The gadolinium and NSF story continues to become clearer. A paper in the July issue of the Clinical Journal of the ASN shows deposition of gadolinium in the skin of a patient who developed Nephrogenic Systemic Fibrosis (NSF). Traces of iron were also found. NSF is seen exclusively in patients with renal failure; most of these patients have received gadolinium based MRI contrast agents. The half life of gadolinium is a little more than one hour in patients with normal renal function, but rises to 120 hours in dialysis patients. It appears that accumulation of gadolinium in the skin and other organs is the trigger for the development of this syndrome. The current study in CJASN provides further support for this view. As stated in an earlier post here, nobody with a glomerular filtration rate of less than 30 ml/min should receive gadolinium unless the indication is stronger than the fear of inducing NSF.
The study’s abstract is reproduced below.
Background and objectives: The pathogenesis of acquired nephrogenic systemic fibrosis recently described for patients with renal insufficiency and a history of exposition to gadolinium-based magnetic resonance contrast agents is not completely understood. A role for circulating fibroblasts in the fibrosing tissue is hypothetical, and the mechanism of the assumed trigger function of gadolinium remains elusive.
Design, setting, participants, & measurements: A skin lesion on a 76-yr-old man with symptoms of nephrogenic systemic fibrosis lasting 5 mo was studied at the ultrastructural level. After confirmation of he diagnosis by histopathologic methods, the presence and distribution of gadolinium, iron, calcium, and magnesium by energy filtering transmission electron microscopy was also examined.
Results: The performed electron spectroscopic imaging and electron energy loss spectroscopic analyses on deparaffinized samples revealed deposition of gadolinium in irregular small aggregates that adhered to cell profiles and collagen fibers of the connective tissue, forming a perivascular “gadolinium-deposit zone” in the skin. Traces of iron signal were demonstrated in singular gadolinium-positive deposits, and iron presence was found in adjacent connective tissue. The ultrastructural cell analysis of the lesion showed among numerous poorly differentiated fibrocytes also higher differentiated cells with myofibroblastic characteristics, including bundles of intermediate filaments and attachment plaques in the cell periphery, indicating an ability of lesional fibroblasts to differentiate into myofibroblastic cells.
Conclusions: These findings support the pivotal role of gadolinium chelates in the development of nephrogenic systemic fibrosis.