Skip to main content

Longevity Library · Lab reference

Written by Daniel Tagge, MD
Updated October 23, 2026
Reviewed October 24, 2026
49 sources · Measured in mmol/mol creatinine

System: Metabolism & Metabolomics

Urine organic acidsOrganic acid test · Urinary organic acid profile · Organic acids panel

Urine organic acid analysis by gas chromatography-mass spectrometry is a validated, decades-old first-tier test for inherited disorders of metabolism, and a handful of its lines have clinical validation in adults: methylmalonic acid for B12 deficiency (above about 4.8 mmol/mol creatinine caught all 7 deficient patients and cleared 88 of 89 who were not, in one prospective study), 5-HIAA for carcinoid tumors (73 percent sensitivity, 100 percent specificity in 133 patients), VMA and HVA for neuroblastoma in children, orotic acid in urea cycle disorders and pyroglutamic acid in acetaminophen-related acidosis; the wellness readings of most other lines, yeast and bacterial markers, single vitamin-cofactor markers, oxidative-stress markers and neurotransmitter metabolites, rest on mechanism and small studies, most elevations have dietary, drug or collection explanations, and the panel as a whole has never been tested against a health outcome.

A urine organic acid panel measures dozens of small acids that cells make while burning fuel and breaking down protein, fat and sugar, plus acids made by gut bacteria and acids from food and medicine. It is the standard first test for inherited metabolic disease, and a few lines answer real adult questions, B12 deficiency above all. Most of the rest are clues rather than diagnoses: the published table of their sources lists diet, supplements, drugs and sample handling beside disease for almost every one.

01 · The scale

Where the laboratory range and the evidence sit.

The panel is a validated diagnostic tool for inherited metabolic disease, and a few lines carry adult validation: methylmalonic acid above about 4.8 mmol/mol creatinine (5 µg/mg) found all 7 B12-deficient patients and cleared 88 of 89 who were not; urinary 5-HIAA had 73 percent sensitivity and 100 percent specificity for carcinoid tumors in 133 patients; HVA and VMA are the established markers of neuroblastoma in children; orotic acid separates the urea cycle defects; and pyroglutamic acid explains a rare acetaminophen-related acidosis. The wellness readings of yeast, bacterial, cofactor, oxidative-stress and neurotransmitter lines rest on mechanism and small or single studies. No cohort has tested whether a urinary organic acid profile predicts any health outcome in adults.

051015

  1. Methylmalonic acid only (one analyte of many; the panel has no single scale): at or below about 4.8 mmol/mol creatinine, where 88 of 89 patients without clinical B12 deficiency fell in one prospective evaluation

    0 to 4.8 mmol/mol creatinine · Matchar 1987 (5 µg/mg, converted)

  2. Methylmalonic acid only: above about 4.8 mmol/mol creatinine, where all 7 clinically deficient patients fell; a reason to read serum B12, serum MMA and homocysteine, not a diagnosis by itself

    4.8 and above mmol/mol creatinine · Matchar 1987; Norman 1993

  • Evidence supports
  • Higher risk in studies
Scale in mmol/mol creatinine. Each analyte is reported per mol of creatinine to correct for how dilute the urine is. Most panels use a single random or first-morning sample; a timed 24-hour collection measures the real excretion rate and is what several tumor markers were validated on. Creatinine correction assumes everyone makes about the same amount of creatinine, which fails at the extremes of muscle mass, in children, and when kidney function is changing. The meals, supplements, medicines and fasting of the previous day or two, and how the sample was stored and shipped, all move the numbers. Older papers print µg/mg creatinine; the conversion depends on each analyte's molar mass. Bands show where studies found something, not a recommendation for any one person.

02 · What it is

What Urine organic acids measures.

Organic acids are the small carbon acids that sit in the middle of metabolism: the steps between food and energy, and between protein, fat and sugar and their waste. Urine contains several hundred of them, from normal and abnormal metabolism, from drugs and their breakdown, and from foreign chemicals and dietary supplements. The laboratory extracts the acidic fraction of a urine sample, chemically tags it, and separates and identifies the compounds by gas chromatography-mass spectrometry. A 2013 survey of the urine metabolome using five analytical platforms identified 445 compounds and quantified 378, and a literature review added another 2,206, describing urine as a waste fluid full of breakdown products of foods, drinks, drugs, environmental contaminants and bacteria, many poorly characterized.1,2Grade B

Its established use is diagnosis of inherited metabolic disease. The 2018 technical standard of the American College of Medical Genetics and Genomics calls organic acid analysis a crucial first-tier laboratory test for a broad spectrum of inborn errors of metabolism and the recommended follow-up for many positive newborn screens. More than 65 organic acidurias are described, each rare (from 1 in 10,000 to fewer than 1 in 1,000,000 births) and together about 1 in 3,000 births; each comes from a missing enzyme or transporter in the breakdown of amino acids, carbohydrates or fats, which makes a specific acid pile up and spill into the urine.3,4Grade A

The same chemistry is sold in a second way, as a broad wellness panel read for vitamin and cofactor needs, gut yeast and bacteria, detoxification, oxidative stress and brain chemistry. One review written from that perspective lists benzoate, hippurate, phenylacetate, phenylpropionate, cresol, the hydroxyphenyl acids, indican, tricarballylate, D-lactate and D-arabinitol as markers of microbial overgrowth and calls their elevation a useful diagnostic tool; its abstract cites no study that tested those readings against an outcome. The interpretation is where the two uses part: the measurement is the same, but what a high line means has been validated for some lines and not for others.5,6Grade C

03 · Origins

Where it came from, and where it sits in the network.

The acids on the panel are the small molecules of central metabolism, shared by every cell. Inherited defects in the breakdown of amino acids, carbohydrates and fats are what define the organic acidurias, and the panel's lines map onto those pathways: the citric acid (TCA) cycle, whose intermediates malate and fumarate correlated best with mitochondrial disease in one retrospective comparison of 67 patients; fatty acid oxidation, with at least 22 inherited defects of beta-oxidation described since the first two in 1973; and amino acid catabolism, where methylmalonic, propionic, isovaleric acidurias and maple syrup urine disease are called the classical organic acidurias.4,7,8Grade B

The field began with a single disease. In 1966 Tanaka and colleagues described isovaleric acidemia as a new genetic defect of leucine metabolism, and the list has grown past 65 disorders since. Gas chromatography-mass spectrometry became the working method: Hoffmann and colleagues' 1989 method isolated organic acids, aldehydes and ketones from urine, plasma and amniotic fluid without deproteinization and set retention indices and adult control ranges for 61 compounds. Liquid chromatography-mass spectrometry is now replacing it in some laboratories: one 2018 method with 71 biomarkers diagnosed all 32 inborn errors in 99 patient samples against 88 controls and outperformed the classical method on an external quality scheme.9,4,10,11Grade B

The metabolomics era widened the lens from a handful of disease acids to the whole profile. In 1999 Nicholson, Lindon and Holmes named 'metabonomics', the study of a living system's metabolic response to disease or injury by multivariate statistics applied to NMR spectra of body fluids. The largest application to urine is INTERMAP: two 24-hour urine samples from each of 4,630 people aged 40 to 59 in China, Japan, the UK and the US, read by NMR, separated East Asian from Western populations, and found formate and alanine (directly) and hippurate (inversely) associated with blood pressure. That study is cross-sectional and population-level; it shows the profile carries information about diet and gut bacteria, not that a person's panel predicts anything.12,13Grade C

Two parts of the network matter for reading the panel beside the blood. The one-carbon network shared with B12 and folate shows up as methylmalonic acid, which rises when B12 fails inside the cell, and formiminoglutamic acid (FIGLU), the histidine breakdown product that was read after a histidine load as a folate test in the 1960s. And some of the panel is not human metabolism at all: hippurate, the glycine conjugate of benzoic acid, comes from microbial breakdown of plant compounds in food, the liver's conjugation and exposure to toluene; in 1,529 women of the TwinsUK cohort it was the blood metabolite most strongly tied to gut microbiome diversity, and rose with fruit and whole-grain intake. When rats were given oral antibiotics for eight days, their urinary hippurate, phenylpropionic acid and indoxyl sulfate fell while citrate, 2-oxoglutarate and fumarate rose: the gut bacteria and the host's TCA cycle write on the same page.14,15,16,17,18Grade C

04 · The laboratory range

What a laboratory calls normal.

Each analyte has its own reference interval, set by the laboratory on its own method and population and printed in mmol/mol creatinine; intervals differ between laboratories, fall with age in children, and are not risk thresholds.

There is no single normal range, only a list. Hoffmann's 1989 method set adult control ranges for 61 compounds; a pediatric study quantified 69 organic acids (32 major, 37 minor) in healthy children aged 2 days to 16 years, found most fall with age with large differences between age groups, and found several tracked protein or calorie intake, so that a child's result means something only against age-matched data. A 2017 review of the classical organic acidurias published updated reference values for the acids most often involved, again laboratory by laboratory.10,19,4Grade B

The reference interval is a distribution of people without a known inborn error, not a map of health. Kumps and colleagues compiled the metabolic, nutritional, iatrogenic and artifactual sources of each urinary organic acid and glycine conjugate into one table because interpretation is hindered by ambiguity about where many of them come from; beside inherited disease, it lists physiological, dietary, drug-related and sample-handling causes and reviews the pre-analytical errors that lead to misinterpretation. A value outside the printed interval is a question about the last two days before it is a question about the person.6Grade A

The method changes the result. In an external quality comparison of 24 organic acids across 28 urine samples, a liquid chromatography method outperformed gas chromatography-mass spectrometry, and screening by tandem mass spectrometry finds different metabolites again. The ACMG standard exists because analysis, interpretation and reporting differ between laboratories; two panels from two laboratories are not directly comparable line by line.11,3Grade B

05 · The evidence

What the studies support.

For inherited metabolic disease, the panel is the standard of care. The ACMG technical standard makes it a first-tier test for a broad spectrum of inborn errors and the follow-up for positive newborn screens, and it is how the organic acidurias, collectively about 1 in 3,000 births, are diagnosed. It is not a complete metabolic screen: in the fatty acid oxidation defects, screening tests that detect other inborn errors are often normal, and a correct diagnosis is made only when those disorders are specifically considered and tested for.3,4,8Grade A

Methylmalonic acid is the best validated adult line on the panel. In a prospective evaluation drawn from 1,599 consecutive B12 tests, all 7 patients with clinical deficiency had a urinary methylmalonic acid above 5 µg/mg creatinine (about 4.8 mmol/mol; sensitivity 100 percent, confidence interval 65 to 100) and 88 of 89 without deficiency were at or below it (specificity 99 percent). Spot urine screening of 809 people over 65 found an elevated value in 3.0 to 5.1 percent depending on the setting; of 35 followed up, 18 had a low serum B12, 12 a low-normal one and 5 a normal one, all 7 low-normal cases assessed further had deficiency, and all 16 retested after B12 injections had normalized. The details of B12 and its serum test are on the Vitamin B12 page.20,21Grade B

Why MMA matters when the blood count is normal: among 141 consecutive patients with nerve or psychiatric problems caused by B12 deficiency, 40 (28 percent) had no anemia or enlarged red cells, and they showed markedly elevated serum methylmalonic acid and homocysteine; all who could be followed improved with B12. Everyday meals raise the urinary value without raising the serum one, and the author concluded that serum MMA separates early deficiency from normal more reliably in people who have not fasted.14,22Grade B

5-HIAA, the breakdown product of serotonin, is the established marker of serotonin-secreting carcinoid tumors. In 133 patients, urinary 5-HIAA had a sensitivity of 73 percent and a specificity of 100 percent, better than any neuropeptide tested; in 75 consecutive carcinoid patients, 75 percent had above-normal excretion. In 116 patients, a 24-hour urine 5-HIAA had an area under the curve of 88 percent and a serum assay 85 percent, and the authors now recommend serum for convenience. An international consensus panel concluded that no single-analyte marker of neuroendocrine tumors meets the bar for detecting minimal disease. The tumor validation was on timed collections in people with symptoms or known tumors, not on a random wellness sample.23,24,25,26Grade B

VMA and HVA, catecholamine metabolites, are the established urinary markers of neuroblastoma, a childhood tumor with a high fatality rate, though age-related reference ranges in children are hard to establish. For pheochromocytoma and paraganglioma in adults, the Endocrine Society guideline recommends plasma free or urinary fractionated metanephrines as the initial test, not VMA or HVA, and asks for attention to the pre-analytical factors that cause false results. On a wellness panel these same lines are often read as a measure of brain dopamine and norepinephrine; no source read for this entry validates that reading.27,28Grade A

Orotic acid is the line that sorts the urea cycle defects, which affect about 1 in 35,000 people. The European guideline asks for urinary organic acids and orotic acid urgently whenever high ammonia is confirmed; high ammonia with low citrulline and arginine is diagnostic of ornithine transcarbamylase deficiency when urinary orotic acid is raised, and strongly suggests carbamoyl phosphate synthetase 1 or N-acetylglutamate synthase deficiency when it is low. Raised orotic acid also supports the diagnosis of citrullinemia type 1 and of arginase 1 deficiency, and an allopurinol challenge that raises orotic acid is used to find female carriers.29,30Grade A

Pyroglutamic acid (5-oxoproline) has one firm adult meaning: a rare, under-recognized high anion gap acidosis linked to regular acetaminophen use. Of 22 adult cases reviewed in 2006, 21 had major acetaminophen exposure and 18 (82 percent) were women, most malnourished with several illnesses and some kidney dysfunction; acetaminophen levels were usually therapeutic or low, and the disorder generally resolves when the drug is stopped. It is attributed to depletion of glutathione and cysteine driving an energy-wasting cycle in glutathione turnover. That is a hospital diagnosis in a very sick person; a mildly raised value on a wellness panel in a well person is a different thing, and in healthy adults sampled weekly it cycled between roughly 15 and 40 µg/mg creatinine on its own.31,32,33Grade C

