Complement activation in early protocol kidney graft biopsies after living-donor transplantation1

Sund, Ståle; Hovig, Torstein; Reisæter, Anna Varberg; Scott, Helge; Bentdal, Øystein; Mollnes, Tom Eirik

doi:10.1097/01.tp.0000062835.30165.2c

Cited by 54 publications

(50 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…C3d (or C3c) was found in PTC in 39 to 60% of biopsies from HLA-mismatched grafts with diffuse PTC C4d (8,(27)(28)(29). In general C3d and C4d were correlated.…”

Section: Other Complement Components Have Not Yet Proved Diagnosticalmentioning

confidence: 78%

“…Lectin pathway components (Figure 1), which activate C4 by binding to microbial carbohydrates, are sometimes detected in conjunction with C4d. Mannose-binding lectin-associated serine protease-1 (MASP-1) was present in one of 11 protocol biopsies with C4d; no mannose-binding lectin was detected (27). Among 18 biopsies with C4d, 16 had diffuse H-ficolin along the PTC, whereas none of the 42 cases without C4d had H-ficolin.…”

Section: Other Complement Components Have Not Yet Proved Diagnosticalmentioning

confidence: 99%

See 1 more Smart Citation

Antibody-Mediated Renal Allograft Rejection

Colvin

2007

Journal of the American Society of Nephrology

493

447

View full text Add to dashboard Cite

Alloantibodies to HLA class I or II and other antigens expressed by endothelium cause a variety of effects on renal transplants, ranging from acute to chronic rejection, and even apparent graft acceptance (accommodation). Recognition of these conditions and appropriate therapy requires demonstration of C4d in biopsies, commonly confirmed by tests for circulating alloantibody. Substantial practical experience by pathologists in the interpretation and pitfalls of C4d stains are reviewed along with considerations of the clinical significance and pathologic mechanisms of the different effects of antibody on the endothelium of the renal allograft. Clinical trials will be needed to ascertain the optimal treatment for the newly appreciated conditions chronic humoral rejection and accommodation.

show abstract

“…C3d (or C3c) was found in PTC in 39 to 60% of biopsies from HLA-mismatched grafts with diffuse PTC C4d (8,(27)(28)(29). In general C3d and C4d were correlated.…”

Section: Other Complement Components Have Not Yet Proved Diagnosticalmentioning

confidence: 78%

Section: Other Complement Components Have Not Yet Proved Diagnosticalmentioning

confidence: 99%

Antibody-Mediated Renal Allograft Rejection

Colvin

2007

Journal of the American Society of Nephrology

493

447

View full text Add to dashboard Cite

show abstract

“…Findings from two recent studies suggest that additional staining of renal allograft biopsies for C3d, a cleavage product of complement component C3 that also binds covalently to tissue, may be useful in identifying particularly aggressive cases of acute AMR (24,25). Sund et al (24), in 37 protocol biopsies that were taken a median of 7 d after transplantation, found C4d in 11, with concurrent C3d deposition in three.…”

Section: Acute Amrmentioning

confidence: 99%

Antibody-Mediated Rejection in Renal Allografts

Racusen¹,

Haas²

2006

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

The past 15 years have seen major advances in the understanding of the effects of anti-donor antibodies on renal allografts at various stages after transplantation. These advances have been due in large part to pathologic examination of both early and late renal allograft biopsies, including both routine histologic evaluation and immunohistology to detect complement split products. As pathologists have become increasingly adept at diagnosing antibody-mediated rejection (AMR) on allograft biopsies, substantial progress has been made in the treatment of AMR and in successful renal transplantation in recipients with pre-existing antibodies against donor blood group (ABO) and/or major histocompatibility (HLA) antigens. This article reviews the pathologic features of hyperacute, acute, and chronic AMR, including some newer findings impacting diagnosis and outcomes, and differences in the implications of similar pathologic findings in ABO-versus HLA-incompatible renal allografts.

show abstract

“…Our data seems to be conflicting with a previous report, which, however, analyzed complement activation in clearly different population of transplanted patients. [41][42][43] In particular, Haas et al 41 reported no C4d deposits in postimplantation biopsies performed 1 hour after reperfusion. Although most of their cases were transplantations from living donors, with a very limited cold ischemia time, they also reported cases of deceased donor kidney transplantations with over 30 hours of cold ischemia.…”

Section: -38mentioning

confidence: 99%

Therapeutic Targeting of Classical and Lectin Pathways of Complement Protects from Ischemia-Reperfusion-Induced Renal Damage

Castellano

Melchiorre

Loverre

et al. 2010

The American Journal of Pathology

134

121

View full text Add to dashboard Cite

Ischemia-reperfusion injury is the major cause of delayed graft function in transplanted kidneys, an early event significantly affecting long-term graft function and survival. Several studies in rodents suggest that the alternative pathway of the complement system plays a pivotal role in renal ischemia-reperfusion injury. However, limited information is currently available from humans and larger animals. Here we demonstrated that 30 minutes of ischemia resulted in the induction of C4d/C1q, C4d/MLB, and MBL/MASP-2 deposits in a swine model of ischemia-reperfusion injury. The infusion of C1-inhibitor led to a significant reduction in peritubular capillary and glomerular C4d and C5b-9 deposition. Moreover, complement-inhibiting treatment significantly reduced the numbers of infiltrating CD163 ؉ , SWC3a ؉ , CD4a ؉ , and CD8a

show abstract

Complement activation in early protocol kidney graft biopsies after living-donor transplantation1

Cited by 54 publications

References 34 publications

Antibody-Mediated Renal Allograft Rejection

Antibody-Mediated Renal Allograft Rejection

Antibody-Mediated Rejection in Renal Allografts

Therapeutic Targeting of Classical and Lectin Pathways of Complement Protects from Ischemia-Reperfusion-Induced Renal Damage

Contact Info

Product

Resources

About