Gadolinium Toxicity

Home » Posts tagged 'Normal Kidney Function' (Page 2)

Tag Archives: Normal Kidney Function

Viewpoint Categories

Initial publication of symptoms of gadolinium toxicity

The results of a 9 question survey about gadolinium exposure and related symptoms in patients with normal renal function were reported in an article by Burke et al titled Self-reported gadolinium toxicity: A survey of patients with chronic symptoms.  The survey provides the initial description in the medical literature of patients with normal renal function who self-described toxicity related to administration of gadolinium-based contrast agents (GBCAs).  There were 50 respondents to the anonymous online survey.  All 50 respondents (100%) received gadolinium-based contrast with an average of 4.2 doses.  All 50 attribute their symptoms to gadolinium exposure.

Thirty-three (66%) subjects described the onset of symptoms immediately following GBCA administration and 16 (32%) within 6 weeks.  The most common symptoms included bone/joint pain and head/neck symptoms including headache, vision change, and hearing change.  Headache and bone/joint pain was described by more than 75% of the cases.  Skin changes were seen in approximately 60% of respondents.

Other symptoms reported include: flu-like symptoms (30.6%); digestive symptoms described as nausea, vomiting, diarrhea (46.9%); chest symptoms described as difficulty breathing (42.9%); generalized whole body symptoms (30.6%); and other (75.5%).

The findings of the survey showed that subjects with normal renal function might develop disease following administration of the majority of GBCAs including macrocyclic agents.

Despite the limitations of the survey, the authors said that it was their opinion “that there most likely is toxicity associated with GBCA administration in patients with normal renal function”.  They concluded that, “at the very least, this study highlights the need to further investigate the subject of patients with normal renal function who complain of severe long-lasting symptomatology following GBCA administration”.

My thoughts –
When Hubbs Grimm and I released the findings of the online symptom survey that we conducted in early 2014, we noted that the results presented in our paper should stimulate further professional investigation into gadolinium retention in all patient populations including those with normal renal function.  It is good to see that the medical community is now looking into the issue of gadolinium retention in patients with normal renal function further.

Our paper, Gadolinium Toxicity – A Survey of the Chronic Effects of Retained Gadolinium from Contrast MRIs can be found in the Research section of our website.

Sharon Williams


Burke, L. M. B., Ramalho, M., AlObaidy, M., Chang, E., Jay, M., & Semelka, R. C. (2016). Self-Reported Gadolinium Toxicity: A Survey of Patients with Chronic Symptoms. Magnetic Resonance Imaging.

Gadolinium Deposition Disease – Part of a Family of Disorders

Important News for Patients who have retained gadolinium –
A recently published article by UNC Radiologist Dr. Richard Semelka and his colleagues proposes naming the histopathologically proven presence of gadolinium in brain tissue “gadolinium storage condition”, and it describes a new entity that represents symptomatic deposition of gadolinium in individuals with normal renal function, for which they propose the designation “gadolinium deposition disease”.  The article titled: Gadolinium in Humans: A Family of Disorders, was published in AJR online.

The article is not freely available to the public at this time.   Because of that, I will provide some important information from the article for patients and their doctors below.

Gadolinium Storage Condition –
“Gadolinium storage condition” is the term proposed for gadolinium tissue deposition. The authors said, “Even in patients with normal renal function, in vivo clinical exposure to gadolinium chelates results in gadolinium incorporation into body tissues such as bone matrix or brain tissues.” (See references below.)

It appears that gadolinium accumulation varies depending on the stability of the agent used.  As with NSF, the least stable GBCAs appear to be most likely to result in gadolinium storage condition, and stable agents either do not cause it or cause it at a very low level.  The clinical significance of gadolinium tissue deposition remains incompletely understood.

Gadolinium Deposition Disease –
“Gadolinium deposition disease” is the name proposed for a disease process observed in subjects with normal or near normal renal function who develop persistent symptoms that arise hours to 2 months after the administration of gadolinium-based contrast agents (GBCAs).  In these cases, no preexistent disease or subsequently developed disease of an alternate known process is present to account for the symptoms.

The authors note that some of these patients are likely to have coexistent gadolinium storage condition, as described above, but gadolinium deposition disease is also described after a single administration of GBCA.  The causal relationship has not been fully established, but it is under investigation.

The article references our MRI Gadolinium-Toxicity support group and notes that the group has reported symptoms it considers to be consistent with the known toxic effects of gadolinium.  They also cite the results of our 2014 Symptom Survey which suggests an association between chronic effects and GBCA exposure.