Lactate and pyruvate earn their place only when mitochondrial disease is a real question. The Mitochondrial Medicine Society includes urinary organic acids in the first evaluation alongside blood lactate, pyruvate, amino acids and acylcarnitines; it notes that a plasma lactate above 3 mmol/L in a properly collected sample suggests mitochondrial dysfunction that may be primary or secondary to many other causes, that urine lactate correlates less well with mitochondrial disease, and that the lactate-to-pyruvate ratio helps only when lactate is high. In 46 children with proven mitochondrial disease, the blood ratio at the recommended cut point of about 25 had a sensitivity of 77 percent and specificity of 91 percent for one subtype, and was no better than chance when lactate was below 2.5 mmol/L.7,34,35Grade A

The fat-burning lines show how often a real chemical signal carries no clinical weight. Ethylmalonic acid in urine is one of the defining markers of short-chain acyl-CoA dehydrogenase deficiency, yet in 31 Dutch patients the condition was far more common than assumed (at least 1 in 50,000 births), its symptoms nonspecific and often transient, the genotype tracked the acid level but not the symptoms, and 7 of 8 affected relatives had none. Dicarboxylic acids rise with fasting, with defects of fatty acid oxidation and with medium-chain triglyceride feeding, and telling them apart takes ratios of specific acids rather than a single raised line.36,37Grade C

The vitamin-cofactor readings are mostly borrowed from loading tests the panel does not perform. The classic vitamin B6 test measured urinary xanthurenic acid in a 24-hour collection after a 2 g tryptophan load, with under 65 µmol suggested as adequate; it is sensitive to deficiency but laborious, and is affected by factors independent of B6 such as estrogen and oral contraceptive use. The review's conclusion is that B6 status is best judged by a combination of markers, of which plasma pyridoxal phosphate is the most used. FIGLU as a folate test was likewise read after a 15 g histidine load, and its authors stressed that urocanic acid had to be measured beside it. A random urine without the load is not the validated test.38,15Grade C

The oxidative-stress line, 8-hydroxy-2'-deoxyguanosine (8-OHdG), is a real marker of DNA oxidation with a measurement problem. It is one of the predominant oxidative lesions in DNA and is widely used in research on cancer risk, smoking and toxic exposures; a European standards committee was set up in 1997 because sample handling itself oxidizes DNA. In an interlaboratory comparison of 20 methods in 17 laboratories, chromatographic methods agreed with each other while immunoassays (ELISA) varied more and read higher; a later study concluded that ELISA cannot determine absolute 8-OHdG levels. Research cohorts use it to compare groups; a single person's value against a commercial reference interval has no outcome study behind it.39,40,41Grade C

The microbial lines are the weakest. D-arabinitol, made by most disease-causing Candida species, is a genuine marker of invasive candidiasis in immunocompromised, usually neutropenic, hospital patients: in a population-based study of 83 people with Candida in the bloodstream, 76 percent had a raised serum D-arabinitol to creatinine ratio, as did 11 percent of 100 hospital controls without infection. Nothing in that literature tests it as a sign of yeast overgrowth in the gut of healthy adults. The claim that a Clostridia metabolite, HPHPA, causes autism-like symptoms rests on a single-author report of children with autism and one adult with acute psychosis whose symptoms remitted with an oral antibiotic, and a 1995 report of tartaric acid, arabinose and related compounds rests on two brothers; no independent replication turned up for this entry.42,43,44,45Grade D

Tryptophan breakdown through the kynurenine pathway is regulated by diet and by inflammation, and peripheral inflammation can drive kynurenine into the brain, where it has been associated with depression and schizophrenia, while exercised muscle clears it. That is a serious research field. It does not yet translate into a validated reading of a single urinary kynurenine-pathway acid in a well adult, and kynurenic and xanthurenic acid excretion also depend on vitamin B6.46,38Grade C

The panel as a whole has no outcome validation. The largest urinary profiling studies are cross-sectional population work, such as INTERMAP's association of hippurate, formate and alanine with blood pressure, and the human urine metabolome project describes a fluid dominated by food, drug, environmental and bacterial products. No prospective cohort read for this entry ties a urinary organic acid profile to mortality, heart disease, diabetes or any other outcome in adults, and no trial has shown that treating the lines of a wellness panel changes health.13,2,6Grade C

06 · What moves it

The levers with evidence behind them.

What is listed here has been tested. The size of each effect, and the size of the study, are in the sentence, so a small effect reads as a small effect.

  • Food in the day or two before the sample

    raises or lowers many lines without any change in metabolism

    Ordinary meals raised urinary methylmalonic acid in healthy people while serum stayed flat; four bananas, a serotonin-rich food, raised urinary 5-HIAA in seven healthy subjects; medium-chain triglyceride oils produce a dicarboxylic acid pattern that mimics a fat-oxidation defect; and in children several organic acids tracked protein or calorie intake. Hippurate rises with fruit, whole grains and other plant compounds. The Kumps table lists dietary sources beside almost every acid.22,24,37,19,17,6Grade B

  • Supplements and medicines

    add their own acids and change others

    Drugs, their metabolites, foreign chemicals and dietary supplements all appear in urine as organic acids, and the Kumps table lists iatrogenic sources for many lines. Regular acetaminophen can raise pyroglutamic acid, and oral contraceptives and other estrogen raise urinary xanthurenic acid and other kynurenines after a tryptophan load independently of vitamin B6. A B12 injection normalized urinary MMA in every deficient older adult retested. Supplements and medicines from the week before the sample belong on the requisition.1,6,31,38,21Grade B

  • Antibiotics

    lower the bacterial lines and can shift the TCA-cycle lines

    In rats given penicillin and streptomycin for eight days, gut bacterial counts fell more than a hundredfold and urinary hippurate, phenylpropionic acid, phenylacetylglycine and indoxyl sulfate fell with them, while taurine, citrate, 2-oxoglutarate and fumarate rose; recolonization was uneven and cage-dependent. The human data are thinner, but a panel drawn during or soon after a course of antibiotics is reading the antibiotic.18Grade C

  • Fasting

    raises ketones and dicarboxylic acids; lowers some protein-derived lines

    Fasting is one of the three recognized causes of dicarboxylic aciduria, beside fat-oxidation defects and medium-chain triglyceride feeding. Going without protein for more than 15 hours lowered urinary methylmalonic acid excretion in healthy people. An overnight or longer fast before the sample changes the profile in ways that read as signals.37,22Grade C

  • Hard exercise

    raises lactate, pyruvate and TCA-cycle lines for hours

    In 12 men who ran repeated 80 m sprints, post-exercise urine separated clearly from pre-exercise urine, driven by lactate, pyruvate, hypoxanthine, citric acid cycle compounds, amino acids and branched-chain amino acid breakdown products, and shorter rests between sprints raised them further. A hard session the day before is a plausible explanation for raised lactate or TCA-cycle lines.47Grade C

  • How the sample is collected

    moves every creatinine-corrected line

    Urinary creatinine in 22,245 NHANES III participants varied with age, sex, race and ethnicity, body mass index and fat-free mass, and slightly with time of day, so creatinine-corrected values should be compared with people of similar build and age. Creatinine excretion also changes when kidney function changes, and the most accurate quantity is a timed collection. For 8-OHdG, spot samples tracked 24-hour excretion reasonably well, and creatinine-adjusted first-morning urine is recommended when a 24-hour sample is not feasible.48,49,41Grade B

07 · Reading it well

Caveats, and what belongs with a physician.

