scholarly journals Causes of Vitamin K Deficiency in Patients on Haemodialysis

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2513
Author(s):  
Signe Wikstrøm ◽  
Katrine Aagaard Lentz ◽  
Ditte Hansen ◽  
Lars Melholt Rasmussen ◽  
Jette Jakobsen ◽  
...  
Keyword(s):  
Vitamin K ◽  
Absorption Capacity ◽  
Protein Supplementation ◽  
Matrix Gla Protein ◽  
Vitamin K1 ◽  
High Concentration ◽  
Vitamin K Deficiency ◽  
Before And After ◽  
K Deficiency ◽  
The Difference

Background: A low vitamin K status is common in patients on haemodialysis, and this is considered one of the reasons for the accelerated atherosclerosis in these patients. The vitamin is essential in activation of the protein Matrix Gla Protein (MGP), and the inactive form, dp-ucMGP, is used to measure vitamin K status. The purpose of this study was to investigate possible underlying causes of low vitamin K status, which could potentially be low intake, washout during dialysis or inhibited absorption capacity. Moreover, the aim was to investigate whether the biomarker dp-ucMGP is affected in these patients. Method: Vitamin K intake was assessed by a Food Frequency Questionnaire (FFQ) and absorption capacity by means of D-xylose testing. dp-ucMGP was measured in plasma before and after dialysis, and phylloquinine (vitamin K1) and dp-ucMGP were measured in the dialysate. Changes in dp-ucMGP were measured after 14 days of protein supplementation. Results: All patients had plasma dp-ucMGP above 750 pmol/L, and a low intake of vitamin K. The absorption capacity was normal. The difference in dp-ucMGP before and after dialysis was −1022 pmol/L (p < 0.001). Vitamin K1 was not present in the dialysate but dp-ucMGP was at a high concentration. The change in dp-ucMGP before and after protein supplementation was −165 pmol/L (p = 0.06). Conclusion: All patients had vitamin K deficiency. The reason for the low vitamin K status is not due to removal of vitamin K during dialysis or decreased absorption but is plausibly due to a low intake of vitamin K in food. dp-ucMGP is washed out during dialysis, but not affected by protein intake to a clinically relevant degree.

Placental Transfer of Vitamin K1 and Its Implications in Fetal Hemostasis

1988 ◽  
Vol 60 (01) ◽  
pp. 039-043 ◽  
Author(s):  
L Mandelbrot ◽  
M Guillaumont ◽  
M Leclercq ◽  
J J Lefrère ◽  
D Gozin ◽  
...  
Keyword(s):  
Vitamin K ◽  
High Performance ◽  
Ultrasound Guidance ◽  
Placental Transfer ◽  
Vitamin K1 ◽  
Vitamin K Deficiency ◽  
Prothrombin Activity ◽  
Oral Supplementation ◽  
K Deficiency ◽  
The Mean

SummaryVitamin K status was evaluated using coagulation studies and/ or vitamin IQ assays in a total of 53 normal fetuses and 47 neonates. Second trimester fetal blood samples were obtained for prenatal diagnosis under ultrasound guidance. Endogenous vitamin K1 concentrations (determined by high performance liquid chromatography) were substantially lower than maternal levels. The mean maternal-fetal gradient was 14-fold at mid trimester and 18-fold at birth. Despite low vitamin K levels, descarboxy prothrombin, detected by a staphylocoagulase assay, was elevated in only a single fetus and a single neonate.After maternal oral supplementation with vitamin K1, cord vitamin K1 levels were boosted 30-fold at mid trimester and 60 fold at term, demonstrating placental transfer. However, these levels were substantially lower than corresponding supplemented maternal levels. Despite elevated vitamin K1 concentrations, supplemented fetuses and neonates showed no increase in total or coagulant prothrombin activity. These results suggest that the low prothrombin levels found during intrauterine life are not due to vitamin K deficiency.

