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4th Annual Yale Nephrogenic Systemic Fibrosis Conference at the New York Academy of Sciences

May 14-15, 2010

In 1997, a new disease was recognized among patients with pre-existing renal dysfunction. Now known as Nephrogenic Systemic Fibrosis (NSF), the disorder is known to be highly associated with, and very likely triggered by, gadolinium based magnetic resonance imaging contrast agents (GBCA). As such, it is a man-made disease, very likely a hitherto uncharacterized fibrosing toxicity to heavy metal deposition in the human body. Much of what we know about NSF stems from the NSF Registry at Yale University, and, in recent years, an annual scientific meeting on NSF hosted at Yale.

The May 2010 Fourth Annual Meeting on NSF and GBCA will have several goals. As the 4th meeting represents a change in venue from New Haven, CT to New York City, a very important aspect will be introducing the disease to a new, and much larger community of practitioners and scientists, chiefly in nephrology, radiology, rheumatology, dermatology and pathology. The introductory sessions will provide the historical context of NSF--how it was discovered, the mechanics of how it is diagnosed, and the significance of gadolinium micro-detection. The core of the meeting will focus on the mechanism of fibrosis in NSF--these derived from animal and tissue culture studies. The discussion will be broadened to include known mechanisms of tissue fibrosis (systemic and organ specific) and potential targets of pharmacologic therapy. Lastly, we will examine the lessons learned from NSF: the current state of prevention, and practical strategies for using GBCA wisely in those at risk.

Overall, the breadth of discussions will extend from the cells and atoms responsible for NSF to the entire population at risk, and therapeutically and mechanistically from the scientific bench-top to the bedside. Of greater importance, perhaps, is the impact this work will have on the fundamental understanding of fibrosis in general, opening up new avenues of understanding into disease mechanisms previously thought to be unchallengeable by medicine.

Click here or here to learn more.

	Announcements

!	4th Annual Yale Nephrogenic Systemic Fibrosis Conference at the New York Academy of Sciences May 14-15, 2010 In 1997, a new disease was recognized among patients with pre-existing renal dysfunction. Now known as Nephrogenic Systemic Fibrosis (NSF), the disorder is known to be highly associated with, and very likely triggered by, gadolinium based magnetic resonance imaging contrast agents (GBCA). As such, it is a man-made disease, very likely a hitherto uncharacterized fibrosing toxicity to heavy metal deposition in the human body. Much of what we know about NSF stems from the NSF Registry at Yale University, and, in recent years, an annual scientific meeting on NSF hosted at Yale. The May 2010 Fourth Annual Meeting on NSF and GBCA will have several goals. As the 4th meeting represents a change in venue from New Haven, CT to New York City, a very important aspect will be introducing the disease to a new, and much larger community of practitioners and scientists, chiefly in nephrology, radiology, rheumatology, dermatology and pathology. The introductory sessions will provide the historical context of NSF--how it was discovered, the mechanics of how it is diagnosed, and the significance of gadolinium micro-detection. The core of the meeting will focus on the mechanism of fibrosis in NSF--these derived from animal and tissue culture studies. The discussion will be broadened to include known mechanisms of tissue fibrosis (systemic and organ specific) and potential targets of pharmacologic therapy. Lastly, we will examine the lessons learned from NSF: the current state of prevention, and practical strategies for using GBCA wisely in those at risk. Overall, the breadth of discussions will extend from the cells and atoms responsible for NSF to the entire population at risk, and therapeutically and mechanistically from the scientific bench-top to the bedside. Of greater importance, perhaps, is the impact this work will have on the fundamental understanding of fibrosis in general, opening up new avenues of understanding into disease mechanisms previously thought to be unchallengeable by medicine. Click here or here to learn more.

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