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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
Study reports elevated cytokine levels in patients with confirmed gadolinium retention
Results of a study to determine whether individuals with proposed gadolinium deposition disease (GDD) have elevated serum levels of pro-inflammatory and pro-fibrotic cytokines were recently published. GDD has been reported in patients with normal renal function after MRIs with a gadolinium-based contrast agent (GBCA). The study by Maecker et al., “An initial investigation of serum cytokine levels in patients with gadolinium retention”, also sought to determine whether specific cytokines are correlated with certain symptoms considered to be characteristic of GDD. The study involved 24 participants who were recruited between May 2016 and June 2017 and met the proposed GDD diagnostic criteria. Some of the participants were recruited from our MRI-Gadolinium-Toxicity support group. A control group of 64 subjects provided serum samples before their flu vaccination. Serum cytokine levels were obtained with Luminex serum cytokine assay using eBiosciences/Affymetrix human 62-plex kits.
In patients who had retained gadolinium, serum levels of 14 cytokines, including 9 pro-inflammatory cytokines, were “statistically significantly elevated” compared to controls (p ≤ 0.05). (more…)
Article says that Gadolinium-Based Contrast Agents should be used with extreme caution
A recently released review article by Drs. Katarina Leyba and Brent Wagner, titled “Gadolinium-based contrast agents: why nephrologists need to be concerned”, doesn’t pull any punches when it comes to the use of gadolinium-based contrast agents (GBCAs) for contrast-enhanced MRIs. The authors said that ‘nephrogenic’ systemic fibrosis is a misnomer since GBCAs are the known trigger for the disease; kidney impairment is a risk factor. They note that “the experimental evidence demonstrates that gadolinium-based contrast agents are biologically active – that is, not inert”. Drs. Leyba and Wagner said that “because GBCAs are biologically active in vitro and in vivo, and patients with normal renal function have reported adverse events that overlap those of ‘nephrogenic’ systemic fibrosis (i.e., rash, muscle/tendon ‘tightness, pain…), and because the other risk factors are undetermined”, medical professionals need to be “open to the possibility that ‘nephrogenic’ systemic fibrosis and these gadolinium-based contrast agent-induced symptoms are part of a continuum”. (more…)
Gadolinium Toxicity 