidence indicates that the dysregulation of cellular redox homeostasis and chronic inflammatory processes are implicated in the pathogenesis of kidney and brain disorders. In this light, endogenous dipeptide carnosine (β-alanyl-L-histidine) and hydrogen sulfide (H2S) exert cytoprotective actions through the modulation of redox-dependent resilience pathways during oxidative stress and inflammation. Several recent studies have elucidated a functional crosstalk occurring between kidney and the brain. The pathophysiological link of this crosstalk is represented by oxidative stress and inflammatory processes which contribute to the high prevalence of neuropsychiatric disorders, cognitive impairment, and dementia during the natural history of chronic kidney disease. Herein, we provide an overview of the main pathophysiological mechanisms related to high levels of pro-inflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and neurotoxins, which play a critical role in the kidney–brain crosstalk. The present paper also explores the respective role of H2S and carnosine in the modulation of oxidative stress and inflammation in the kidney–brain axis. It suggests that these activities are likely mediated, at least in part, via hormetic processes, involving Nrf2 (Nuclear factor-like 2), Hsp 70 (heat shock protein 70), SIRT-1 (Sirtuin-1), Trx (Thioredoxin), and the glutathione system. Metabolic interactions at the kidney and brain axis level operate in controlling and reducing oxidant-induced inflammatory damage and therefore, can be a promising potential therapeutic target to reduce the severity of renal and brain injuries in humans.

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Native Hypovitaminosis D in CKD Patients: From Experimental Evidence to Clinical Practice

Cited by 19 publications

References 80 publications

Vitamin D and Cardiovascular Disease: An Updated Narrative Review

Vitamin D and Cardiovascular Disease: An Updated Narrative Review

CYP24A1 Polymorphism Effect on Chronic Drugs Administration and Development of Osteomalacia: A Review Article

Hydrogen Sulfide and Carnosine: Modulation of Oxidative Stress and Inflammation in Kidney and Brain Axis

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