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Ten Years Later: Gadolinium Toxicity – A Disease of Degrees
Editorial by Sharon Williams
November 12, 2025
In early 2015, I opened a post with the following question: Why does a Gadolinium Toxicity diagnosis have to be full-blown NSF (Nephrogenic Systemic Fibrosis) or nothing at all? I went on to say that we believe Gadolinium Toxicity is a “disease of degrees”, which can manifest itself in many ways depending on how much gadolinium someone retains. And it can occur in patients with normal renal function.
Here we are ten years later, in 2025, and our belief about retained gadolinium causing a disease with varying degrees of severity is stronger than ever. That belief is based on the results of the Patient Survey that Hubbs Grimm and I conducted last year along with patient advocates Sarah Ratnam and Catriona Walsh. We recently released our first paper that focuses on the symptoms reported by 316 survey participants after MRIs with a gadolinium-based contrast agent (GBCA). The patients had normal and near normal renal function at the time of their MRIs. 185 of the participants have one or more test results that confirm they retained gadolinium for more than 30 days and for as long as 22 years after contrast administration, including 14 years in pelvic bone, and 13 years in sigmoid colon tissue.
The similarities between the symptom reporting patterns of the survey participants closely mirror those published about the clinical presentation of early-phase NSF as described by Marckmann & Skov (2009). Based on what Marckmann wrote about NSF, it seems that NSF itself had varying degrees of severity. Marckmann (2009 & 2011) wrote that there were significant individual differences in the clinical course of NSF, even in end-stage renal disease (ESRD) patients, which seems to indicate that retained gadolinium could trigger a range of symptoms, with a varied clinical outcome in all patient populations.
The variability of the symptoms shows that even in severely renally impaired patients, gadolinium-induced NSF did not cause the exact same set of symptoms or level of severity.
Is NSF itself the “disease of degrees”? Do all patients affected by gadolinium manifest NSF to varying extents, but without the “N” or nephrogenic component? The many similarities between the early clinical picture of NSF and the symptoms reported by participants in our Patient Survey suggest that they do.
Rather than a new or separate disease entity for patients with normal renal function, such as Gadolinium Deposition Disease (GDD) as described by Semelka & Ramalho (2023), our survey findings suggest that GDD and NSF may reflect different points along a continuum of gadolinium-induced toxicity. In other words, what we are observing may be one gadolinium-induced disease process manifesting with varying degrees of severity, which is how Marckmann described NSF in his Severity Grading in 2009.
Gadolinium has the Potential to Harm All Patients (more…)
Can Symptoms of Gadolinium Toxicity be explained?
On August 25, 2020, I wrote an open letter to the FDA, Radiologists and Researchers about the symptoms of gadolinium toxicity that have not, as yet, been recognized by the FDA or medical community as being caused by retained gadolinium (Gd). I believe part of the problem stems from the fact that histopathological examination has not found any evidence that deposited Gd caused “harm” in the brain. However, the lack of physical evidence and abnormal blood tests does not mean that harmful events have not taken place in patients’ bodies. What if gadolinium affected the function of cells, especially nerve cells, and triggered a cascade of adverse events, experienced by the person as decidedly abnormal and unpleasant sensations? Would that be easily detected on histological examination of tissue, or blood tests?
In my letter, I reviewed facts that we already know about Gd from the literature, in terms of both its retention after contrast administration and its effects at a cellular level. Given that Gd has been shown to induce mitochondrial toxicity, interfere with ion channels, create neuronal hyperexcitability, and affect inflammatory processes, could Gd be affecting not only the part of the brain that controls many processes, but also peripheral and autonomic nerve endings, as well as dorsal root ganglia, to produce the many and varied symptoms that patients are experiencing?
We know that retention of Gd has been demonstrated in humans, that unexplained symptoms are occurring, and the neuronal effects of Gd have been demonstrated experimentally. Could it just be that the connection has not yet been made, and when considered together, all these facts might explain how patients’ symptoms are being caused by retained Gd from gadolinium-based contrast agents (GBCAs)?
I believe many symptoms of gadolinium toxicity can be explained by Gd-induced small fiber neuropathy (SFN) and long-standing neuropathic pain. Interestingly, as you will see in my letter, many symptoms of SFN are the same as the clinical symptoms associated with nephrogenic systemic fibrosis (NSF), which makes sense to me since the cause is the same.
