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Optimal range: 6.8 - 101 mmol/mol creatinine
Oxalic acid may be associated with dysbiosis from Aspergillus, Penicillium, Candida, or high dose vitamin C. If yeast or fungal markers are elevated, antifungal therapy may reduces oxalates. Also associated with anti-freeze (ethylene glycol) poisoning.
Optimal range: 15 - 174 mmol/mol creatinine
Oxalic acid may be associated with dysbiosis from Aspergillus, Penicillium, Candida, or high dose vitamin C. If yeast or fungal markers are elevated, antifungal therapy may reduces oxalates. Also associated with anti-freeze (ethylene glycol) poisoning.
Optimal range: 8.9 - 67 mmol/mol creatinine
Oxalic acid may be associated with dysbiosis from Aspergillus, Penicillium, Candida, or high dose vitamin C. If yeast or fungal markers are elevated, antifungal therapy may reduces oxalates. Also associated with anti-freeze (ethylene glycol) poisoning.
Optimal range: 35 - 185 mmol/mol creatinine
Oxalic acid may be associated with dysbiosis from Aspergillus, Penicillium, Candida, or high dose vitamin C. If yeast or fungal markers are elevated, antifungal therapy may reduces oxalates. Also associated with anti-freeze (ethylene glycol) poisoning.
Optimal range: 144.9 - 1749.5 nmol/mg Creatinine
Oxalic acid may be associated with dysbiosis from Aspergillus, Penicillium, Candida, or high dose vitamin C. If yeast or fungal markers are elevated, antifungal therapy may reduces oxalates. Also associated with anti-freeze (ethylene glycol) poisoning.
Optimal range: 0 - 78 Units
Oxalic acid is the metabolic end-product of the glyoxylase pathway and is derived from the oxidation of glyoxylate. In the cell, the majority of glyoxylate is converted into glycine or glycolic acid. However, in some instances there may be greater oxidation of glyoxylate to oxalic acid. This leads to increased urinary excretion of oxalic acid. As 80% of kidney stones are calcium-oxalate stones, an increase in oxalic acid is strongly correlated to frequency of urolithiasis. As mentioned previously, there are inborn errors of metabolism that cause elevated oxalic acid such as primary hyperoxaluria.
Optimal range: 0 - 78 mmol/mol creatinine
Oxalic acid is the metabolic end-product of the glyoxylase pathway and is derived from the oxidation of glyoxylate.
In the cell, the majority of glyoxylate is converted into glycine or glycolic acid. However, in some instances there may be greater oxidation of glyoxylate to oxalic acid. This leads to increased urinary excretion of oxalic acid.
As 80% of kidney stones are calcium-oxalate stones, an increase in oxalic acid is strongly correlated to frequency of urolithiasis.
Optimal range: 0.01 - 0.07 Healthy Relative Abundance IQR (%)
Oxalobacter formigenes is a bacterium that colonizes the colon of a substantial proportion of the normal population and metabolizes dietary and endogenous oxalate and hence reducing the incidence of kidney stones.
Optimal range: 5 - 500 x10^6 CFU/g
Oxalobacter formigenes is a bacterium that colonizes the colon of a substantial proportion of the normal population and metabolizes dietary and endogenous oxalate and hence reducing the incidence of kidney stones.
Optimal range: 5 - 500 x10^6 CFU/g
Oxalobacter formigenes is a bacterium that colonizes the colon of a substantial proportion of the normal population and metabolizes dietary and endogenous oxalate and hence reducing the incidence of kidney stones.
Optimal range: 0 - 11000000 CFU/g stool
Oxalobacter formigenes is a bacterium that colonizes the colon of a substantial proportion of the normal population and metabolizes dietary and endogenous oxalate and hence reducing the incidence of kidney stones.
Optimal range: 10 - 170 ng/mL
Oxidized LDL is LDL cholesterol (the “bad” cholesterol) that has been modified by oxidation. Oxidized LDL triggers inflammation leading to the formation of plaque in the arteries, also known as atherosclerosis. Oxidized LDL may also play a role in increasing the amount of triglycerides the body produces, as well as increasing the amount of fat deposited by the body. In turn, fat tissue can enhance the oxidation of LDL, creating a vicious cycle.
Optimal range: 0 - 60 U/L
Oxidized LDL is LDL cholesterol (the “bad” cholesterol) that has been modified by oxidation. Oxidized LDL triggers inflammation leading to the formation of plaque in the arteries, also known as atherosclerosis. Oxidized LDL may also play a role in increasing the amount of triglycerides the body produces, as well as increasing the amount of fat deposited by the body. In turn, fat tissue can enhance the oxidation of LDL, creating a vicious cycle.
Optimal range: 0 - 2 nmol/L
Oxidized phospholipids are found on all apoB-containing lipoproteins, namely, LDL, VLDL, and especially Lp(a). When taken up by the artery wall, oxidized lipoproteins accelerate atherosclerosis, thereby, increasing the risk of myocardial infarctions, strokes, and calcific aortic valve stenosis. Oxidized phospholipids are highly pro-inflammatory and contribute to many diseases of aging.
Clinicians can use OxPL-apoB levels to reclassify patients into higher or lower risk categories allowing better personalized care.
Optimal: <2.0 nM/L
Borderline: 2.0-3.0 nM/L
Increased Risk: >3.0 nM/L
