The Utility of 1- and 3-Month Protocol Biopsies on Renal Allograft Function: A Randomized Controlled Study

Kurtkoti, Jagadeesh; Sakhuja, Vinay; Sud, Kamal; Minz, Mukut; Nada, Ritambhra; Kohli, Harbir Singh; Gupta, Krishan Lal; Joshi, Kusum; Jha, Vivekanand

doi:10.1111/j.1600-6143.2007.02049.x

Cited by 83 publications

(57 citation statements)

References 35 publications

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“…It is noteworthy that IFTAþi is associated with episodes of acute rejection and increased levels of HLA mismatch [15,17], as well as a rejectionlike gene expression signature [16,20]. Taken together, these findings expand upon earlier work that demonstrates that subclinical TCMR is associated with poor graft outcomes [21][22][23][24] and suggests that IFTAþi may represent an ongoing, low-grade cellular rejection state that is not recognized in the current Banff schema [15,25] and may be amenable to intervention.…”

Section: Introductionsupporting

confidence: 71%

Urinary biomarkers of renal transplant outcome

Rush²,

Nickerson³

2015

Current Opinion in Organ Transplantation

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Urinary chemokines may identify recipients who are at high risk of graft loss. The early detection of high-risk recipients may allow for more intensive posttransplant surveillance; avoidance of drug minimization/withdrawal protocols; and the identification of patients who may benefit from enrolment in novel interventional trials. Prospective trials are needed to demonstrate that urinary chemokine-guided posttransplant surveillance strategies improve long-term graft outcomes.

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Section: Introductionsupporting

confidence: 71%

Urinary biomarkers of renal transplant outcome

Rush²,

Nickerson³

2015

Current Opinion in Organ Transplantation

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“…This result confirms the findings of recent clinical trials showing that indolent TCMR can be adequately treated and is not associated per se with graft loss in adherent patients. 10,24 However, late TCMR could be a warning sign of nonadherence, which can have a devastating effect on kidney allograft survival, often precipitating ABMR. 5 In our study, all patients with subclinical TCMR received steroid pulse-based therapy, suggesting that early screening and adapted therapy may be beneficial over the long term.…”

Section: Discussionmentioning

confidence: 99%

Subclinical Rejection Phenotypes at 1 Year Post-Transplant and Outcome of Kidney Allografts

Loupy

Vernerey

Tinel

et al. 2015

Journal of the American Society of Nephrology

264

237

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Kidney allograft rejection can occur in clinically stable patients, but long-term significance is unknown. We determined whether early recognition of subclinical rejection has long-term consequences for kidney allograft survival in an observational prospective cohort study of 1307 consecutive nonselected patients who underwent ABO-compatible, complement-dependent cytotoxicity-negative crossmatch kidney transplantation in Paris (2000Paris ( -2010. Participants underwent prospective screening biopsies at 1 year post-transplant, with concurrent evaluations of graft complement deposition and circulating anti-HLA antibodies. The main analysis included 1001 patients. Three distinct groups of patients were identified at the 1-year screening: 727 (73%) patients without rejection, 132 (13%) patients with subclinical T cell-mediated rejection (TCMR), and 142 (14%) patients with subclinical antibody-mediated rejection (ABMR). Patients with subclinical ABMR had the poorest graft survival at 8 years post-transplant (56%) compared with subclinical TCMR (88%) and nonrejection (90%) groups (P,0.001). In a multivariate Cox model, subclinical ABMR at 1 year was independently associated with a 3.5-fold increase in graft loss (95% confidence interval, 2.1 to 5.7) along with eGFR and proteinuria (P,0.001). Subclinical ABMR was associated with more rapid progression to transplant glomerulopathy. Of patients with subclinical TCMR at 1 year, only those who further developed de novo donor-specific antibodies and transplant glomerulopathy showed higher risk of graft loss compared with patients without rejection. Our findings suggest that subclinical TCMR and subclinical ABMR have distinct effects on long-term graft loss. Subclinical ABMR detected at the 1-year screening biopsy carries a prognostic value independent of initial donor-specific antibody status, previous immunologic events, current eGFR, and proteinuria.

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“…Therapy of subclinical rejection remains to be a subject of debate. While some authors referred benefits of subclinical rejection treatment [7][8][9][10], others did not [11,12].…”

Section: Introductionmentioning

confidence: 99%

Molecular Patterns of Subclinical and Clinical Rejection of Kidney Allograft: Quantity Matters

Wohlfahrtová¹,

Tycova²,

Honsová

et al. 2015

Kidney Blood Press Res

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Background/Aims: Subclinical rejection diagnosed from protocol biopsies is thought to be a risk factor of long- term allograft dysfunction. The reason why in some patients subclinical rejection does not represent risk for progression is not fully understood. Methods: The intragraft expression of 376 target genes involved in chemokine defense, apoptosis, inflammation, tolerance and TGF-β signalling pathways was measured using quantitative real-time RT-PCR (2^-∆∆^Ct) method in subclinical inflammation (SCI, n=10), clinical inflammation in acute T-cell mediated rejection (CI, n=10) and no rejection samples (n=9). Results: Clinical inflammation group showed a increased expression of genes for chemotaxis mediating cytokines (CCL1, CCL17, CCL24, CCL25, CCL26), cytokine receptors (CCR1, CCRL2, IL1RAPL2, CXCR5), proinflammatory cytokines (IL12A, LTA), inflammatory mediator (PTAFR), complement protein C3, executioner protein of apoptosis (CASP7), growth factor (TGFA), colony stimulating factor (CSF-2), proteins involved in dendritic cells differentiation and interaction (CD209, LAMP3), regulation of immune response (LILRB2, LILBRB4). The quantitative difference in transcripts signature between SCI and CI is consistent with stronger proinflammatory setting of CI. Prostaglandin E2 receptor gene expression was independently associated with lower risk of further graft function deterioration (OR 0.11, CI 0.01-0.78, p<0.0001). Conclusion: Subclinical acute kidney inflammation has transcriptional profile of immune injury of lower extend compared to clinical acute inflammation.

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The Utility of 1- and 3-Month Protocol Biopsies on Renal Allograft Function: A Randomized Controlled Study

Cited by 83 publications

References 35 publications

Urinary biomarkers of renal transplant outcome

Urinary biomarkers of renal transplant outcome

Subclinical Rejection Phenotypes at 1 Year Post-Transplant and Outcome of Kidney Allografts

Molecular Patterns of Subclinical and Clinical Rejection of Kidney Allograft: Quantity Matters

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