*Purpose: Accurate identification of successful treatment for rejection (R) without repeat kidney biopsy (KB) in kidney transplantation is an unmet need. The few existing biomarkers which are monitored during treatment (tx) of active transplant kidney injury e.g. serum creatinine/eGFR can be insensitive markers. DD-cfDNA detected in patients’ plasma has been proposed as a discriminative quantitative marker of allograft injury; validated in adults, but not in children (C). We propose that dd-cfDNA might be a useful adjuvant to follow C after KB and tx.

*Methods: During a 6 month period spanning January to November 2018 we studied the course of dd-cfDNA and eGFR (ml/min/1.73m²)in 9 C(12-18yrs) with kidney transplants: 6 with biopsy-proven R (5 with antibody-mediated R and 1 with Banff 1a cellular R) and 3 C who were stable.RB was performed for unstable clinical data. As dd-cfDNA has not been evaluated in C, CareDx provided compassionate testing. Figure 1 shows the course of dd-cfDNA %. A rank sum test was used to determine differences between treated and stable C.

*Results: The median dd-cfDNA at RB in C with R was 3.6 (2.05,7.45; IQR) and at last follow-up 0.88(0.35,1.40). For stable C, dd-cfDNA at baseline was 0.31(0.19,0.78) and at last follow-up (f/u) 0.27(0.19,0.75). Table 1. Comparison of C with R with those who were stable was significantly different (SD), p=0.034 at KB but not at last f/u, p=0.289. eGFR was not significantly different at either period.

*Conclusions: DD-cfDNA appears to be a distinguishing and reassuring biomarker of a return to a clinically ‘stable’ condition and perhaps successful tx of R in C with kidney transplants, importantly more so than the change in eGFR. Our small cohort study is preliminary, but we feel worthy of further and larger investigation.

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