Symptoms of Gadolinium Toxicity: Can their cause be explained? is available for download as a PDF and it will be posted in Our Research in the Research section of our website. The reason for making my letter available to the public now is to inform doctors, researchers, and affected patients about gadolinium-related facts that do not seem to be widely recognized. My hope is that more research will be conducted that involves evaluation and testing of patients who have retained gadolinium and are experiencing SFN-like symptoms, which, until now, have been unexplained and perplexing to clinicians who are not familiar with the potential toxic effects of retained gadolinium.
Sharon Williams
Gadolinium Reference Range for those with no GBCA exposure
The article, “Establishing Reference Intervals for Gadolinium Concentrations in Blood, Plasma, and Urine in Individuals Not Previously Exposed to Gadolinium-Based Contrast Agents” by Layne et al., was published in Investigative Radiology earlier this year. Their study set out to determine whether healthy people who have never received a gadolinium-based contrast agent (GBCA) have detectable concentrations of gadolinium (Gd) in their blood and urine, and to then develop a reference range for Gd concentrations in blood and spot urine. A secondary aim of the study was to determine whether spot urine Gd concentrations are equivalent to those in timed 24-hour urine collections. In the majority (93.3%) of their 120 healthy volunteers, the Gd concentrations were undetectable in blood, plasma, spot urine samples, and 24-hour urine collections. No participants had detectable concentrations of Gd in their plasma. The authors noted that those subjects who did have detectable Gd concentrations in their spot urine samples had considerably lower concentrations than those identified in the reference interval published on the Mayo Clinic web site, which is less than 0.8 mcg/g creatinine.
Proposed Gadolinium Reference Intervals, Layne et al. (2020):
- Whole blood: <0.008 ng/mL or <0.050 nmol/L
- Plasma: <0.009 ng/mL or <0.057 nmol/L
- Spot urine: <0.036 μg/g creatinine or <0.0250 nmol/mmol
More Study Details –
Twenty subjects also did a timed 24-hour urine collection, and urine Gd concentrations were measured in samples from those collections. None of the 24-hour urine collections had detectable Gd concentrations, and those 20 subjects also did not have detectable Gd in their spot urine specimens.
Study participants were recruited from the staff at Guy’s and St Thomas’ NHS Foundation Trust, London, and students from King’s College London who are based at St Thomas’ Hospital. Potential subjects completed a basic health questionnaire to determine suitability for inclusion in the study. Participants had to be 18 years or older with no significant medical history, no history of smoking or vaping within the previous 6 months, and no prior exposure to gadolinium or GBCAs. All participants had an estimated glomerular filtration rate (eGFR) of 70 or greater. Of the 120 subjects, 79 (65.8%) were female and 41 (34.2%) were male. The median age was 29.6 years.
Although no subjects reported having an MRI with a GBCA, detectable concentrations of Gd were found in 10 of the 120 subjects. Four of those 10 reported undergoing an MRI without contrast in the past, which could not be confirmed, so those 4 were excluded from further data analysis.
The authors noted that it is possible that subjects had a degree of background Gd exposure from anthropogenic gadolinium which is known to be in tap water. (more…)
Gadolinium in Ovaries 9.5 Years after GBCA Administration
Editorial by Sharon Williams
May 2020
While being in the middle of the COVID-19 pandemic might not seem like the best time to write an editorial about long-term gadolinium retention, waiting longer was not a good option for me. I believe that the information I want to share with patients, doctors, and gadolinium researchers needs to be in the public domain.
Anyone who follows our posts knows that none have been made since mid-2019. I will not go into all the reasons for that, but one of the issues resulted in the removal of my ovaries late last year. Thankfully, no cancer was found, but something else that should not have been there was – gadolinium. Testing performed by Doctor’s Data determined that there was gadolinium in both of my ovaries which were removed more than 9.5 years after my last dose of a gadolinium-based contrast agent (GBCA). I must admit that I was not surprised, since gadolinium was also found in my thyroid tissue that was removed in 2014.
At the time of all my MRIs, I had what the NSF literature refers to as “normal” renal function, meaning an eGFR greater than 60. I have had 5 MRIs with a linear GBCA that is no longer on the market, and my last dose was 10 years ago in March of 2010. I have no history of brain tumors or cancer anywhere in my body. Based on what patients like me have been told, I should not have retained gadolinium from the contrast agent, but I did, and I have proof of long-term gadolinium deposition in my organs. While I understand that deposition alone does not prove causation, I believe it raises serious questions about the long-term effects of gadolinium retention that need to be answered.
