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Updated: May 9, 2026
16:15
Mouse Kidney Transplantation: Models of Allograft Rejection
Published on: October 11, 2014
Microvascular Inflammation in Kidney Transplantation
Emmett Tsz Yeung Wong1,2,3, Robert Balshaw4, Ian W Gibson5,6
1Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.
Summary
Microvascular inflammation in kidney transplants, defined by glomerulitis and peritubular capillaritis scores, does not independently predict graft loss when adjusted for T-cell-mediated rejection and de novo donor-specific antibodies.
Area of Science:
- Nephrology
- Transplantation Immunology
- Pathology
Background:
- Microvascular inflammation (g+ptc≥2) is common in kidney transplants, often occurring with T-cell-mediated rejection (TCMR) or de novo donor-specific antibodies (dnDSA).
- The independent prognostic value of microvascular inflammation without DSA is not well understood.
Purpose of the Study:
- To determine the independent impact of microvascular inflammation (g+ptc≥2), TCMR, and dnDSA on death-censored allograft loss.
- To analyze these factors in a modern kidney transplant cohort using time-dependent analyses.
Main Methods:
- A single-center cohort of 689 kidney transplant recipients (2004-2021) was analyzed.
- Cox models with time-dependent covariates were used to assess the impact of g+ptc≥2, TCMR, and dnDSA on graft survival.
- Events were analyzed individually and in a combined model.
Main Results:
- Microvascular inflammation (g+ptc≥2) occurred in 15% of recipients, with 88% having concurrent or sequential TCMR and/or dnDSA.
- Individually, g+ptc≥2, TCMR, and dnDSA were associated with graft loss.
- In a combined model, only TCMR and dnDSA remained independently associated with death-censored allograft loss.
Conclusions:
- In contemporary kidney transplant recipients on tacrolimus, microvascular inflammation (g+ptc≥2) without DSA does not independently predict graft loss.
- TCMR and dnDSA are the primary drivers of graft loss in this context.
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