Vitamin K in Chronic Kidney Disease

Cozzolino, Mario; Mangano, Michela; Galassi, Andrea; Ciceri, Paola; Messa, Piergiorgio; Nigwekar, Sagar U.

doi:10.3390/nu11010168

Cited by 72 publications

(65 citation statements)

References 65 publications

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“…CKD patients frequently suffer from subclinical vitamin K deficiency [20], resulting in increased plasma levels of inactive uncarboxylated MGP protein, a condition that may be associated with an increased risk of cardiovascular disease (CVD) [21] and mortality in patients with CKD [22,23]. This deficiency might be caused by exhaustion of vitamin K due to its high requirement by vitamin K-dependent proteins to inhibit calcification or due to dietary recommendations for CKD patients, such as a diet low in potassium (fewer leafy green vegetables rich in K1) and phosphate (fewer dairy products rich in K2) [24].…”

Section: Introductionmentioning

confidence: 99%

Cholesterol-Lowering Action of a Novel Nutraceutical Combination in Uremic Rats: Insights into the Molecular Mechanism in a Hepatoma Cell Line

Lupo

Biancorosso

Brilli³

et al. 2020

Nutrients

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Appropriate nutraceutical combinations may represent a valid approach to prevent vascular calcification associated with chronic kidney disease (CKD). In the present study, we tested the effect of a new nutraceutical combination named RenaTris®, containing MK-7, magnesium carbonate, and Sucrosomial® Iron, on vascular calcification in uremic rats. Rats were randomly divided into three groups, i.e., control (high-phosphate diet), uremic (high-phosphate diet containing 0.5% adenine), and supplemented uremic diet (0.5% adenine, MK-7, magnesium carbonate, and Sucrosomial® Iron). After six weeks, sera and vascular calcification were examined. The uremic diet increased creatinine and phosphate levels and induced extensive vascular calcification. The uremic condition also induced a mild hypercholesterolemic condition (+52% of total cholesterol; p < 0.05). The supplemented uremic diet did not reduce creatinine, phosphate levels, or vascular calcification, however, we observed a significant hypocholesterolemic effect (−18.9% in supplemental uremic vs. uremic diet; p < 0.05). Similar to simvastatin, incubation of cultured human hepatoma cells (Huh7) with MK-7 significantly reduced cholesterol biosynthesis (−38%) and induced 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase and low-density lipoprotein receptor (LDLR) at both mRNA and protein levels. The effect of MK-7 on LDLR was counteracted by the co-incubation with squalene. Unlike simvastatin, MK-7 reduced PCSK9 in Huh7. These results indicated that the new nutraceutical combination significantly impacts cholesterol metabolism and its supplementation may help to control mild hypercholesterolemic conditions in CKD patients.

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Section: Introductionmentioning

confidence: 99%

Cholesterol-Lowering Action of a Novel Nutraceutical Combination in Uremic Rats: Insights into the Molecular Mechanism in a Hepatoma Cell Line

Lupo

Biancorosso

Brilli³

et al. 2020

Nutrients

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“…There are two main natural forms of Vitamin K: K1 (or phylloquinone, PK) contained in green vegetables, and K2 (including several different vitamers called menaquinones, MKs) mostly derived from fermented foods and intestinal bacteria (e.g., cheeses and the Japanese soybean product known as "natto") [15]. There are up to 12 different types of MKs, from MK-4 to MK-15; the most common MKs in humans are the short-chain MK-4 and MK-7 to MK-10, which are respectively produced by systemic conversion of phylloquinone to menaquinones and synthesized by bacteria [16]. The pivotal biological role of vitamin K is to act as a cofactor for the carboxylation (and thereby activation) of vitamin-K-dependent proteins (VKDPs).…”

Section: Vitamin K and Gla Proteinsmentioning

confidence: 99%

“…Krueger speculated that uncarboxylated Gla proteins are less secreted from the cells, maybe in attempt to prevent inactive proteins from entering the tissues. A reduced phosphorylation of the three serine residues of MGP seems equally important as it would result in reduced secretion of MGP [16][17][18][19]36,41].…”

Section: Vitamin K and Gla Proteinsmentioning

confidence: 99%

Current Therapy in CKD Patients Can Affect Vitamin K Status

et al. 2020

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Chronic kidney disease (CKD) patients have a higher risk of cardiovascular (CVD) morbidity and mortality compared to the general population. The links between CKD and CVD are not fully elucidated but encompass both traditional and uremic-related risk factors. The term CKD-mineral and bone disorder (CKD-MBD) indicates a systemic disorder characterized by abnormal levels of calcium, phosphate, PTH and FGF-23, along with vitamin D deficiency, decreased bone mineral density or altered bone turnover and vascular calcification. A growing body of evidence shows that CKD patients can be affected by subclinical vitamin K deficiency; this has led to identifying such a condition as a potential therapeutic target given the specific role of Vitamin K in metabolism of several proteins involved in bone and vascular health. In other words, we can hypothesize that vitamin K deficiency is the common pathogenetic link between impaired bone mineralization and vascular calcification. However, some of the most common approaches to CKD, such as (1) low vitamin K intake due to nutritional restrictions, (2) warfarin treatment, (3) VDRA and calcimimetics, and (4) phosphate binders, may instead have the opposite effects on vitamin K metabolism and storage in CKD patients.

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“…One more interesting evidence is that CKD patients suffer from subclinical vitamin K deficiency [8], suggesting that this represents a population at risk for any biological consequences of poor vitamin K status. This deficiency might be caused by exhaustion of vitamin K due to its high requirement by vitamin K-dependent proteins to inhibit VC.…”

Section: Doi: 101159/000506178mentioning

confidence: 99%