This test is most useful if any of these apply to you.
If you eat a lot of grains, rice, or take a red yeast rice supplement, some of what you swallow may include a fungal poison that your kidneys have to filter out. This urine test shows whether that has happened recently.
It will not diagnose a disease, but it gives you a direct window into a specific dietary exposure that no standard blood panel checks for.
CIT (citrinin) is a toxin made by molds, mainly species of Penicillium, Aspergillus, and Monascus, that grow on stored grains, fruits, herbs, spices, and fermented rice products. It is not something your body makes. It gets into you through contaminated food, and this test measures how much of it, along with its main breakdown product, ended up in your urine.
Once you swallow citrinin, your body converts most of it into a related molecule called DH-CIT (dihydrocitrinone). This breakdown product is usually the bigger signal in urine, often several times higher than the parent toxin, and it is considered a detoxification product because it is less toxic than citrinin itself. A complete read on your exposure measures both.
This is a research and exposure-monitoring marker, not an established clinical test. There are no standardized reference ranges or cutoff levels that map a specific urine number to a specific health outcome. What it tells you is whether, and roughly how much, you were exposed in the last day or two.
Human biomonitoring studies across Germany, Belgium, Portugal, Italy, Bangladesh, Nigeria, and Spain consistently find citrinin in a large share of urine samples. In one German study, at least one citrinin biomarker was detected in every single urine sample tested, and in healthy German adults the toxin or its breakdown product turned up in 82 to 84 percent of samples. Exposure is common, not exotic.
Because citrinin is not routinely checked in food or in standard lab panels, most people have no idea what their exposure looks like. This test is one of the few ways to find out.
The clearest health concern tied to citrinin is kidney toxicity. In animal studies and toxicology reviews, the kidney is repeatedly identified as the main target organ after repeated exposure, with damage concentrated in the small filtering tubes of the kidney. Higher urine levels mean greater recent exposure to a toxin that stresses the kidneys, not proof that kidney damage has occurred.
How risk is judged: rather than naming a urine concentration that causes harm, researchers convert your urine levels into an estimated daily intake and compare it to the European Food Safety Authority's level of no concern for kidney toxicity, which is 0.2 micrograms per kilogram of body weight per day (a very small amount relative to body size). In Germany, median estimated intake was well below that in adults, but 6.3 percent of children exceeded it. In one Bangladeshi adult group, estimated intake crossed the concern level in 10 percent of people in summer and 24 percent in winter.
Citrinin exposure during pregnancy is common. In rural Bangladesh, citrinin was detected in 61 percent of pregnant women's urine, and it frequently occurred alongside a related kidney toxin called ochratoxin A. Under a moderate exposure scenario, estimated citrinin intake was of public health concern in about 16 to 17 percent of these women.
The direct outcome evidence is limited and, so far, does not show harm. A prospective study of 436 singleton pregnancies found no clear link between maternal citrinin exposure and pregnancy loss, preterm birth, low birth weight, or small-for-gestational-age babies. The catch is that the confidence intervals were wide, meaning the data cannot rule out either a protective or a meaningfully harmful effect. This is best read as insufficient evidence, not a clean bill of health.
You may see citrinin described as a potential carcinogen. The human evidence does not support that framing. The International Agency for Research on Cancer classifies citrinin as Group 3, meaning it cannot be classified as to whether it causes cancer in humans, because the evidence is limited. In a case-control study of colorectal cancer patients, urinary citrinin was detected in 74 percent of samples but did not distinguish cancer patients from healthy controls.
Tentative links to kidney tumors and to endemic kidney disease exist in the literature, but they are confounded by the fact that citrinin almost always occurs together with ochratoxin A, making it hard to separate the two. Treat these as open questions, not established facts.
This is a genuinely counterintuitive marker, and it is worth resolving the apparent contradiction directly. A detectable result does not mean poisoning, and an undetectable result does not mean zero lifetime exposure. Citrinin clears fast. Human data show half-lives of about 6.7 hours for citrinin and 8.9 hours for its breakdown product, with most urinary excretion happening within 24 to 48 hours. It does not build up strongly in the body.
So this test is a snapshot of the last day or two, not a measure of long-term body burden. That is exactly why it is not a good marker of established kidney disease. A telling example: in a Nicaraguan population with declining kidney function, urinary citrinin was below the limit of detection and was not supported as a cause of their disease. Abnormal kidney results do not imply citrinin exposure, and citrinin is not a general kidney injury test.
Because citrinin reflects recent intake and normalizes within a day or two, a single spot reading tells you about a single window in time. If you ate a contaminated meal yesterday, the number is up; if you did not, it may be undetectable even if you are exposed regularly through your usual diet. That day-to-day swing is the whole point of tracking over time.
Get a baseline. If you are trying to identify or remove a dietary source, such as a specific grain product or a red yeast rice supplement, retest after you make the change to see whether your levels drop. Repeat testing across different times of year is also informative, because studies show levels vary by season depending on how food is grown and stored. A pattern of repeatedly elevated results is far more meaningful than any single number, and both the parent toxin and its breakdown product should be measured together each time.
Urine is a moving target, and several things can distort a single reading without reflecting a true change in exposure. Lead with the biggest one: how dilute your urine is.
No specific medication is known to falsely raise or lower urinary citrinin on its own. Medication is listed in the broader biomonitoring literature only as a general influence on urine chemistry, not as a citrinin-specific confounder.
A single detectable result is not a reason to panic, but a repeatedly elevated one is a reason to investigate your diet. Because urine cannot tell you which food is responsible, the practical next step is to review likely sources: stored grains and cereal products, and especially red yeast rice supplements, which can contain very high citrinin levels. Removing a suspected source and retesting is the cleanest way to confirm it.
If you are pregnant, managing kidney disease, or taking supplements that could be contaminated, this result is worth bringing to a licensed clinician or toxicology specialist. Citrinin should be interpreted alongside your exposure history and, where kidney concern exists, alongside actual kidney injury markers such as NAG, beta-2-microglobulin, KIM-1, or NGAL rather than on its own. Because it frequently co-occurs with ochratoxin A, checking that companion toxin at the same time gives a fuller picture of your total nephrotoxic mycotoxin exposure.
Evidence-backed interventions that affect your CTN level
Citrinin is best interpreted alongside these tests.
Citrinin is included in these pre-built panels.