The authors said, in their experience, “Symptoms of gadolinium deposition disease are similar but not identical to those observed in NSF”.   They said that their preliminary investigation has convinced them that this phenomenon is a true disease process. (more…)

Study finds more Gadolinium in Bone than Brain Tissue

A recent study by Murata et al, “Macrocyclic and Other Non-Group 1 Gadolinium Contrast Agents Deposit Low Levels of Gadolinium in Brain and Bone Tissue: Preliminary Results from 9 Patients with Normal Renal Function”, adds to the mounting evidence of gadolinium deposition and retention in patients with normal renal function.  The study, published online ahead of print in Investigative Radiology, found that “Gadolinium deposition in normal brain and bone tissue occurs with macrocyclic and linear protein interacting agents in patients with normal renal function”.  The authors noted that, “Deposition of Gd in cortical bone occurs at much higher levels compared with brain tissue and shows a notable correlation between the two”.

The linear gadolinium-based contrast agents (GBCAs) most frequently associated with NSF were designated as Group 1 agents by the FDA in 2010.  Those agents are gadodiamide (Omniscan), gadoversetamide (OptiMARK), and gadopentetate (Magnevist).  The linear protein binding agents include gadobenate dimeglumine (MultiHance), gadoexetate (Eovist), and gadofosveset (Ablavar).  (more…)

New Study calls for FDA action on Gadolinium-based Contrast Agents

Details of a new article about gadolinium-based contrast agent safety concerns were posted to EurekAlert! by MedInsight Research Institute.  The article, “Gadolinium-Based Contrast Agent Toxicity – A Review of Known and Proposed Mechanisms”, by Rogosnitzky and Branch, was published in the Springer journal BioMetals 

Of special interest to us is the fact that the authors referenced the Lighthouse Project and results from our 2014 paper, Gadolinium Toxicity: A Survey of the Chronic Effects of Retained Gadolinium from Contrast MRIs.  As we have done, the authors called for FDA action on Gadolinium-Based Contrast Agents.

The following release can be found at



Study raises questions about the safety of MRI contrast agent; authors call for FDA action


APRIL 6, 2016, Ariel, Israel – An article published today in the Springer journal BioMetalsraises serious questions about the safety of the gadolinium-based contrast agents that are used in about 30 percent of magnetic resonance imaging (MRI) scans. In their literature review, researchers from MedInsight Research Institute and Israel’s Ariel University analyzed studies detailing the known and proposed mechanisms of retained gadolinium toxicity. According to lead author Moshe Rogosnitzky, “Although gadolinium is bound to chelating agents designed to flush out the rare metal following an MRI, it has been found to deposit in the brain, bone, and other organs.”

Rogosnitzky said that this finding contradicts the longstanding belief that patients with normal kidney function are not at risk for gadolinium accretion. In 2007, the U.S. Food and Drug Administration (FDA) ordered a black box warning for gadolinium-based contrast agents following the discovery that patients with kidney disease were developing nephrogenic systemic fibrosis (NSF) due to the inability to clear gadolinium from their bodies. In July 2015, the FDA announced it was evaluating the risk of brain-deposits in patients who undergo repeated exposure to gadolinium-based contrast agents. “At the time, FDA claimed that available information did not identify any adverse health effects. In the face of the information contained in our study, we believe this position is no longer tenable,” said Rogosnitzky.

Study author and toxicologist Dr. Stacy Branch underscored the urgent need for the FDA to take action. “Given the ever-growing toxicological and gadolinium tissue retention data, it is vital that the FDA promptly leads efforts, including retrospective and prospective clinical studies, to better define the connection between GBCA-exposure and adverse health events,” she said. “This is needed to guide the choice of preventive methods, achieve accurate diagnoses, implement effective treatment approaches, and spark research for the design of safer contrast agents and imaging protocols.”

Rogosnitzky, who heads the Center for Drug Repurposing at Ariel University, called upon the scientific community to quickly develop treatments for gadolinium overload. “Our literature review did not reveal a single suitable drug to swiftly remove gadolinium from the body,” he said. “In one study, the authors estimated it might take up to 156 years to remove a patient’s stored gadolinium using a particular drug.” Rogosnitzky believes that a good first step is to study existing chelator drugs used for other metal toxicities in order to assess their possible utility in gadolinium accumulation.

The published article sounds the alarm about the gap in scientific knowledge about treatment for gadolinium toxicity. “With the ominous discovery that gadolinium is retained in healthy patients, there is a critical shortage of scientific information regarding how to assess gadolinium toxicity, and perhaps most importantly, how to treat it,” Rogosnitzky said.


The article, “Gadolinium-Based Contrast Agent Toxicity – A Review of Known and Proposed Mechanisms,” can be accessed at

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

%d bloggers like this: