Table 2.

Summary of different studies analyzing the transcriptome on surveillance biopsies. IFTA, interstitial fibrosis and tubular atrophy; TCMR, T-cell mediated rejection; QCATs (infiltration of cytotoxic T cells); GRIT1 (interferon-gamma and rejection-induced transcripts); QCMAT (infiltration of macrophages; AMAT1 (alternative macrophage activation); IRITD3 (injury and repair induced transcripts); ENDATs (endothelial transcripts); KT1 and KT2 (kidney parenchymal transcripts).

Reference	Time & Type of Biopsy Sample Size	Methods & Results	Main Conclusion
Sherer A et al. Nephrol Dial Transplant 2009 [49]	Paired 3- and 6-month protocol biopsies.	Affymetrix GeneChip Human Genome U133 Plus 2.0 Arrays	Gene expression profiling of early protocol biopsies identified changes in the transcriptome of grafts, which may be important for development of IFTA.
	Non IFTA progression (n = 12)	IFTA progression is associated with overexpression of T-, B-cell activation, immune response and profibrotic genes.
	IFTA progression (n = 8)	Under expression of genes related with transporter and metabolic functions in IFTA progression.
Vitalone MJ et al.	Paired 0-, 1-, 3- and 12-month protocol biopsies (59 biopsies from 18 patients)	Human 8K cDNA microarrays, Australian Genome Research	Allografts display immune and fibrotic gene expression profiles with patterns of expression gradually varying by time after transplantation.
Transplantation 2010 [48]	Subclinical rejection = 14%	Immune pathway activity peaked at 1-month, fibrotic expression at 3 months, wound healing-remodelling and cell proliferation-repair processes were activated between 3 and 12 months, whereas macrophage-related gene expression occurred late by 12 months	Gene expression predated histologic damage.
Naesens M et al.	Paediatric transplants.	Affymetrix Gene Chip Human Genome U133 Plus 2.0 Arrays	Progressive chronic histological damage is associated with regulation of both innate and adaptive immune responses that cannot be evaluated by histology.
Kidney Int 2011 [50]	24 patients with paired 0-, 6- and 24 months protocol biopsies. 24 patients with TCMR.	Upregulation of adaptive (T- and B-cell signatures) and innate immune cell transcripts (dendritic cell and NK cell transcripts) is already present in biopsies of kidneys several months before chronic histological damage occurs.
Mengel M et al.	6-weeks protocol biopsies (n = 107). TCMR (n = 9), Borderline (n = 20)	Affymetrix Gene Chip Human Genome U133 Plus 2.0 Arrays	The molecular phenotype reflects the injury–repair response to implantation stresses, and has little relationship to future events.
Am J Transplant 2011 [51]		↑ QCAT, QCMAT, GRIT1, AMAT; ↓ KT1-KT2 in TCMR and borderline.
		PBTs correlated with DGF but not with ΔeGFR at 2 years, ΔIF/TA at 6 months or i-Banff at 6 months.
O’Conell PJ et al.	Discovery set: 3-month (n = 159) and 12-month paired protocol biopsies (n = 101).	Affymetrix human exon 1.0 ST array in the discovery set and qPCR in the validation set. 13 genes related with active repair and regeneration pathways predicts the development and progression of chronic allograft damage and subsequent allograft loss	Kidney transplant recipients at risk of allograft loss can be identified before the development of irreversible damage.
The Lancet 2016 [52]	Validation set (n = 45)