Most elevations have mundane explanations. The comprehensive table of sources lists diet, medicines, supplements, physiological states and sample handling beside inherited disease for almost every acid, and the reviewers note that pre-analytical errors lead to misinterpretation. A single raised line deserves a check of food, drugs and collection before it deserves a supplement.6,1Grade A

Creatinine correction is a convenience with known failures. It assumes steady creatinine output, which varies with muscle mass, age, sex and body composition, and with changing kidney function; a very muscular person's values read low and a frail or small person's read high. A timed collection is more accurate when the number matters.48,49Grade B

Lines move from week to week in healthy people. In adults sampled weekly for a month or more, pyroglutamic acid rose and fell in roughly month-long cycles between about 15 and 40 µg/mg creatinine, most clearly in 8 of 13 menstruating women; the day-to-day variation of creatinine-corrected 8-OHdG was about 20 percent. One sample is one day.33,41Grade C

Method and laboratory matter. Mass spectrometry methods differ from each other in which analytes they catch and how well, immunoassays for 8-OHdG read higher and vary more than chromatography, and reference intervals are set on each laboratory's own method and population, by age in children. Comparing two panels from two laboratories line by line is not reliable.11,40,19Grade B

Several lines were validated on a different test. Xanthurenic acid for B6 and FIGLU for folate were validated after a tryptophan or histidine load, 5-HIAA and the tumor markers on timed collections in people with symptoms, and serum MMA is more reliable than urine in someone who has eaten. A random wellness sample borrows those meanings without the conditions that produced them.38,15,25,22Grade B

A normal panel does not rule out a metabolic disease. Fat-oxidation defects can leave the screening tests normal under many circumstances, and the urea cycle and mitochondrial disorders need plasma amino acids, acylcarnitines, ammonia, lactate and other tests beside the urine. Nothing on this page applies to a newborn, a child being evaluated for an inherited disorder, or a person acutely ill; those panels belong with a metabolic specialist.8,29,7Grade A

See a physician

  • Anyone, child or adult, with episodes of vomiting, unusual sleepiness, confusion or unsteadiness after fasting, an illness or a high-protein meal, which is the pattern of a urea cycle disorder or an organic aciduria and calls for an ammonia level and urgent metabolic testing, not a wellness panel.
  • A raised methylmalonic acid, especially with numbness or tingling in the hands or feet, balance trouble, memory change, a sore tongue, or a low or low-normal serum B12, which needs serum B12, serum MMA and homocysteine and a physician who can treat deficiency; the Vitamin B12 page has the details.
  • Flushing, diarrhea or wheezing, or episodes of pounding headache, sweating and palpitations with high blood pressure, which call for the guideline tests (serum or 24-hour urine 5-HIAA, or plasma or urine metanephrines) rather than a random organic acid sample.
  • Feeling very unwell, breathing fast or being told of an acid build-up in the blood while taking acetaminophen regularly, especially with poor eating or kidney disease, which can be pyroglutamic acidosis and needs emergency care.
  • Muscle weakness, exercise intolerance, dark urine after exertion, or low blood sugar on fasting, which suggest a disorder of fat oxidation or of the mitochondria and need a specialist evaluation with blood tests the urine panel does not replace.
  • A panel read as showing yeast, bacterial overgrowth or a toxin, before starting an antifungal, an antibiotic, a binder or a restrictive diet: the gut symptoms belong with a physician who can examine you, and the urinary markers are not a diagnosis.
  • A parent told that a child's autism or behavior comes from a gut bacterial metabolite on a urine test, before any antibiotic or antifungal is given: the evidence for that reading is a single uncontrolled report.

This page is education, not individual medical advice, and reading it creates no physician-patient relationship.

08 · Open questions

What the literature does not settle.

  • No prospective cohort has tested whether a urinary organic acid profile, read as a whole, predicts mortality, cardiovascular disease, diabetes or any other outcome in adults; whatever the panel adds to the blood markers is untested.
  • Whether the wellness readings of single cofactor lines (for B vitamins, carnitine, biotin, coenzyme Q10 or glutathione) agree with the direct blood measures of the same nutrients has not been tested head to head in healthy adults, and no trial has shown that supplementing to normalize a line changes how a person feels or fares.
  • Whether any urinary microbial marker, alone or as a pattern, can identify a clinically meaningful gut problem in a healthy adult is unknown; the validated microbial line, D-arabinitol, was studied in immunocompromised patients with invasive infection.
  • How much of a well person's panel is diet, collection and the previous day's activity rather than metabolism has never been quantified for most lines; formal biological variation studies, with repeat sampling under controlled diets, are missing for most analytes.
  • Whether neurotransmitter metabolites in urine (HVA, VMA, 5-HIAA, quinolinic and kynurenic acids) say anything about brain chemistry in a person without a tumor is unproven; most of these molecules are made and cleared in the body as well as the brain.
  • Liquid chromatography and untargeted metabolomics now measure hundreds of urinary compounds; which of them, if any, will earn validated adult meanings, and whether a pattern of many will do better than any single line, is an active and unsettled question.

09 · In practice

How Dr. Tagge reads it in his own practice.

I order a urine organic acid panel as a map of the network, not as a list of deficiencies to fill. One marker is a clue; three that point the same way are a story. The lines I trust are the few with real validation: methylmalonic acid, which I read beside the serum B12 and homocysteine; FIGLU, which I read with folate and homocysteine rather than alone; lactate and pyruvate when mitochondrial disease is a real question and not a label; and the tumor markers when symptoms point there, in which case I order the guideline test rather than rely on a random sample. The lines I read as questions are the yeast and bacterial markers, the single cofactor markers and the oxidative-stress markers. When one line is off, I go through food, drink, supplements, medicines, exercise and how the sample was collected before I reach for a supplement, because the published table of sources lists an ordinary explanation for almost every acid on the panel, and I repeat it if the answer matters. I read the panel beside the blood, B12, folate, homocysteine, ferritin, fasting insulin and magnesium, and beside the person in front of me; if the urine and the blood disagree, the blood usually wins. I will say plainly where I am ahead of the evidence: I think the pattern across the panel tells me something about how a person's metabolism is running and how their gut and their diet are talking to it, and I use it to choose which questions to ask next, but no study has shown that reading a panel this way improves anyone's health, and I do not treat a line that has no symptom or blood finding behind it.

