title: SDF-1 expression is elevated in chronic human renal allograft rejection.
abstract: The exact mechanism of acute and chronic allograft rejection still remains unclear. The chemokine SDF-1 as mediator of allograft rejection has been under intensive investigation in liver, cardiac and bone marrow transplantation, whereas in renal transplantation, there are no reports about SDF-1 to date. This study was performed to evaluate if SDF-1 might also play an important role in human renal graft biopsies. One hundred and ninety formalin-fixed, paraffin-embedded renal allograft biopsies were included in the analysis from patients with normal renal graft morphology (according to Banff 97 classification grade 1, n = 84), with acute interstitial rejection (Banff grade 4 type I, n = 10), with acute vascular rejection (Banff grade 4 type II, n = 21), with chronic allograft nephropathy (CAN, Banff grade 5, n = 23), and without rejection but with various other lesions (Banff grade 6, n = 42). SDF-1 was localized by immunohistochemistry. In biopsies with CAN, SDF-1 expression was significantly elevated in interstitial infiltrates and infiltrating neointimal cells of arteries compared with biopsies with normal renal graft morphology. This is the first study describing a role of SDF-1 in human renal allograft rejection. We were able to demonstrate in a large number of biopsies an upregulation of SDF-1 in patients with CAN. Whether SDF-1 has pro-inflammatory or protective properties in this setting has to be evaluated in further trials.
authors.affiliation: Klinik und Poliklinik für Innere Medizin II, University of Regensburg, Regensburg, Germany. ute.hoffmann@klinik.uni-regensburg.de
authors.forename: U
authors.initials: U
authors.lastname: Hoffmann
authors.forename: B
authors.initials: B
authors.lastname: Banas
authors.forename: B
authors.initials: B
authors.lastname: Krüger
authors.forename: M
authors.initials: M
authors.lastname: Banas
authors.forename: T
authors.initials: T
authors.lastname: Bergler
authors.forename: C
authors.initials: C
authors.lastname: Böger
authors.forename: M
authors.initials: M
authors.lastname: Kammerl
authors.forename: A
authors.initials: A
authors.lastname: Obed
authors.forename: P
authors.initials: P
authors.lastname: Rümmele
authors.forename: S
authors.initials: S
authors.lastname: Segerer
authors.forename: G A J
authors.initials: GA
authors.lastname: Riegger
authors.forename: B K
authors.initials: BK
authors.lastname: Krämer
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D054377:Chemokine CXCL12; D019743:Chemokines, CXC / Q000096:biosynthesis*; D002908:Chronic Disease; D018450:Disease Progression; D005500:Follow-Up Studies; D006084:Graft Rejection / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D016030:Kidney Transplantation / Q000473:pathology*; D011379:Prognosis; D012189:Retrospective Studies; D012720:Severity of Illness Index; D017154:Stromal Cells / Q000378:metabolism; D014184:Transplantation, Homologous
chemical_list: D015415:Biomarkers; C515255:CXCL12 protein, human; D054377:Chemokine CXCL12; D019743:Chemokines, CXC