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.

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.

What Does the Oxalate, Serum/Plasma Test Measure?

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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