A practice judgment, labeled as one (Grade D): it is how one physician reads the number for the people he cares for, not a recommendation for you.

10

Questions

11 · Sources

49 sources, read in full.

Numbered in the order they appear. Each line says what this page relies on from the paper; the link opens the record at PubMed or the publisher.

  1. 1.

    Jones PM, Bennett MJ. Urine organic acid analysis for inherited metabolic disease using gas chromatography-mass spectrometry. Methods in Molecular Biology. 2010. PMID 20077094. DOI 10.1007/978-1-60761-459-3_41.

    Laboratory method study · Urine organic acid analysis is an essential part of the workup for suspected inborn errors; urine contains several hundred organic acids from normal and abnormal metabolism, drugs and drug metabolism, xenobiotics and dietary supplements; the method extracts, derivatizes and identifies them by GC-MS.

  2. 2.

    Bouatra S, Aziat F, Mandal R, et al.. The human urine metabolome. PLoS One. 2013. PMID 24023812. DOI 10.1371/journal.pone.0073076.

    Laboratory method study · Multi-platform analysis (NMR, GC-MS, LC-MS/MS, ICP-MS, HPLC) identified 445 and quantified 378 urine metabolites (179 identified by GC-MS); literature review added 2,206 more, for 2,651 confirmed urine metabolite species; urine contains breakdown products of foods, drinks, drugs, environmental contaminants, endogenous waste and bacterial by-products.

  3. 3.

    Gallagher RC, Pollard L, Scott AI, Huguenin S, Goodman S, Sun Q; ACMG Biochemical Genetics Subcommittee of the Laboratory Quality Assurance Committee. Laboratory analysis of organic acids, 2018 update: a technical standard of the American College of Medical Genetics and Genomics (ACMG). Genetics in Medicine. 2018. PMID 29543224. DOI 10.1038/gim.2018.45.

    Guideline · Organic acid analysis, typically by GC-MS, is a crucial first-tier laboratory test for a broad spectrum of inborn errors of metabolism and recommended follow-up for positive newborn screens; the standard guides laboratory analysis, interpretation and reporting.

  4. 4.

    Villani GR, Gallo G, Scolamiero E, Salvatore F, Ruoppolo M. Classical organic acidurias: diagnosis and pathogenesis. Clinical and Experimental Medicine. 2017. PMID 27613073. DOI 10.1007/s10238-016-0435-0.

    Review · Organic acidurias are inherited enzyme or transporter defects in the catabolism of amino acids, carbohydrates or lipids; more than 65 are described, individually 1 in 10,000 to fewer than 1 in 1,000,000 births and collectively about 1 in 3,000; methylmalonic, propionic, isovaleric aciduria and maple syrup urine disease are the classical ones; updated GC-MS reference values given.

  5. 5.

    Lord RS, Bralley JA. Clinical applications of urinary organic acids. Part 2. Dysbiosis markers. Alternative Medicine Review. 2008. PMID 19152477.

    Review · Presents benzoate, hippurate, phenylacetate, phenylpropionate, cresol, hydroxyphenyl acids, indican, tricarballylate, D-lactate and D-arabinitol as urinary markers of intestinal microbial overgrowth and calls their elevation a useful diagnostic tool; no outcome validation is cited in the abstract.

  6. 6.

    Kumps A, Duez P, Mardens Y. Metabolic, nutritional, iatrogenic, and artifactual sources of urinary organic acids: a comprehensive table. Clinical Chemistry. 2002. PMID 11978597.

    Review · A comprehensive table of urinary organic acids and glycine conjugates listing, beside inborn errors, other pathologic causes and physiological, nutritional, iatrogenic and artifactual sources, compiled because ambiguity about sources hinders interpretation; pre-analytical issues and possible misinterpretations are reviewed.

  7. 7.

    Parikh S, Goldstein A, Koenig MK, et al.. Diagnosis and management of mitochondrial disease: a consensus statement from the Mitochondrial Medicine Society. Genetics in Medicine. 2015. PMID 25503498. DOI 10.1038/gim.2014.177.

    Consensus statement · Initial evaluation should include blood lactate, pyruvate, amino acids and acylcarnitines with urinary organic acids; plasma lactate above 3 mmol/L in a properly collected sample suggests mitochondrial dysfunction, primary or secondary; urine lactate correlates less well; the lactate/pyruvate ratio is of value only when lactate is elevated; malate and fumarate best correlated with mitochondrial disease in 67 patients versus 21 with organic acidemias.

  8. 8.

    Vockley J, Whiteman DA. Defects of mitochondrial beta-oxidation: a growing group of disorders. Neuromuscular Disorders. 2002. PMID 11801395. DOI 10.1016/s0960-8966(01)00308-x.

    Review · At least 22 inborn errors of beta-oxidation have been identified since the first two in 1973; recurrent rhabdomyolysis and hypoglycemia are frequent; screening tests that detect other inborn errors are often normal in these patients, so the disorders must be specifically considered and tested for.

  9. 9.

    Tanaka K, Budd MA, Efron ML, Isselbacher KJ. Isovaleric acidemia: a new genetic defect of leucine metabolism. Proceedings of the National Academy of Sciences of the United States of America. 1966. PMID 5229850. DOI 10.1073/pnas.56.1.236.

    Laboratory method study · Described isovaleric acidemia as a new genetic defect of leucine metabolism (cited for the historical fact only; the 1966 paper has no PubMed abstract).

  10. 10.

    Hoffmann G, Aramaki S, Blum-Hoffmann E, Nyhan WL, Sweetman L. Quantitative analysis for organic acids in biological samples: batch isolation followed by gas chromatographic-mass spectrometric analysis. Clinical Chemistry. 1989. PMID 2702744.

    Laboratory method study · A GC-MS method for organic acids, aldehydes and ketones in urine, plasma and amniotic fluid without deproteinization; retention indices, discriminating ions and adult control ranges were determined for 61 biologically important compounds.

  11. 11.

    Körver-Keularts IMLW, Wang P, Waterval HWAH, et al.. Fast and accurate quantitative organic acid analysis with LC-QTOF/MS facilitates screening of patients for inborn errors of metabolism. Journal of Inherited Metabolic Disease. 2018. PMID 29435781. DOI 10.1007/s10545-017-0129-0.

    Laboratory method study · An LC-QTOF/MS panel of 71 biomarkers diagnosed all 32 inborn errors in 99 patient urines against 88 controls, and on cross-validation of 24 organic acids in 28 external-quality-scheme urines outperformed the GC-MS method.

  12. 12.

    Nicholson JK, Lindon JC, Holmes E. 'Metabonomics': understanding the metabolic responses of living systems to pathophysiological stimuli via multivariate statistical analysis of biological NMR spectroscopic data. Xenobiotica. 1999. PMID 10598751. DOI 10.1080/004982599238047.

