*Purpose: Macrophage infiltration, as an expression of early inflammation, is associated with unfavorable kidney graft outcome in protocol biopsies. However, few studies have evaluated the impact of interstitial CD68⁺ cells infiltration in for cause biopsies performed in clinical practice.

*Methods: We therefore prospectively evaluated 52 kidney transplant recipients (KTRs) who underwent kidney biopsy for mild graft dysfunction, as expressed by slight increase in serum creatinine, and/or mild proteinuria (greater than 0.3 g/24 hr), occurring in the first post-transplant year. Biopsies showing acute rejection (12), BKV nephropathy (2) or recurrent glomerular disease (1) were excluded. Thus, 38 KTRs were finally included in the study. Banff score, CD68⁺ count by immunohistochemistry, and 1-yr de novo donor-specific antibodies (DSA) were assessed in all.

*Results: Fifteen KTRs showed high CD68⁺ infiltration (greater than 400 cells/mm²), and 47% of them developed de novo DSA, vs 18% in the lower CD68⁺ group. During a 6.2±2.7 year follow-up, 17 KTRs lost their graft (12 in the high CD68⁺ group). Graft survival was lower in KTRs with higher CD68⁺ infiltration (P=0.0009; log-rank test). Multivariate Cox regression analysis showed that high CD68⁺ infiltrate was the most significant predictor of graft loss (HR 5.41, 95% CI 1.74 to 16.8; P=0.003), together with more severe graft dysfunction at biopsy (HR 6.41, 95% CI 2.57 to 16; P<0.001), whereas both IFTA and de novo DSA were not associated with outcome in the multivariable model.

*Conclusions: Early subclinical CD68⁺ interstitial infiltration regardless of IFTA and de novo DSA development, was the most significant predictor of subsequent graft loss in KTRs with early, subclinical, mild kidney graft dysfunction.

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