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Optimal range: 0 - 1.8 ELISA Index
ANTIBODIES ASSOCIATED WITH:
This test by itself is not diagnostic for any condition or disease
Autoimmune Endocrine Disorders
Autoimmune Polyendocrine Syndrome Type 1
Hypogonadism
Premature Menopause
Premature Ovarian Failure
BODY TISSUE:
Reproductive
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 - 2 mcmol/L
What is Oxalate?
Oxalate (or oxalic acid) is a naturally occurring substance found in many foods and also produced as a waste product in the body. It is not essential for human health and is typically excreted in the urine. In the bloodstream, oxalate levels are usually very low under normal circumstances.
The Oxalate, Serum/Plasma test measures the concentration of oxalate circulating in your blood. This test is primarily used to:
Evaluate primary or secondary hyperoxaluria (a condition of excessive oxalate production or absorption)
Assess risk for calcium oxalate kidney stones
Monitor kidney function in patients with known oxalate-related disorders
Help diagnose oxalate nephropathy, a rare but serious kidney condition
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: 0.013 - 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.
