Nephrogenic systemic fibrosis is associated with transforming growth factor β and Smad without evidence of renin-angiotensin system involvement

Brent Kelly, Matthew Petitt, Ramon Sanchez

Research output: Contribution to journalArticle

27 Scopus citations

Abstract

Background: The mechanisms of fibrosis associated with nephrogenic systemic fibrosis (NSF) are largely unknown. Transforming growth factor beta (TGF-β), a known profibrotic cytokine, is theorized to play a central role. The renin-angiotensin system has been linked with both TGF-β expression and fibrosis in other organ systems. Objective: We sought to investigate whether these mechanisms were involved with NSF. Method: Eleven biopsy specimens from 8 patients with NSF were evaluated by immunohistochemistry for the expression of TGF-β, Smad 2/3, angiotensin-converting enzyme (ACE), and angiotensin II receptor 1 (AT1). Results: TGF-β was detected in 8 of 11 samples of NSF. Smad 2/3 nuclear staining was seen in 8 of 11 samples. Conversely, only faint staining for ACE was seen in 2 of the 11 specimens. No AT1 staining was seen. Limitations: We did not perform our studies on a cohort of comparable patients with renal dysfunction without NSF. Our technique may not have been sufficiently sensitive to detect renin-angiotensin system involvement. Conclusions: TGF-β, as well as its second messengers, Smad 2/3, appears to be associated with the fibrosis seen in NSF. No definitive evidence of renin-angiotensin system involvement could be determined.

Original languageEnglish (US)
Pages (from-to)1025-1030
Number of pages6
JournalJournal of the American Academy of Dermatology
Volume58
Issue number6
DOIs
StatePublished - Jun 1 2008

ASJC Scopus subject areas

  • Dermatology

Fingerprint Dive into the research topics of 'Nephrogenic systemic fibrosis is associated with transforming growth factor β and Smad without evidence of renin-angiotensin system involvement'. Together they form a unique fingerprint.

  • Cite this