You might be wondering if I made the FDA or anyone else aware of the fact that gadolinium was found in my ovarian tissue 9.5+ years after my last dose of a GBCA, and the answer is, yes, I did. I sent the FDA and more than 20 other doctors and scientists a copy of a document that contained details of my GBCA history and results of testing my blood, urine, and thyroid and ovarian tissue for gadolinium. While I heard back from the FDA and a few doctors, nothing else has come from it at this time.
Whether the gadolinium level in my tissue was high or not is not the issue since gadolinium should not remain in the body many years after MRIs with a GBCA. As the FDA noted on page 16 of its Briefing Document for the September 8, 2017, MIDAC public meeting about Gadolinium Retention, “detection of gadolinium weeks or months following GBCA administration is considered abnormal as gadolinium is a trace element and not involved in any physiologic processes.” Sherry et al. (2009) reported that gadolinium is toxic in biological systems that require calcium for proper function due to the very similar radius of the Gd3+ and Ca2+ ions. Surely, based on what we have learned about gadolinium (Gd) and Nephrogenic Systemic Fibrosis (NSF), no one can honestly think that patients who retain toxic gadolinium for many months or years will not be harmed by it in some way at some point in time.
Until mid-2015, the FDA had not recognized that patients with normal renal function were retaining gadolinium from GBCAs administered for MRIs. While the FDA and Radiology community now acknowledge that everyone who has an MRI with a GBCA likely retains gadolinium from each dose of contrast they receive, so far, they continue to say that they have seen no evidence that retained gadolinium causes harm. I find that statement hard to reconcile with what we know already from the published facts about NSF, GBCAs, and the toxic effects of gadolinium.
While some may think the long-term effects of gadolinium retention are still unknown, I cannot believe it is a benign substance since I continue to experience symptoms of gadolinium toxicity more than 10 years later. It seems clear that a gadolinium study to evaluate patients like me is urgently needed. In my opinion, the issue is not about the toxic effects of gadolinium when it is retained in the human body since the NSF-related literature already informed us about that. The problem is no one understands what it is doing to patients with normal renal function when less gadolinium may have been retained.
As we have said many times before, Gadolinium Toxicity is a “Disease of Degrees” with NSF being the worst manifestation of it when large amounts of gadolinium are retained. However, based on the published facts about gadolinium and GBCAs, we see no reason to think that retained gadolinium will cause full-blown NSF or nothing at all.
It is my belief that the medical community will not fully-appreciate the scope of the problems related to gadolinium retention until symptomatic patients with normal renal function are interviewed, examined, and tested. If all patients retain some gadolinium from every dose of contrast that they receive, why is it that only a small percentage of people report having symptoms of toxicity? Could asymptomatic patients who have retained Gd go on to develop gadolinium-induced health issues later? Why are patients who have received macrocyclic agents for their MRIs experiencing intense symptoms; could they be retaining the intact macrocyclic GBCA?
There are many unanswered questions about the long-term effects of gadolinium retention, and I believe patients who have been affected by the toxic effects of gadolinium are key to finding some of those answers. What you learn from patients like me might help guide new research.
Researchers interested in conducting a study with me or other patients with normal renal function who have evidence of gadolinium retention and symptoms of gadolinium toxicity, should email me at Sharon@GadoliniumToxicity.com. I sincerely hope that researchers contact me since this problem is not going away.
Sharon Williams
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References
9/8/2017 FDA Briefing Document for Medical Imaging Drugs Advisory Committee Meeting about Gadolinium Retention. https://www.fda.gov/media/107133/download
Sherry, A. D., Caravan, P., & Lenkinski, R. E. (2009). Primer on gadolinium chemistry. Journal of Magnetic Resonance Imaging : JMRI, 30(6), 1240–1248. Retrieved from http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2853020&tool=pmcentrez&rendertype=abstract
7/27/15 FDA Safety Announcement – https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-fda-evaluating-risk-brain-deposits-repeated-use-gadolinium-based
5/22/2017 FDA Safety Communication – https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-fda-identifies-no-harmful-effects-date-brain-retention-gadolinium
12/19/2017 & 5/16/2018 FDA Safety Announcements can be found here:
https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-fda-warns-gadolinium-based-contrast-agents-gbcas-are-retained-body
Gadolinium Toxicity 