P1645VITAMIN K DEPENDENT PROTEINS AFTER KIDNEY TRANSPLANTATION: RESULTS FROM PROSPECTIVE STUDY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Maria Fusaro ◽  
Pascale Khairallah ◽  
Andrea Aghi ◽  
Mario Plebani ◽  
Martina Zaninotto ◽  
...  
Keyword(s):  
Kidney Transplantation ◽  
Prospective Study ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Matrix Gla Protein ◽  
Bone Gla Protein ◽  
Vitamin K Deficiency ◽  
Prospective Data ◽  
K Deficiency ◽  
The Impact

Abstract Background and Aims Two Vitamin K-dependent proteins (VDKPs) link bone and vasculature in CKD-MBD: Bone Gla Protein (BGP) and Matrix Gla Protein (MGP). In ESKD, Vitamin K deficiency is highly prevalent and leads to increased levels of inactive VKDPs (undercaboxylated (ucBGP and dephosphorylated (dp)-uMGP), which are linked to greater risk of fractures and severity of vascular calcification. We hypothesized that kidney transplantation (KT) would improve Vitamin K status and lower levels of inactive VKDPs. Method Between 2014-2017, we conducted a study in 34 patients to assess changes in VKDPs during the 1st year of KT. In a specialized lab we determined VKDPs pre- and 1-year post-KT: total BGP, uc BGP, total MGP, and dp-uc MGP. We determined the prevalence of Vitamin K deficiency based on levels of uc BGP and dp-uc MGP. Results Our cohort had a mean +/- SD age of 48+/-14 years, 32% were female and 97% were Caucasian. 1 year post-KT, there was a decrease in the levels of all VKDPs and the prevalence of Vitamin K deficiency (Table 1 and Figure 1). Patients with greatest severity of Vitamin K deficiency pre-KT had the largest decreases of inactive VDKPs post-KT. Conclusion KT was associated with improvement in Vitamin K status as manifested by decreased levels of inactive VKDPs. These are the first prospective data on VKDPs in CKD patients pre- and post-KT. Studies are needed to assess the impact of improvement in VKDP status after KT on CKD-MBD outcomes.

scholarly journals Association of the Inactive Circulating Matrix Gla Protein with Vitamin K Intake, Calcification, Mortality, and Cardiovascular Disease: A Review

2019 ◽  
Vol 20 (3) ◽  
pp. 628 ◽  
Author(s):  
Stefanos Roumeliotis ◽  
Evangelia Dounousi ◽  
Theodoros Eleftheriadis ◽  
Vassilios Liakopoulos
Keyword(s):  
Cardiovascular Disease ◽  
Renal Function ◽  
Vitamin K ◽  
Serum Levels ◽  
Matrix Gla Protein ◽  
Biologically Active ◽  
Vitamin K Deficiency ◽  
K Deficiency ◽  
Dependent Protein ◽  
Existing Data

Matrix Gla Protein (MGP), a small Gla vitamin K-dependent protein, is the most powerful natural occurring inhibitor of calcification in the human body. To become biologically active, MGP must undergo vitamin K-dependent carboxylation and phosphorylation. Vitamin K deficiency leads to the inactive uncarboxylated, dephosphorylated form of MGP (dpucMGP). We aimed to review the existing data on the association between circulating dpucMGP and vascular calcification, renal function, mortality, and cardiovascular disease in distinct populations. Moreover, the association between vitamin K supplementation and serum levels of dpucMGP was also reviewed.

Evaluation of a Daily Dose of 25 μg Vitamin K1 to Prevent Vitamin K Deficiency in Breast-Fed Infants

1993 ◽  
Vol 16 (3) ◽  
pp. 301-305 ◽  
Author(s):  
E. A. M. Cornelissen ◽  
L. A. A. Kollée ◽  
T. G. P. J. van Lith ◽  
K. Motohara ◽  
L. A. H. Monnens
Keyword(s):  
Vitamin K ◽  
Vitamin K1 ◽  
Vitamin K Deficiency ◽  
Daily Dose ◽  
K Deficiency ◽  
Breast Fed

scholarly journals Difference in the metabolism of vitamin K between liver and bone in vitamin K-deficient rats

