Gadolinium-Based Contrast Exposure, Nephrogenic Systemic Fibrosis, and Gadolinium Detection in Tissue
Clark D. Wiginton1,
Brent Kelly2,
Aytekin Oto3,4,
Mary Jesse5,
Patricia Aristimuno6,7,
Randy Ernst3,8 and
Gregory Chaljub1
1 Department of Radiology, University of Texas Medical Branch, 301 University
Blvd., Galveston, TX 77555.
2 Department of Dermatology, University of Texas Medical Branch, Galveston,
TX.
3 Department of Radiology, University of Texas Medical Branch, Galveston,
TX.
4 Present address: Department of Radiology, University of Chicago, Chicago,
IL.
5 School of Medicine, University of Texas Medical Branch, Galveston, TX..
6 Department of Nephrology, University of Texas Medical Branch, Galveston,
TX
7 Present address: Division of Nephrology, Texas Tech University, Lubbock,
TX.
8 Present address: Department of Radiology, M. D. Anderson Cancer Center,
Houston, TX.

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Fig. 1 —Over 10-year time course in our local outpatient dialysis
clinic population, 83 patients underwent MRI, 72 of whom received MR contrast
material. Sixty-three of 72 received gadodiamide, 54 of whom received
gadodiamide only and nine also received gadopentetate. Eighteen received
gadopentetate, of whom nine received gadopentetate only and nine received
gadodiamide also.
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Fig. 2 —Both cases of nephrogenic systemic fibrosis (NSF) discovered
in our local outpatient dialysis center's population exclusively followed at
our institution were diagnosed in our dermatology department and were archived
in our dermatopathology database. Five additional cases of NSF were discovered
in dermatopathology database, two of which were followed up at dialysis
centers in other cities, whereas the other three never required treatment at
outpatient dialysis center.
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Fig. 3 —Plot of total time to develop nephrogenic systemic fibrosis
(NSF) symptoms after onset of gadolinium contrast exposure in renal failure
versus cumulative dose of gadolinium-based contrast agent before symptom onset
in each patient ( ) shows no linear correlation between two factors
(r = 0.01).
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Fig. 5 —Diagram of possible mechanism of fibrosis in nephrogenic
systemic fibrosis (NSF) illustrates points at which various potential risk
factors may interact to potentiate development of fibrosis. Note that
angiotensin-converting enzyme (ACE) inhibitors may inhibit fibrosis found in
NSF. TGF-β = transforming growth factor-β.
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Copyright © 2008 by the American Roentgen Ray Society.