Interestingly, even CXCL9 and CXCL10 baseline recipient's serum levels assessed before KTx may predict AR [101,102].

Additionally, urinary CXCR3—the receptor for CXCL9 and CXCL10, expressed on activated T-lymphocytes—was shown to detect subclinical inflammation and correlate with evolution towards chronic damage; of interest, its level decreased after immunosuppression intensification [103].

In another study, serum concentration of chemokine CXCL13, a B lymphocyte chemoattractant, was significantly higher in TCMR than in stable graft and in borderline rejection; furthermore, a marked increase (>5-fold) was found in patients developing AR within first post-transplant week and correlated with entity of B cell infiltration in renal biopsy. A similar correlation was found in a mouse model of TCMR, indicating that CXCL13 serum levels may be a marker of B cell-involvement in TCMR, identifying a severe subset of this type of rejection [104].

On the whole, growing evidence points to a role of urinary and serum chemokines as biomarkers of both types of AR.