    Review · Introduced 'metabonomics', the study of the metabolic response of living systems to pathophysiological stimuli by multivariate statistical analysis of NMR spectra of biological samples (cited from title; no PubMed abstract).

  13. 13.

    Holmes E, Loo RL, Stamler J, et al.. Human metabolic phenotype diversity and its association with diet and blood pressure. Nature. 2008. PMID 18425110. DOI 10.1038/nature06882.

    Cross-sectional study · NMR spectra of two 24-hour urines from each of 4,630 INTERMAP participants aged 40 to 59 in China, Japan, the UK and the US separated East Asian from Western populations; urinary formate and alanine (direct) and hippurate (inverse) were associated with individual blood pressure.

  14. 14.

    Lindenbaum J, Healton EB, Savage DG, et al.. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. New England Journal of Medicine. 1988. PMID 3374544. DOI 10.1056/NEJM198806303182604.

    Prospective cohort · Of 141 consecutive patients with neuropsychiatric abnormalities from cobalamin deficiency, 40 (28 percent) had no anemia or macrocytosis and showed markedly elevated serum methylmalonic acid and total homocysteine; all treated patients followed improved.

  15. 15.

    Mohamed SD, Roberts M. Relative importance of formiminoglutamic and urocanic acid excretion after a histidine load. Journal of Clinical Pathology. 1966. PMID 5904980. DOI 10.1136/jcp.19.1.37.

    Laboratory method study · After a 15 g histidine load in 15 controls and 49 patients, upper limits of FIGLU and urocanic acid excretion were set per 8 hours; urocanic acid detected abnormal tests that FIGLU missed, and both metabolites should be measured in tests for folate deficiency.

  16. 16.

    Lees HJ, Swann JR, Wilson ID, Nicholson JK, Holmes E. Hippurate: the natural history of a mammalian-microbial cometabolite. Journal of Proteome Research. 2013. PMID 23342949. DOI 10.1021/pr300900b.

    Review · Hippurate, the glycine conjugate of benzoic acid, is a normal urinary metabolite long associated with microbial degradation of dietary components, hepatic function and toluene exposure, and varies with sex, age and the gut microbiota.

  17. 17.

    Pallister T, Jackson MA, Martin TC, et al.. Hippurate as a metabolomic marker of gut microbiome diversity: Modulation by diet and relationship to metabolic syndrome. Scientific Reports. 2017. PMID 29057986. DOI 10.1038/s41598-017-13722-4.

    Prospective cohort · Among 292 blood metabolites in 1,529 TwinsUK women, hippurate was the top marker of gut microbiome diversity (replicated in 420 others); higher fruit and whole-grain intake went with higher hippurate, and a rising hippurate trend with lower odds of metabolic syndrome (OR 0.795). Blood, not urine.

  18. 18.

    Swann JR, Tuohy KM, Lindfors P, et al.. Variation in antibiotic-induced microbial recolonization impacts on the host metabolic phenotypes of rats. Journal of Proteome Research. 2011. PMID 21591676. DOI 10.1021/pr200243t.

    Laboratory method study · In rats given oral penicillin and streptomycin for 8 days (n = 6 per group), all bacterial groups fell and urinary hippurate, phenylpropionic acid, phenylacetylglycine and indoxyl sulfate decreased, while taurine, glycine, citrate, 2-oxoglutarate and fumarate rose; recolonization was cage-dependent.

  19. 19.

    Guneral F, Bachmann C. Age-related reference values for urinary organic acids in a healthy Turkish pediatric population. Clinical Chemistry. 1994. PMID 8087979.

    Laboratory method study · In healthy children aged 2 days to 16 years, 69 organic acids (32 major, 37 minor) were quantified per creatinine; most fell with age with substantial differences between age groups, and several correlated with protein or caloric intake.

  20. 20.

    Matchar DB, Feussner JR, Millington DS, Wilkinson RH Jr, Watson DJ, Gale D. Isotope-dilution assay for urinary methylmalonic acid in the diagnosis of vitamin B12 deficiency. A prospective clinical evaluation. Annals of Internal Medicine. 1987. PMID 3551712. DOI 10.7326/0003-4819-106-5-707.

    Prospective cohort · From 1,599 consecutive B12 assays, 96 evaluable patients were studied prospectively; all 7 with clinical deficiency had urinary MMA above 5 µg/mg creatinine (sensitivity 100 percent, 65 to 100) and 88 of 89 without deficiency were at or below it (specificity 99 percent).

  21. 21.

    Norman EJ, Morrison JA. Screening elderly populations for cobalamin (vitamin B12) deficiency using the urinary methylmalonic acid assay by gas chromatography mass spectrometry. American Journal of Medicine. 1993. PMID 8506883. DOI 10.1016/0002-9343(93)90209-8.

    Prospective cohort · In 809 people over 65 screened by spot urine, elevated MMA was found in 3.0 to 5.1 percent by setting; of 35 followed up, 18 had low, 12 low-normal and 5 normal serum B12; all 7 low-normal cases assessed further had deficiency; all 16 retested after intramuscular B12 had normal urinary MMA.

  22. 22.

    Rasmussen K. Studies on methylmalonic acid in humans. I. Concentrations in serum and urinary excretion in normal subjects after feeding and during fasting, and after loading with protein, fat, sugar, isoleucine, and valine. Clinical Chemistry. 1989. PMID 2591042.

    Laboratory method study · Everyday meals increased urinary MMA excretion without significantly raising serum MMA; urinary excretion declined after more than 15 hours without protein; serum measurement best separates early cobalamin deficiency from normal in nonfasting patients.

  23. 23.

    Feldman JM, O'Dorisio TM. Role of neuropeptides and serotonin in the diagnosis of carcinoid tumors. American Journal of Medicine. 1986. PMID 2432780. DOI 10.1016/0002-9343(86)90583-8.

    Prospective cohort · In 133 patients grouped by carcinoid status, urinary 5-HIAA excretion had a sensitivity of 73 percent and a specificity of 100 percent for carcinoid tumors, outperforming plasma substance P and neurotensin.

  24. 24.

    Feldman JM. Urinary serotonin in the diagnosis of carcinoid tumors. Clinical Chemistry. 1986. PMID 2421946.

    Prospective cohort · In 75 consecutive carcinoid patients, 75 percent had above-normal urinary 5-HIAA; ingestion of four bananas raised urinary 5-HIAA (but not urinary serotonin) in seven normal subjects.

  25. 25.

    Becker A, Schalin-Jäntti C, Itkonen O. Comparison of Serum and Urinary 5-Hydroxyindoleacetic Acid as Biomarker for Neuroendocrine Neoplasms. Journal of the Endocrine Society. 2021. PMID 34195530. DOI 10.1210/jendso/bvab106.

    Prospective cohort · In 116 patients, serum 5-HIAA by LC-MS/MS had an area under the curve of 85 percent and 24-hour urine 5-HIAA 88 percent for neuroendocrine neoplasms; both separated active disease from remission, and serum is recommended for its more reliable, convenient sampling.

