vitamin-k-1 and Kidney-Failure--Chronic

Vascular calcification occurs when calcium accumulates in the intima (associated with atherosclerosis) and/or media layers of the vessel wall. Coronary artery calcification (CAC) reflects the calcium burden within the intima and media of the coronary arteries. In population-based studies, CAC independently predicts cardiovascular disease (CVD) and mortality. A preventive role for vitamin K in vascular calcification has been proposed based on its role in activating matrix Gla protein (MGP), a calcification inhibitor that is expressed in vascular tissue. Although animal and in vitro data support this role of vitamin K, overall data from human studies are inconsistent. The majority of population-based studies have relied on vitamin K intake to measure status. Phylloquinone is the primary dietary form of vitamin K and available supplementation trials, albeit limited, suggest phylloquinone supplementation is relevant to CAC. Yet observational studies have found higher dietary menaquinone, but not phylloquinone, to be associated with less calcification. Vascular calcification is highly prevalent in certain patient populations, especially in those with chronic kidney disease (CKD), and it is plausible vitamin K may contribute to reducing vascular calcification in patients at higher risk. Subclinical vitamin K deficiency has been reported in CKD patients, but studies linking vitamin K status to calcification outcomes in CKD are needed to clarify whether or not improving vitamin K status is associated with improved vascular health in CKD. This review summarizes the available evidence of vitamin K and vascular calcification in population-based studies and clinic-based studies, with a specific focus on CKD patients.

Topics: Adult; Aged; Animals; Calcium-Binding Proteins; Dietary Supplements; Evidence-Based Medicine; Extracellular Matrix Proteins; Female; Humans; Kidney Failure, Chronic; Male; Matrix Gla Protein; Middle Aged; Vascular Calcification; Vitamin K; Vitamin K 1; Vitamins

Vitamin K denotes a group of lipophilic vitamins determining post-translational modification of proteins. There are 2 main forms of vitamin K: vitamin K1 (phylloquinone, found in vegetables); vitamin K2 (menaquinone, produced by bacteria in the intestine and in fermented foods). Vitamin K stores are limited in humans, but it can be recycled. Vitamin K1 is principally transported to the liver, regulating the production of coagulation factors. Vitamin K2, instead, is also transported to extra-hepatic tissues, such as bone and arteries, regulating the activity of matrix Gla-protein (MGP) and osteocalcin [bone Gla-protein (BGP)]. In patients with chronic kidney disease (CKD), cardiovascular mortality is the first cause of death. Some pathogenetic mechanisms of vascular calcification (such as hyperparathyroidism, hyperphosphatemia, hypercalcemia, role of vitamin D) have been widely investigated, but the potential role of vitamin K is still uncertain. Vitamin K could play a key role, as it transforms glutamic acid residues into γ-carboxyglutamic acid, through a carboxylation process, makings both MGP (cMGP) and BGP (cBGP) biologically active. cMGP inhibits vascular calcifications (VC), while cBGP has an important role for a proper mineralization process. Uncarboxylated MGP and BGP (ucMGP and ucBGP) concentrations are indirect markers of vitamin K2 deficiency. The purpose of this review is to analyze the current literature to understand the relationship between vitamin K2 status, fragility fractures and VC in CKD patients. This analysis could be of help in planning investigations of Vitamin K status and its possible supplementation in CKD patients to avert fragility fractures and VC.

Topics: Animals; Calcinosis; Fractures, Bone; Humans; Kidney Failure, Chronic; Molecular Structure; Osteocalcin; Renal Dialysis; Vitamin K 1; Vitamin K 2

Topics: Alkaline Phosphatase; Biomarkers; Calcium; Dietary Supplements; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Parathyroid Hormone; Phosphates; Renal Dialysis; Vitamin K 1

To investigate the influence of liver lesions and vitamin K1 on bleeding after liver biopsy in patients with chronic renal failure and hepatitis virus infection.. Ninety-two renal transplant recipients on hemodialysis with hepatitis B or C virus infection received percutaneous liver biopsy. The severities of liver inflammation and fibrosis were evaluated by semi-quantitative technique. Thirty-four patients were given intramuscular injection of vitamin K1 before liver biopsy at the dose of 10 mg twice daily for 3 days.. The total incidence of bleeding after liver biopsy was 12.0% (11/92) in these patients, and the use of vitamin K1 did not significantly influence the incidence of bleeding, nor did the degree of liver lesions.. Bleeding occurred with a relatively high incidence after liver biopsy in patients with chronic renal failure and hepatitis virus B or C infection; vitamin K1 before liver biopsy could not reduce the incidence of bleeding, which is not correlated with the degree of liver lesions.

Topics: Biopsy; Hemorrhage; Humans; Incidence; Kidney Failure, Chronic; Liver; Vitamin K 1

Serum level of vitamin K1 (= phylloquinone, hereinafter K1) and K dependent blood coagulation factors were determined by HPLC in normal subject, liver cirrhosis, hepatocellular carcinoma, acute hepatitis, chronic hepatitis, chronic renal failure with hemodialysis and patients under warfarin therapy. Normal range of serum K1 concentration was decided on 0.20-2.30 (0.87 +/- 0.53, n = 96) ng/ml. Serum K1 level showed no significant differences among normal subject, various diseases and warfarin therapy. Correlation between serum K1 level and F-VII (r = 0.879, p less than 0.001) or protein C activity (r = 0.839, p less than 0.01) was found in patients whose thrombotest was 20% and less. However serum K1 level didn't correlate with any K dependent coagulation factors in patients if thrombotest was over 20%.

Topics: Adolescent; Adult; Blood Coagulation Factors; Female; Heart Diseases; Humans; Kidney Failure, Chronic; Liver Diseases; Male; Protein C; Vitamin K 1; Warfarin

Antibiotic therapy, using penicillins or cephalosporins, is frequently required in patients on maintenance hemodialysis. Points to consider are dose adjustment for drugs which are excreted via the kidney, drug dialysability, and cumulation with frequent occurrence of side reactions, neurotoxicity and bleeding being the clinically most important ones. For third-generation cephalosporins with N-methylthiotetrazole side chain, impaired intrahepatic vitamin K metabolism may cause problems of hemostasis which can be avoided by dose adjustment and prophylactic administration of vitamin K1.

Topics: Bacterial Infections; Body Weight; Cephalosporins; Dose-Response Relationship, Drug; Drug Administration Schedule; Hemorrhage; Humans; Kidney Failure, Chronic; Kinetics; Penicillin Resistance; Penicillins; Renal Dialysis; Tetrazoles; Vitamin K 1