Vitamin K2 Eases Artery Stiffness in Kidney Transplant Patients

clinical-trial PMID: 36695702

Vitamin K2 Eases Artery Stiffness in Kidney Transplant Patients

Quick Summary: A 2023 study tested vitamin K2 supplements on kidney transplant patients low in vitamin K. While it didn't stop artery calcification, it did reduce artery stiffness after 12 weeks. This could help lower heart risks for these patients.

What The Research Found

Researchers wanted to see if vitamin K2 could fight artery hardening in kidney transplant patients who lack this vitamin. Vitamin K2 helps keep calcium from building up in arteries, which can make them stiff and raise heart disease risk.

Key results from the trial:
- Artery stiffness improved: Patients taking vitamin K2 saw their arteries get more flexible. Stiffness dropped by 0.7 meters per second, a meaningful change that beats the placebo group (P=0.01).
- No big change in calcification risk: The supplement didn't lower the blood's tendency to form calcium deposits, as measured by a test called T50. Both groups showed similar small shifts (+2.3 minutes for vitamin K2 vs. +0.8 minutes for placebo; P=0.88).
- Vitamin K levels bounced back: The supplement worked well to fix the deficiency. A marker called dp-ucMGP fell by 392 pmol/L in the vitamin K2 group, proving it activated the body's natural protectors against artery damage (P<0.001).
- Safe with no side effects: No one reported problems from the supplement.

These findings suggest vitamin K2 targets artery flexibility but may not directly block calcium buildup in this group.

Study Details

Who was studied: 40 kidney transplant patients who were low in vitamin K (tested by high dp-ucMGP levels over 500 pmol/L). About 35% were women, with an average age of 57. They had no recent heart issues or blood thinners.
How long: 12 weeks, or about 3 months.
What they took: Daily oral capsules of 360 micrograms of vitamin K2 (menaquinone-7, or MK-7) or a fake placebo pill. Everyone got the same routine, and researchers didn't know who got what to keep it fair.

The study was double-blind and randomized at one hospital, ensuring reliable results.

What This Means For You

If you or a loved one had a kidney transplant and tests show low vitamin K, this research points to a simple fix. Adding 360 mcg of vitamin K2 daily might make your arteries less stiff, cutting heart risks without side effects. It's not a cure-all for calcification, but improving flexibility is a win for blood flow and overall health.

Talk to your doctor before starting supplements, especially with kidney issues—they can check your levels and tailor advice. For healthy folks, this doesn't apply directly, but it highlights vitamin K2's role in heart health from foods like fermented soy or cheese.

Study Limitations

This trial has some hurdles that mean it's not the final word:
- Small group: Only 40 people, so results might not hold for everyone.
- Short time frame: 12 weeks may not show long-term effects on calcification or heart events.
- One location: Done at a single center, so it might not fit all hospitals or patient types.
- High variability: Calcification tests fluctuated a lot, making it hard to spot small differences.
- Specific to this group: Findings are for vitamin K-deficient kidney patients only—not for general kidney disease or healthy people.

Bigger, longer studies are needed to confirm if vitamin K2 truly prevents heart problems over time.

Key Findings

This 12-week clinical trial found that daily supplementation with 360 μg of vitamin K2 (menaquinone-7) in vitamin K-deficient kidney transplant recipients (KTRs) significantly reduced arterial stiffness (measured by pulse wave velocity [PWV]) by -0.7 m/s compared to placebo (P=0.01). However, no significant effect was observed on serum calcification propensity (change in T50: +2.3 ± 27.4 minutes vs. +0.8 ± 34.4 minutes in placebo; P=0.88). Vitamin K status improved markedly, with a 392 pmol/L decrease in dp-ucMGP (P<0.001), confirming the supplement’s bioactivity.

Study Design

A double-blind, randomized, placebo-controlled trial conducted at a single center. 40 vitamin K-deficient KTRs (plasma dp-ucMGP ≥500 pmol/L) were randomized 1:1 to vitamin K2 or placebo. Participants were 35% female, aged 57 ± 13 years. Exclusion criteria included prior cardiovascular events or anticoagulant use.

Dosage & Administration

Participants received 360 μg/day of menaquinone-7 (MK-7) or placebo capsules orally for 12 weeks. Compliance was monitored via capsule return counts.

Results & Efficacy

Arterial stiffness: PWV decreased by -0.7 m/s in the K2 group vs. placebo (P=0.01; 95% CI not reported).
Calcification propensity: No significant change in T50 (P=0.88), though variability was high (±27.4 vs. ±34.4 minutes).
Vitamin K status: dp-ucMGP levels dropped by -392 pmol/L in the K2 group vs. placebo (P<0.001), indicating improved carboxylation of MGP.
Safety: No adverse events reported.

Limitations

Small sample size (n=40) and short duration (12 weeks) may limit detection of long-term calcification effects.
Single-center design reduces generalizability.
T50 variability: High standard deviations in both groups suggest potential measurement inconsistency or heterogeneity in calcification pathways.
Population specificity: Results apply only to KTRs with severe vitamin K deficiency, not to the general population or those with chronic kidney disease.
No clinical endpoints: The trial did not assess hard outcomes like cardiovascular events or mortality.

Clinical Relevance

For vitamin K-deficient KTRs, MK-7 supplementation at 360 μg/day may improve arterial stiffness, a risk factor for cardiovascular disease. However, the lack of effect on calcification propensity (T50) suggests it does not directly inhibit vascular calcification in this population. Clinicians should consider screening KTRs for vitamin K deficiency (via dp-ucMGP) and address arterial stiffness through targeted interventions. Supplement users with kidney disease should consult healthcare providers before use, as individual responses may vary. Larger, longer trials are needed to confirm these findings and explore effects on calcification in broader populations.

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