Kynurenate is product of the metabolism of L-Tryptophan and appears in urine in Vitamin B6 deficiencies. Your body needs vitamin B6 (pyridoxine) to utilize amino acids derived from dietary protein. Inadequate vitamin B6 is one factor that leads to increased concentrations of kynurenate and xanthurenate in urine. These products of amino acid breakdown cannot be further metabolized in the absence of vitamin B6.
Xanthurenate and kynurenate are metabolic byproducts in the production of tryptophan to NAD in the liver. If either xanthurenate or kynurenate build up in the urine, it can indicate a need for vitamin B6. This need is amplified if BOTH markers are elevated, and often indicates a more severe deficiency of vitamin B6. Vitamin B6 is critical as a co-factor to over 100 important reactions that occur in the human body and is stored in the highest concentration in muscle tissue.
Tryptophan is converted to NAD by the liver and one of the steps in this pathway requires B6. When B6 is insufficient, xanthurenate is made instead. Xanthurenate can also bind to iron and create a complex that increases DNA oxidative damage resulting in higher 8-OHdG levels. If both the xanthurenate and 8OhdG levels are elevated, there is likely an antioxidant insufficiency.
Kynurenate may also become elevated when patients are B6 deficient because of a different, possibly less B6 dependent pathway. While there is always some tryptophan going down the kynurenine pathway towards NAD, and possibly xanthurenate, this process is up regulated by inflammation, estrogen and cortisol elevations. If levels of estrogen or cortisol are high, it may exacerbate kynurenic acid and increase the need for vitamin B6. As the Xanthurenate and Kynurenate pathways lead to biomarkers with other influence in the body, elevations in these markers may not always agree.
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