Vitamins For Healthy Kidney Function – Free Fatty Acid Receptor 4 (FFA4) Activation Ameliorates Ovalbumin-Induced Allergic Asthma by Omnibus Activation of Dendritic and Malignant Cells in Mice.
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Vitamins For Healthy Kidney Function
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By Federica Bellone 1, †, Maria Cincograni 1, †, Ramona Nicotra 2, Nazarno Carollo 3, Alessandro Casarella 3, Pirangela Presta 3, Michel Andrucci 3, Giovanni Squadrito 2, Marpino 1, Giovanni Squadrito 1, Giovanni Rossi 1, Giovanni 3 , Saro 3 , David Bolinano 3 , and Giuseppe Capolino 3 , *
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Received: March 29, 2022 / Revised: May 7, 2022 / Accepted: May 7, 2022 / Published: May 9, 2022
Chronic kidney disease (CKD) is common with vitamin K deficiency. Some serious complications of CKD are represented by cardiovascular disease (CVD) and skeletal fragility with increased risk of morbidity and mortality. There is a complex pathogenic relationship between hormonal and ionic disturbances, changes in bone tissue and metabolism, and vascular calcification (VC) and is defined as chronic kidney disease-mineral and bone disorders (CKD-MBD). Poor vitamin K status appears to play a key role in the development of CKD, but also in the initiation and progression of bone and cardiovascular complications. Three forms of vitamin K are now known: vitamin K1 (phylloquinone), vitamin K2 (menaquinone), and vitamin K3 (menadione). Vitamin K plays a variety of roles, including activating vitamin K-dependent proteins (VKDPs) and modulating bone metabolism and helping to inhibit VC. This review focuses on the biochemical and functional properties of vitamin K, suggesting this nutrient as a possible marker of renal, CV, and bone damage in the CKD population and exploring its potential use for health promotion in this clinical setting. Treatment strategies for osteoporosis and CV disease associated with CKD should include vitamin K supplementation. However, randomized clinical trials are still needed to evaluate safety and adequate dosing to prevent CKD complications.
Chronic kidney disease (CKD) is characterized by concomitant vascular calcification and impaired bone metabolism [1]. In particular, bone-vascular imbalances have been shown with subsequent vascular and bone changes. Although the mechanistic link of this vascular-skeletal junction is still poorly understood, certain hormones, including parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D3, are known to regulate both skeletal and vascular mineralization. Regeneration of stem cells [3]. Therefore, the term “calcification paradox” has been coined to denote the association of ectopic mineralization in the vessels with decreased bone turnover and decreased bone mineral density (BMD) [4]. In recent years, knowledge about the important role of vitamin K has increased exponentially due to its known involvement in vascular calcification, cardiovascular diseases and bone resorption. Recently, increasing evidence suggests that vitamin K supplementation may be a tool to prevent rapid vascular calcification and maintain bone health in CKD patients [5]. In this context, we will focus on the current knowledge about the biological functions of vitamin K, its involvement in the relationship between cardiovascular diseases (especially in hypertensive patients) and bone metabolism in CKD patients, and the potential utilization of vitamin K. . To promote health in this hospital
A review of this literature was made available. First, studies were retrieved from PubMed, Scope and Web of Science online databases, using the following keywords: “chronic kidney disease”, “vitamin K”, “vascular calcification”, “bone metabolism”, “osteoporosis”. and “cardiovascular diseases”. An initial filter was applied for online search language (Latin) and availability of full-text articles. In addition, indexes of included studies were reviewed to identify potentially relevant studies further required in the database search. Online survey definitively completed on March 15, 2022.
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The term vitamin K or naphthoquinone refers to a family of fat-soluble molecules that have a similar structure of the 2-methyl-1, 4-naphthoquinone ring, but have different origins and functions. Currently, three primary forms are known, defined as vitamins, which differ in the anodic bonds of the 2-methyl-1,4-naphthoquinone ring at the 3-position [6]. These are vitamin K1 (phylloquinone), vitamin K2 (menaquinone), and vitamin K3 (menadione). The main known biological role of vitamin K1 is in blood coagulation, as it acts as a cofactor for the enzymatic conversion of glutamic acid (Glu) residues to gamma-carboxyglutamic acid (Gla) in vitamin K-dependent proteins (VKDPs) via vitamin he does. K-gamma-glutamyl-dependent carboxylase, located in the endoplasmic reticulum of cells of all mammalian tissues [7, 8, 9], and for the conversion of protein-bound glutamate to carboxyglutamate, required for II, VII, IX. , and cases of coagulation factor X and natural anticoagulant proteins S, C [10, 11]. Sources of vitamin K1 are mainly leafy or flowering vegetables (spinach, lettuce, kale, cabbage, Brussels sprouts, turnips), but grains, peas, soybeans, green tea, eggs, pork, and beef liver also contain vitamin K1. . [12]. Vitamin K2 is primarily absorbed by the gut microbiota as menaquinone (MK). Depending on the length of the isoprene chain attached to the methylated naphthoquinone ring, various forms such as 4 to 13 are found. MK-4 is numbered from the conversion of phylloquinone or menadione and is mainly found in meat and animals. – Products such as eggs, milk and yogurt [13, 14, 15]. MK-VII, on the other hand, is a long-chain form produced by gut bacteria and found in fermented foods such as cheese and soy. MK4 and MK7, along with MK8, MK9 and MK10, are the two most common menaquinones in the human diet. Vitamin K3, also known as menadione, was once thought to be a synthetic form of vitamin K. However, it has been shown that vitamin K3 can also be formed in the intestine as an intermediate product of the conversion of oral vitamin K1 to vitamin K2, i.e., MK4. [17, 18].
Vitamin K absorption occurs in different intestinal tracts: Vitamin K1 is absorbed in the ileum. Vitamin K2 in sections of the colon. Efficient functioning of the pancreas is essential for bile and adequate absorption. Vitamin K molecules are incorporated into chylomicrons and then released into high-density lipoprotein (VLDL) and low-density lipoprotein (LDL) and then released into the fibers. Due to their relatively short half-life (17 hours), vitamin K1 and K2 must be continuously synthesized and supplied by intestinal bacteria. Catabolism of vitamin K1 and vitamin K2 share common mechanisms, with initial hydroxylation mediated by CYP4F2, followed by shortening of the polyisoprenoic side chain by b-oxidation to carboxylic acids (to 5C, 7C, or 10C metabolites). which are glucuronidated and excreted through urine and bile [7, 19, 20].
In healthy subjects, fasting plasma phylloquinone concentrations have been reported to range from 0.29 to 2.64 nmol/L [21]. However, serum vitamin K levels are difficult to estimate because they are affected by multiple factors (eg, low plasma levels, nonpolar nature, and lipid barrier). Diet and inflammation are other variables that affect plasma levels. Therefore, vitamin K levels are often assessed indirectly by measuring prothrombin time (vitamin K1) or gamma-carboxyglutamic acid (Gla) carboxylated protein concentration (not available in all laboratories) [22, 23].
The recommended intake of vitamin K by the World Health Organization (WHO) and the Food and Agriculture Organization (FAO) is 65 μg/day for men and 55 μg/day for women, based on a calculated requirement of 1 μg/kg/day. body weight. The Italian Society of Human Nutrition (SINU) recommended an age-level vitamin K intake: 140 μg/day or 170 μg/day for 18–59 years and over 60 years, respectively [ 24 ]. Vitamin K deficiency is associated with an increased rate of cardiovascular events [7]. Observational studies of the inverse relationship between vitamin K2 and