The clinical relevance of low urinary glyceric acid has not been studied in the peer-reviewed literature. However, knowing that glyceric acid accumulation is the result of breakdown of both serine and fructose, it is possible that low glyceric acid may be caused by low amino acid status and/or low fructose intake.

Aside from these rare inborn errors of metabolism, elevated levels of glyceric acid have been demonstrated in a few metabolomic studies. One study demonstrated that glyceric acid was among 3 metabolites that correlated in patients with rheumatoid arthritis.

Furthermore, correlation between glyceric acid was amongst a small handful of metabolites that were able to effectively identify patients with schizophrenia and bipolar as compared to controls.

These profiles suggest that more subtle metabolic abnormalities may result in elevated urinary glyceric acid excretion. It is known that a deficiency in the enzyme glyoxylate reductase leads to excessive levels of glyceric acid resulting in primary hyperoxaluria type 2 and oxalosis.

This enzyme requires vitamin B3 in the form of NAD as a cofactor. Whether subclinical elevations in glyceric acid could be an indication of a functional need for vitamin B3 has not been studied in the literature. Interestingly, niacin has been shown to be effective in clinical trials with patients suffering from schizophrenia. Glycerate kinase requires magnesium as a cofactor to convert glyceric acid. Therefore, magnesium deficiency may play a role in glyceric acid levels.

Lastly, glyceric acid is formed during metabolism of fructose and serine (previously mentioned). The contribution of fructose intake to total urinary glyceric acid excretion has not been fully elucidated. A careful dietary recall should be considered with increased glyceric acid in the absence of suspected metabolic defects.