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What is a Vitamin K Blood Test?

REVIEWED BY
Bill Maish, MD
Clinical Content Consultant
Published
May 30, 2026
Last updated
May 30, 2026
Quick answer:

Vitamin K blood testing measures circulating phylloquinone (K1) or menaquinones (K2) — fat-soluble nutrients the liver uses to activate clotting factors II, VII, IX, X and calcium-regulating proteins like osteocalcin and matrix Gla protein. Deficiency elevates INR/PT, is associated with easy bruising and prolonged bleeding, and may impair bone mineralisation and vascular health. Pairing serum K with PT/INR and PIVKA-II helps assess haemostatic balance and long-term cardiovascular risk.

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Table of contents

Phylloquinone and menaquinones: the vitamin K family

Vitamin K blood testing evaluates your body's vitamin K status. Vitamin K is a fat-soluble family of nutrients that we get mainly as K1 from leafy greens and plant oils (phylloquinone) and as K2 from animal and fermented foods and from gut bacteria (menaquinones). After absorption with dietary fat, vitamin K travels in the bloodstream with lipoproteins and is stored and used in the liver and other tissues.

Vitamin K's core job is to help "activate" certain proteins by adding a specific chemical tag (gamma-carboxylation). This switch turns on key blood-clotting factors (II, VII, IX, X) and natural anticoagulants (proteins C and S), and it also enables proteins that manage calcium in bone and soft tissues, such as osteocalcin and matrix Gla protein. A vitamin K blood test therefore reflects the body's supply of vitamin K available for these activation steps and, by extension, the readiness of clotting and calcium-handling systems to function properly.

Why vitamin K bridges clotting, bone, and vascular biology

A vitamin K blood test gauges your supply of a fat-soluble vitamin that activates clotting factors and calcification-controlling proteins. It integrates nutrition, gut absorption, and liver function, signaling how safely you form clots while maintaining bone and vascular health.

A Vitamin K blood test typically measures circulating phylloquinone (vitamin K1), the fat-soluble vitamin the liver and other tissues use to activate proteins by gamma-carboxylation. Adequate availability supports stable blood clotting, bone mineralization (osteocalcin), and protection against arterial calcification (matrix Gla protein), linking it to cardiovascular integrity and skeletal health.

Reading low and high vitamin K values

Labs measure vitamin K1 or functional markers. There's no single universal range; mid-range values, with a normal PT/INR, usually indicate adequate status rather than living at the low edge. Being in range suggests adequate activation of vitamin K-dependent proteins in liver and extrahepatic tissues, with stable hemostasis, balanced bone remodeling, and vascular maintenance. For most labs, fasting, mid-range values align with steady physiologic status.

When values are low, the liver cannot fully gamma-carboxylate clotting factors (II, VII, IX, X) and proteins C/S. Low values usually reflect too little intake or poor absorption of fat, reduced bile flow, or interference with vitamin K recycling (e.g., warfarin). Blood clots more slowly, causing easy bruising, gum or nose bleeding, heavy periods, or blood in stool. Physiology shifts toward undercarboxylated clotting factors II, VII, IX, and X and proteins C and S, which shows up as easy bruising or bleeding. Bone proteins stay undercarboxylated, weakening bone quality; arteries lose matrix Gla protein activity, favoring calcification. Over time, undercarboxylated osteocalcin and matrix Gla protein can weaken bone and permit vascular calcification. Risks rise with fat-malabsorption, prolonged antibiotics, liver disease, and in pregnancy and especially newborns, where deficiency can cause dangerous bleeding. Newborns and late pregnancy are higher-risk states for deficiency-related bleeding.

Higher results usually reflect recent diet or supplements; toxicity is rare. High values usually reflect recent supplementation or a fat-containing meal, since plasma vitamin K rises postprandially. In people taking warfarin, abundant vitamin K counteracts the drug, lowering the INR and shifting risk toward clotting. Phylloquinone and menaquinones rarely cause toxicity, and elevated levels do not typically produce hypercoagulability. Liver disease may show normal vitamin K with impaired clotting because the liver cannot make the proteins, so functional tests can clarify context. Marked elevations can also reflect lipemia or assay interference.

Why a plasma K result can be misleading

Plasma vitamin K fluctuates with recent diet, fasting status, and lipid levels, and may not mirror tissue status. Liver disease, fat-malabsorption, antibiotics, anticonvulsants, pregnancy, and assay method influence interpretation. Functional markers (PT/INR, PIVKA-II) are often used alongside direct vitamin K measurements.