2002 ◽  
Vol 87 (4) ◽  
pp. 307-314 ◽  
Author(s):  
Toshiro Sato ◽  
Yutaka Ohtani ◽  
Yoko Yamada ◽  
Sanshiroh Saitoh ◽  
Hiroshi Harada
Keyword(s):  
Body Weight ◽  
Vitamin K ◽  
Initial Level ◽  
Undercarboxylated Osteocalcin ◽  
Vitamin K Deficiency ◽  
Dose Administration ◽  
Osteocalcin Level ◽  
Short Period ◽  
K Deficiency ◽  
The Difference

The difference between vitamin K metabolism in the liver and that in the bone of vitamin K-deficient rats was examined. After 17 d administration of vitamin K-deficient food, vitamin K in the liver was almost depleted, and prothrombin time (PT) was prolonged. Serum total osteocalcin level was slightly decreased by vitamin K deficiency, whereas serum undercarboxylated osteocalcin level did not change. The level of menaquinone (MK)-4 as well as that of phylloquinone was decreased, but approximately 40 % of the initial level still existed in the femur after the 17 d period. A single-dose administration of vitamin K (250 nmol/kg body weight) markedly increased vitamin K level in the liver but not in the femur. These results suggest that the turnover of vitamin K in the bone is slower than that in the liver, and bone metabolism may be little affected by the short period of intake of vitamin K-deficient food. However, intake of a larger amount of vitamin K is required for its accumulation in the bone than in the liver. Furthermore, the counteracting effect of MK-7 on prolonged PT in vitamin K-deficient rats was found to be higher than phylloquinone or MK-4.

Finding the optimal dose of vitamin K1 to treat vitamin K deficiency and to avoid anaphylactoid reactions

2017 ◽  
Vol 31 (5) ◽  
pp. 495-505 ◽  
Author(s):  
Yan-ni Mi ◽  
Na-na Ping ◽  
Bo Li ◽  
Xue Xiao ◽  
Yan-bing Zhu ◽  
...  
Keyword(s):  
Vitamin K ◽  
Optimal Dose ◽  
Vitamin K1 ◽  
Vitamin K Deficiency ◽  
K Deficiency ◽  
Anaphylactoid Reactions

scholarly journals Sevelamer Use in End-Stage Kidney Disease (ESKD) Patients Associates with Poor Vitamin K Status and High Levels of Gut-Derived Uremic Toxins: A Drug–Bug Interaction?

Toxins ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 351
Author(s):  
Lu Dai ◽  
Björn K. Meijers ◽  
Bert Bammens ◽  
Henriette de Loor ◽  
Leon J. Schurgers ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Vitamin K ◽  
Phosphate Binder ◽  
Microbial Metabolism ◽  
Uremic Toxins ◽  
Matrix Gla Protein ◽  
Vitamin K Deficiency ◽  
End Stage Kidney Disease ◽  
K Deficiency ◽  
End Stage

Gut microbial metabolism is not only an important source of uremic toxins but may also help to maintain the vitamin K stores of the host. We hypothesized that sevelamer therapy, a commonly used phosphate binder in patients with end-stage kidney disease (ESKD), associates with a disturbed gut microbial metabolism. Important representatives of gut-derived uremic toxins, including indoxyl sulfate (IndS), p-Cresyl sulfate (pCS), trimethylamine N-oxide (TMAO), phenylacetylglutamine (PAG) and non-phosphorylated, uncarboxylated matrix-Gla protein (dp-ucMGP; a marker of vitamin K status), were analyzed in blood samples from 423 patients (65% males, median age 54 years) with ESKD. Demographics and laboratory data were extracted from electronic files. Sevelamer users (n = 172, 41%) were characterized by higher phosphate, IndS, TMAO, PAG and dp-ucMGP levels compared to non-users. Sevelamer was significantly associated with increased IndS, PAG and dp-ucMGP levels, independent of age, sex, calcium-containing phosphate binder, cohort, phosphate, creatinine and dialysis vintage. High dp-ucMGP levels, reflecting vitamin K deficiency, were independently and positively associated with PAG and TMAO levels. Sevelamer therapy associates with an unfavorable gut microbial metabolism pattern. Although the observational design precludes causal inference, present findings implicate a disturbed microbial metabolism and vitamin K deficiency as potential trade-offs of sevelamer therapy.

scholarly journals Late vitamin K deficiency bleeding despite intramuscular prophylaxis at birth - is there a need for additional supplementation?

