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An Assessment of the Value of Donor-derived Cell-free DNA Surveillance in Patients With Preserved Kidney Allograft Function. | LitMetric

AI Article Synopsis

  • Donor-derived cell-free DNA (dd-cfDNA) is a potential biomarker for detecting kidney transplant rejection, but its value in routine monitoring amidst overall stable kidney function remains uncertain.
  • In a study involving 317 kidney transplant recipients with good function, patients were grouped based on dd-cfDNA levels to observe future adverse events like rejection or graft loss.
  • Results showed higher rejection rates in those with elevated dd-cfDNA compared to low levels, but most patients with elevated levels remained stable over time, prompting the need for further research to identify which patients with high dd-cfDNA may actually experience negative outcomes.

Article Abstract

Background: Donor-derived cell-free DNA (dd-cfDNA) is a biomarker validated to detect rejection when measured to assess kidney allograft dysfunction. However, it remains unclear whether routine surveillance with dd-cfDNA provides additional information over standard monitoring of kidney allografts with creatinine and donor-specific antibodies (DSAs), particularly among those with little suspicion of rejection or injury. We investigated the value of measuring dd-cfDNA in patients with preserved allograft function and describe its association with future events.

Methods: Three-hundred seventeen kidney transplant recipients with a creatinine ≤1.5 mg/dL, no current DSA, and no prior rejection were assessed with dd-cfDNA and categorized into low (dd-cfDNA <0.5%; n = 239), moderate (dd-cfDNA 0.5% to <1.0%; n = 43), and high (dd-cfDNA ≥1.0%; n = 35) groups. The occurrence of rejection, DSA, graft loss, and change in estimated glomerular filtration rate over time after dd-cfDNA assessment was compared.

Results: Over follow-up, rejections were more commonly found among patients with high vs low dd-cfDNA (17% versus 5%; P = 0.01); a similar nonsignificant trend was observed among patients with moderate compared to low dd-cfDNA (12% versus 5%; P = 0.13). DSA development was uncommon and not different between groups (low: 4%; moderate: 3%; high: 0%; P = 0.52). There was only 1 graft loss in a patient with low dd-cfDNA, and dd-cfDNA was not associated with graft dysfunction over time.

Conclusions: Most patients with elevated dd-cfDNA in conjunction with preserved allograft function remained stable over follow-up without deterioration in function or graft loss. Studies are needed to differentiate patients with elevated dd-cfDNA who will develop adverse outcomes from those who will remain clinically stable.

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Source
http://dx.doi.org/10.1097/TP.0000000000004267DOI Listing

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