Big picture: vitamin K status links diet, microbiome, bile-mediated absorption, and hepatic protein synthesis with skeletal strength and vascular flexibility. Persistent inadequacy is associated with fractures and arterial calcification; excess chiefly matters for those on vitamin K antagonists. Vitamin K is most informative alongside PT/INR and PIVKA-II, which capture undercarboxylated clotting factors, plus liver tests when synthesis itself is in question.

FAQs

Vitamin K is a family of fat-soluble vitamins, including vitamin K1 (phylloquinone) from leafy greens and plant oils, and vitamin K2 (menaquinones) from fermented foods, animal products, and gut bacteria. Vitamin K is essential for activating proteins that control blood clotting, bone mineralization, and calcium regulation in blood vessels. It enables the body to stop bleeding after injury, supports strong bones by activating osteocalcin, and is studied for its potential effects on calcium buildup in arteries through matrix Gla protein. Adequate vitamin K status is crucial for normal hemostasis, bone strength, and vascular health.

Vitamin K deficiency leads to under-activation of clotting factors, resulting in easy bruising, gum or nosebleeds, heavy menstrual bleeding, or prolonged bleeding after injury. Laboratory tests may show a high INR or prolonged PT. In bones, deficiency causes higher levels of undercarboxylated osteocalcin, reducing bone mineralization and increasing fracture risk. Deficiency also impairs matrix Gla protein, raising the risk of arterial calcification. Groups at higher risk include those with fat malabsorption, liver disease, prolonged antibiotic use, older adults, and newborns.

Vitamin K1 (phylloquinone) is primarily found in leafy green vegetables such as spinach, kale, and broccoli, as well as in plant oils. Vitamin K2 (menaquinones) is present in fermented foods like natto, some cheeses, and animal products such as egg yolks and liver. Additionally, gut bacteria produce small amounts of K2. A balanced diet with plenty of leafy greens and some fermented or animal foods helps maintain within reference ranges vitamin K status.

Vitamin K status is assessed using serum vitamin K levels and functional markers like INR, PIVKA-II (des-γ-carboxy prothrombin), and undercarboxylated osteocalcin. Normal vitamin K status is indicated by a standard INR, low PIVKA-II, and low undercarboxylated osteocalcin, with serum levels in the mid-range. Results should be interpreted alongside liver function tests, medications, and bleeding symptoms, as well as factors like recent food intake and triglyceride levels.

Conditions that impair fat absorption, such as chronic gastrointestinal or liver disease, bile or pancreatic insufficiency, and use of fat-blocking agents or bile acid binders, can reduce vitamin K absorption. Prolonged use of broad-spectrum antibiotics disrupts gut bacteria that produce vitamin K2. Newborns are at high risk due to low stores and limited placental transfer. Vitamin K antagonist medications (e.g., warfarin) also interfere with vitamin K activity, increasing bleeding risk.

Superpower currently offers at-home blood testing in the following states: Alabama, Arizona, California, Colorado, Connecticut, Delaware, District of Columbia, Florida, Georgia, Idaho, Illinois, Indiana, Kansas, Maine, Maryland, Massachusetts, Michigan, Minnesota, Missouri, Montana, Nebraska, Nevada, New Hampshire, New Jersey, New Mexico, New York, North Carolina, Ohio, Oklahoma, Oregon, Pennsylvania, South Carolina, Tennessee, Texas, Utah, Vermont, Virginia, Washington, West Virginia, and Wisconsin.

We’re actively expanding nationwide, with new states being added regularly. If your state isn’t listed yet, stay tuned.

References

  1. National Institutes of Health, Office of Dietary Supplements. (2021). Vitamin K: Fact sheet for health professionals. https://ods.od.nih.gov/factsheets/VitaminK-HealthProfessional/
  2. Shearer, M. J., Fu, X., & Booth, S. L. (2012). Vitamin K nutrition, metabolism, and requirements: Current concepts and future research. Advances in Nutrition, 3(2), 182-195. https://doi.org/10.3945/an.111.001800
  3. DiNicolantonio, J. J., Bhutani, J., & O'Keefe, J. H. (2015). The health benefits of vitamin K. Open Heart, 2(1), e000300. https://doi.org/10.1136/openhrt-2015-000300
  4. El Asmar, M. S., Naoum, J. J., & Arbid, E. J. (2014). Vitamin K dependent proteins and the role of vitamin K2 in the modulation of vascular calcification: a review. Oman Medical Journal, 29(3), 172-177. https://doi.org/10.5001/omj.2014.44
  5. Sankar, M. J., Chandrasekaran, A., Kumar, P., Thukral, A., Agarwal, R., & Paul, V. K. (2016). Vitamin K prophylaxis for prevention of vitamin K deficiency bleeding: a systematic review. Journal of Perinatology, 36(Suppl 1), S29-S35. https://doi.org/10.1038/jp.2016.30

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