2017 ◽  
Vol 145 (5-6) ◽  
pp. 254-258 ◽  
Author(s):  
Jelena Martic ◽  
Katarina Pejic ◽  
Dobrila Veljkovic ◽  
Zorica Rakonjac ◽  
Milos Kuzmanovic ◽  
...  
Keyword(s):  
Vitamin K ◽  
Tertiary Care ◽  
Newborn Infants ◽  
Antibiotic Use ◽  
Daily Weight Gain ◽  
Vitamin K1 ◽  
Vitamin K Deficiency ◽  
Vitamin K Deficiency Bleeding ◽  
Breastfed Infants ◽  
K Deficiency

Introduction/Objective. Vitamin K deficiency is common in newborn infants and without prophylaxis there is a risk of vitamin K deficiency bleeding (VKDB). The most frequent prophylactic approach is an intramuscular (IM) injection of vitamin K1 immediately after birth. Its efficiency to prevent late VKDB has been recently questioned by several reports. Based on our experience, we discuss the need for additional vitamin K1 supplementation after its IM administration at birth. Methods. We present a retrospective review of 12 infants, 11 with confirmed and one with probable late VKDB despite IM prophylaxis at birth, who were treated in the two largest tertiary care pediatric hospitals in Serbia during the last 15 years. Results. All the patients were exclusively breastfed. In 11 patients, daily weight gain was normal or increased, and one patient had failure to gain weight. Six infants were previously healthy, three infants received antibiotics prior to bleeding, and in two diarrhea and cholestasis, respectively, existed previously. An intracranial bleeding was documented in nine infants, four of whom died. Conclusion. Low content of phytomenadione in human milk could occasionally be attributed to late VKDB despite postnatal IM injection of vitamin K1 in otherwise healthy, exclusively breastfed infants. This might be aggravated by transient disturbance of vitamin K turnover due to antibiotic use, acute diarrhea, or transient cholestasis. We suggest that an additional vitamin K1 supplementation after postnatal IM prophylaxis could be justified in exclusively breastfed infants.

scholarly journals Functional vitamin K insufficiency, vascular calcification and mortality in advanced chronic kidney disease: A cohort study

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247623
Author(s):  
Lu Dai ◽  
Longkai Li ◽  
Helen Erlandsson ◽  
Armand M. G. Jaminon ◽  
Abdul Rashid Qureshi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Matrix Gla Protein ◽  
Vitamin K Deficiency ◽  
Increased Risk ◽  
Ckd Stage ◽  
All Cause Mortality ◽  
K Deficiency

Patients with chronic kidney disease (CKD) suffer from vitamin K deficiency and are at high risk of vascular calcification (VC) and premature death. We investigated the association of functional vitamin K deficiency with all-cause mortality and whether this association is modified by the presence of VC in CKD stage 5 (CKD G5). Plasma dephosphorylated-uncarboxylated matrix Gla-protein (dp-ucMGP), a circulating marker of functional vitamin K deficiency, and other laboratory and clinical data were determined in 493 CKD G5 patients. VC was assessed in subgroups by Agatston scoring of coronary artery calcium (CAC) and aortic valve calcium (AVC). Backward stepwise regression did not identify dp-ucMGP as an independent determinant of VC. During a median follow-up of 42 months, 93 patients died. Each one standard deviation increment in dp-ucMGP was associated with increased risk of all-cause mortality (sub-hazard ratio (sHR) 1.17; 95% confidence interval, 1.01–1.37) adjusted for age, sex, cardiovascular disease, diabetes, body mass index, inflammation, and dialysis treatment. The association remained significant when further adjusted for CAC and AVC in sub-analyses (sHR 1.22, 1.01–1.48 and 1.27, 1.01–1.60, respectively). In conclusion, functional vitamin K deficiency associates with increased mortality risk that is independent of the presence of VC in patients with CKD G5.

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