  26. 26.

    Oberg K, Modlin IM, De Herder W, et al.. Consensus on biomarkers for neuroendocrine tumour disease. Lancet Oncology. 2015. PMID 26370353. DOI 10.1016/S1470-2045(15)00186-2.

    Consensus statement · A Delphi consensus panel concluded that monoanalyte biomarkers of neuroendocrine tumors have poor sensitivity, specificity and predictive ability and that none has fulfilled the criteria for minimal disease detection; the meeting was funded by a company selling a multianalyte test.

  27. 27.

    Kavalakatt S, Ivica J. Homovanillic acid and vanillylmandelic acid as neuroblastoma biomarkers in children. Biochemia Medica. 2026. PMID 42299350. DOI 10.11613/BM.2026.020505.

    Review · Neuroblastoma, the most common pediatric tumor with the highest fatality rate, is characterized by elevated catecholamines and their metabolites, particularly HVA and VMA; urinary methods support early diagnosis, but age-related reference ranges in children are difficult to establish.

  28. 28.

    Lenders JW, Duh QY, Eisenhofer G, et al.; Endocrine Society. Pheochromocytoma and paraganglioma: an endocrine society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism. 2014. PMID 24893135. DOI 10.1210/jc.2014-1498.

    Guideline · Initial biochemical testing for pheochromocytoma and paraganglioma should include plasma free or urinary fractionated metanephrines, with attention to pre-analytical factors that cause false-positive or false-negative results; all positive results require follow-up.

  29. 29.

    Häberle J, Boddaert N, Burlina A, et al.. Suggested guidelines for the diagnosis and management of urea cycle disorders. Orphanet Journal of Rare Diseases. 2012. PMID 22642880. DOI 10.1186/1750-1172-7-32.

    Guideline · If hyperammonemia is confirmed, plasma amino acids, acylcarnitines, urinary organic acids and orotic acid should be requested urgently; hyperammonemia with low citrulline and arginine is diagnostic of OTC deficiency with raised urinary orotic acid and suggests CPS1 or NAGS deficiency when it is low; the allopurinol test identifies female carriers (full text).

  30. 30.

    Häberle J, Burlina A, Chakrapani A, et al.. Suggested guidelines for the diagnosis and management of urea cycle disorders: First revision. Journal of Inherited Metabolic Disease. 2019. PMID 30982989. DOI 10.1002/jimd.12100.

    Guideline · Urea cycle disorders, with an estimated incidence of 1 in 35,000, cause hyperammonemia of neonatal (about 50 percent) or late onset that can lead to intellectual disability or death; under-recognition and delayed diagnosis remain widespread; the revision uses GRADE methodology.

  31. 31.

    Fenves AZ, Kirkpatrick HM 3rd, Patel VV, Sweetman L, Emmett M. Increased anion gap metabolic acidosis as a result of 5-oxoproline (pyroglutamic acid): a role for acetaminophen. Clinical Journal of the American Society of Nephrology. 2006. PMID 17699243. DOI 10.2215/CJN.01411005.

    Review · Four new and 18 previously reported adults with 5-oxoproline acidosis: 21 had major acetaminophen exposure, 18 (82 percent) were women, most were malnourished with multiple comorbidities and some kidney dysfunction; the condition is underdiagnosed because 5-oxoproline assays are not readily available.

  32. 32.

    Emmett M. Acetaminophen toxicity and 5-oxoproline (pyroglutamic acid): a tale of two cycles, one an ATP-depleting futile cycle and the other a useful cycle. Clinical Journal of the American Society of Nephrology. 2014. PMID 24235282. DOI 10.2215/CJN.07730713.

    Review · Acquired 5-oxoproline acidosis was first described in 1989 and linked to chronic acetaminophen the next year; most cases are malnourished, chronically ill women with therapeutic or low acetaminophen levels; it resolves with stopping the drug, and an ATP-depleting futile cycle activated by glutathione and cysteine depletion explains it.

  33. 33.

    Lord RS. Long-term patterns of urinary pyroglutamic acid in healthy humans. Physiological Reports. 2016. PMID 26908712. DOI 10.14814/phy2.12706.

    Prospective cohort · In healthy adults sampled weekly, urinary pyroglutamic acid showed roughly 4-week cycles between about 15 and 40 µg/mg creatinine, most prominently in 8 of 13 menstruating women and also in 3 of 8 men.

  34. 34.

    Mitochondrial Medicine Society's Committee on Diagnosis; Haas RH, Parikh S, Falk MJ, et al.. The in-depth evaluation of suspected mitochondrial disease. Molecular Genetics and Metabolism. 2008. PMID 18243024. DOI 10.1016/j.ymgme.2007.11.018.

    Consensus statement · Confirming mitochondrial disease requires extensive clinical and laboratory evaluation; compiling blood and tissue analytes, neuroimaging, provocative testing, enzyme assays and DNA analysis can often establish an etiology.

  35. 35.

    Debray FG, Mitchell GA, Allard P, Robinson BH, Hanley JA, Lambert M. Diagnostic accuracy of blood lactate-to-pyruvate molar ratio in the differential diagnosis of congenital lactic acidosis. Clinical Chemistry. 2007. PMID 17384007. DOI 10.1373/clinchem.2006.081166.

    Prospective cohort · In 11 children with pyruvate dehydrogenase deficiency and 35 with other mitochondrial disease, the blood lactate:pyruvate ratio at the recommended cut point of about 25 had 77 percent sensitivity and 91 percent specificity, and no better than chance discrimination when lactate was below 2.5 mmol/L.

  36. 36.

    van Maldegem BT, Duran M, Wanders RJ, et al.. Clinical, biochemical, and genetic heterogeneity in short-chain acyl-coenzyme A dehydrogenase deficiency. JAMA. 2006. PMID 16926354. DOI 10.1001/jama.296.8.943.

    Prospective cohort · In 31 Dutch patients defined by raised butyrylcarnitine or urinary ethylmalonic acid with ACADS variants, birth prevalence was at least 1 in 50,000, symptoms were nonspecific and often transient, genotype tracked ethylmalonic acid but not clinical features, and 7 of 8 affected relatives were symptom-free.

  37. 37.

    Tserng KY, Griffin RL, Kerr DS. Distinction of dicarboxylic aciduria due to medium-chain triglyceride feeding from that due to abnormal fatty acid oxidation and fasting in children. Metabolism. 1996. PMID 8596483. DOI 10.1016/s0026-0495(96)90047-5.

    Laboratory method study · Dicarboxylic aciduria occurs with medium-chain triglyceride feeding, abnormal fatty acid oxidation and fasting; relative amounts of saturated dicarboxylic acids do not distinguish them, but specific ratios (unsaturated to saturated below 0.1, among others) identify the MCT pattern.

  38. 38.

    Ueland PM, Ulvik A, Rios-Avila L, Midttun Ø, Gregory JF. Direct and Functional Biomarkers of Vitamin B6 Status. Annual Review of Nutrition. 2015. PMID 25974692. DOI 10.1146/annurev-nutr-071714-034330.

    Review · B6 status is best assessed by a combination of biomarkers, plasma PLP most used; the tryptophan load test (urinary xanthurenic acid under 65 µmol per 24 hours after 2 g suggested adequate) is sensitive but invasive and laborious and is affected by factors independent of B6, including estrogen and oral contraceptives; kynurenic and xanthurenic acid are end-stage metabolites with high renal clearance (full text).

  39. 39.

    Valavanidis A, Vlachogianni T, Fiotakis C. 8-hydroxy-2' -deoxyguanosine (8-OHdG): A critical biomarker of oxidative stress and carcinogenesis. Journal of Environmental Science and Health, Part C. 2009. PMID 19412858. DOI 10.1080/10590500902885684.

    Review · 8-OHdG is one of the predominant free-radical lesions of nuclear and mitochondrial DNA and widely used as a biomarker of oxidative stress and carcinogenesis; the European Standards Committee for Oxidative DNA Damage was set up in 1997 to resolve artifactual oxidation during sample processing.

  40. 40.

    European Standards Committee on Urinary (DNA) Lesion Analysis; Evans MD, Olinski R, Loft S, Cooke MS. Toward consensus in the analysis of urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine as a noninvasive biomarker of oxidative stress. FASEB Journal. 2010. PMID 19966135. DOI 10.1096/fj.09-147124.

    Laboratory method study · Across 17 laboratories and 20 methods given identical samples, mass spectrometric and electrochemical methods agreed well, while ELISA showed more within-technique variation, reported higher urine values and deviated with concentration.

  41. 41.

    Barregard L, Møller P, Henriksen T, et al.. Human and methodological sources of variability in the measurement of urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine. Antioxidants and Redox Signaling. 2013. PMID 23198723. DOI 10.1089/ars.2012.4714.

    Laboratory method study · ELISAs varied far more between laboratories and generally overestimated 8-oxodG, and cannot determine absolute levels; timed spot excretion correlated with 24-hour excretion (r 0.67 to 0.90); variation across days was about 17 percent for 24-hour and 20 percent for creatinine-corrected first-void samples; creatinine- or specific-gravity-adjusted first-morning samples are recommended when 24-hour collection is not feasible.

  42. 42.

    Christensson B, Sigmundsdottir G, Larsson L. D-arabinitol--a marker for invasive candidiasis. Medical Mycology. 1999. PMID 10647119. DOI 10.1046/j.1365-280x.1999.00249.x.

    Review · D-arabinitol is a metabolite of most pathogenic Candida species; elevated ratios in serum or urine have been found in immunocompromised, usually neutropenic, patients with invasive candidiasis; serum levels rise in renal dysfunction; only a few prospective studies with adequate methods exist.

  43. 43.

    Yeo SF, Huie S, Sofair AN, Campbell S, Durante A, Wong B. Measurement of serum D-arabinitol/creatinine ratios for initial diagnosis and for predicting outcome in an unselected, population-based sample of patients with Candida fungemia. Journal of Clinical Microbiology. 2006. PMID 16957030. DOI 10.1128/JCM.01045-06.

    Prospective cohort · Serum D-arabinitol/creatinine ratios at or above 3.9 µM/mg/dL were found in 63 of 83 (76 percent) patients with Candida fungemia and 11 of 100 (11 percent) hospitalized controls without it; persistent elevation 3 or more days after onset went with higher mortality.

  44. 44.

    Shaw W. Increased urinary excretion of a 3-(3-hydroxyphenyl)-3-hydroxypropionic acid (HPHPA), an abnormal phenylalanine metabolite of Clostridia spp. in the gastrointestinal tract, in urine samples from patients with autism and schizophrenia. Nutritional Neuroscience. 2010. PMID 20423563. DOI 10.1179/147683010X12611460763968.

    Cross-sectional study · A single-author report of higher urinary HPHPA in children with autism than controls and in an adult with recurrent C. difficile; the highest value (7,500 mmol/mol creatinine) was in a patient with acute psychosis that remitted with oral vancomycin; the abstract gives no group sizes.

  45. 45.

    Shaw W, Kassen E, Chaves E. Increased urinary excretion of analogs of Krebs cycle metabolites and arabinose in two brothers with autistic features. Clinical Chemistry. 1995. PMID 7628083.

    Cross-sectional study · Two brothers with autistic features had markedly increased urinary citramalic, tartaric and 3-oxoglutaric acids, a tentatively identified citric acid analog (up to 137 mmol/mol creatinine) and arabinose.

  46. 46.

    Cervenka I, Agudelo LZ, Ruas JL. Kynurenines: Tryptophan's metabolites in exercise, inflammation, and mental health. Science. 2017. PMID 28751584. DOI 10.1126/science.aaf9794.

    Review · Kynurenine-pathway enzymes are regulated by nutritional and inflammatory signals; peripheral inflammation can contribute to kynurenine accumulation in the brain, associated with depression and schizophrenia, while exercised skeletal muscle activates kynurenine clearance.

  47. 47.

    Pechlivanis A, Kostidis S, Saraslanidis P, et al.. (1)H NMR-based metabonomic investigation of the effect of two different exercise sessions on the metabolic fingerprint of human urine. Journal of Proteome Research. 2010. PMID 20932058. DOI 10.1021/pr100684t.

    Laboratory method study · In 12 men performing repeated 80 m sprints with 10 s or 1 min rests, post-exercise urine separated from pre-exercise urine through lactate, pyruvate, hypoxanthine, Krebs cycle compounds, amino acids and BCAA catabolites, all higher with the shorter rest.

  48. 48.

    Barr DB, Wilder LC, Caudill SP, Gonzalez AJ, Needham LL, Pirkle JL. Urinary creatinine concentrations in the U.S. population: implications for urinary biologic monitoring measurements. Environmental Health Perspectives. 2005. PMID 15687057. DOI 10.1289/ehp.7337.

    Cross-sectional study · In 22,245 NHANES III participants, urinary creatinine varied significantly with age, sex, race and ethnicity, body mass index and fat-free mass, and slightly with time of day; creatinine-adjusted values should be compared with reference ranges from similar demographic groups.

  49. 49.

    Waikar SS, Sabbisetti VS, Bonventre JV. Normalization of urinary biomarkers to creatinine during changes in glomerular filtration rate. Kidney International. 2010. PMID 20555318. DOI 10.1038/ki.2010.165.

    Laboratory method study · Creatinine normalization assumes constant creatinine excretion, but excretion varied across and within hospitalized patients with changing kidney function, so ratios can under- or overestimate a biomarker; timed collections give the most accurate excretion rate.

Related

Keep reading.

Reading a number well is the start of the work, not the end of it. If you would like a physician to read yours over time, Explore working with Dr. Tagge.