Acute kidney injury after transplantation = Delayed graft function (DGF)
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1 Acute kidney injury after transplantation = Delayed graft function (DGF) PD Dr. med. Bernd Schröppel Section of Nephrology University Hospital Ulm, Germany 1
2 DGF and donor source Live donor: 3% Standard criteria: 21% Expanded criteria donor (ECD): 33% Donation after cardiac death (DCD): 40% SRTR 2008
3 cumulative probability of patient survival with graft function DGF and transplant outcome Tapiawala SN, JASN, 2010
4 Biological processes implicated in ischemia and reperfusion Eltzschig, Nat Med 2011
5 Innate immune system Not a separate system, but rather an overlapping response to disturbed tissue integrity. Components: Toll-like receptors Autophagy Complement
6 Concept of donor-derived inflammation: Islet-derived MCP-1 attracts recipient immune cells Schröppel, JASN 2005
7 Damage-associated molecular patterns (DAMPs) cause sterile inflammation Arslan F, Nat. Rev. Cardiol. 2011
8 Islets release HMGB1 and TLR sense injury and mediate early graft failure after transplantation Hypoxia DAMPs TLR2 TLR4 DAMPs Cold ischemia and reperfusion Islet isolation TLR4 TLR2 DAMPs Islets DAMPs TLR2 TLR4 Necrotic cells (exocrine debris) Cytokines Chemokines Sterile peritransplant inflammation activates adaptive immune response (T cells) Islet failure Kruger, Eur J Immunol, 2010
9
10 PNAS 2009
11 TLR4 is up-regulated in deceased donor compared to living donor kidneys Kruger, B, PNAS 2009
12 What are the endogenous TLR ligands? Fibronectin/ Fibrinogen Heparan sulfate Defensins Heat shock proteins Histones High mobility group box protein (HMGB1)
13 What are the endogenous TLR ligands? Fibronectin/ Fibrinogen Heparan sulfate Defensins Heat shock proteins Histones High mobility group box protein (HMGB1)
14 HMGB1 is only expressed in decreased donor kidneys
15 Kidneys with loss-of-function TLR4 mutation have higher rate of immediate graft function n=267 Multivariate P HR (95% CI) TLR4 mutant ( ) Donor Age (y) ( ) Donor Type ( ) CIT (min) ( ) Center ( )
16 HMGB1/TLR4 are critical mediators in IR injury Donor TLR4 affects graft failure in liver transplant recipients. Dhillon, J Hepatol 2010; Oeting, Liver Transpl 2012 Neutralization of HMGB1 protects against renal IR injury. Li J, NDT 2011 HMGB1 contributes to kidney IR injury. Wu, H, JASN 2010 TLR4 regulates endothelial activation during ischemic AKI. Chen J, Kidney Int HMGB1 mediates liver IR injury. Tsung, JEM 2010 HMGB1/TLR4 mediates cardiac IR injury. Zhu, Transplantation 2013
17 HMGB1 as therapeutic target? Oxidation or selective mutation of Cys106 abolished the HMGB1- induced activities. BoxA, a HMGB1 inhibitor, interferes with leukocyte recruitment but not with activation. Anderson, Ann Rev Imm 2011 Kamaza, Immunity 2008; Yang, PNAS 2010, Venereau JEM 2012
18 TLRs as therapeutic targets OPN-305, Humanised Monoclonal Antibody blocking TLR2 Start Feb 2013; Phase 2 (n = 278); NCT Intravenous infusion for 1 hour at start of transplant procedure
19 Autophagy
20 auto - (self), phagy (eating) Quality control & removal of disfunct organelles Energy source during starvation Effector and regulator of innate and adaptive immunity Cell survival and death Schröppel B. Autophagy: Basic Principles and Relevance to Transplant Immunity, Am J Transplant 2014
21 Autophagy and apoptosis autosis Schröppel, B. Am J Transplant 2014
22 Dynamic changes of autophagy in proximal tubules Renal tubular cells of CAG-RFP-EGFP-LC3 mice - puncta outside the autolysosome Resolution of autophagy is accompanied by activation of mtor and by tubular repair Ling Li et al. JASN 2014
23 Autophagie is protective during IR injury Liu, Autophagy 2012
24 Autophagy in Renal Ischemia Reperfusion Injury: Friend or Foe? P. Decuypere, AJT 2014
25 Autophagy in Renal Ischemia Reperfusion Injury: Friend or Foe?
26 Autophagy as therapeutic target? PRO Huge clinical interest (Crohns disease, cancer, aging, diabetes, infection, Alzheimer). CON No validated clinical markers Lack of safe and selective inducers or inhibitors
27 Complement
28 Terminal complement activation is critical in IR injury Damman, AJT 2011
29 Renal cell and bone marrow cell expressed C3aR / C5aR are important Peng Q et al. JASN 2012
30 Complement activation during brain death Werkhoven, AJT 2013
31 Therapeutic interventions? Pilot study, Mount Sinai: Eculizumab in DGF. Pilot study at Mount Sinai: C5a inhibitor eclizumab
32 Complement as therapeutic target C5a inhibitor Eculizumab Start Mai 2014; Phase 2/3 (n = 283) IV infusion on day of transplant then hours later C1 Esterase Inhibitor Start Jul 2014; Phase 1/2 (n = 70) IVP administered on day of transplant, and another dose 24 hours post op.
33 Since activation of innate immune system occurs already before organ donation, complement-based strategies should start shortly after the diagnosis of brain death and extent into the recipient.
34 Barriers for DGF therapeutics To date no validated prognostic tools to predict allograft outcome of the individual donor kidney Defining surrogate endpoints is instrumental to test new treatments. No consensus on the definition of DGF.
35 Schröppel, JASN 2010
36 ATN-diagnosis in the donor kidney is not helpful in predicting DGF or graft failure P=0.01 P=0.3 P=0.9 Hall IE, CJASN 2014
37 Danger and damage is everywhere Hall IE, CJASN 2010
38 Glutathione S-transferase (GST) in perfusion solution Hall, IE, AJT 2014
39 Glutathione S-transferase at the end of perfusion correleates with DGF alpha-gst: released by damaged proximal tubule cells pi-gst: released by distal tubules Hall IE, AJT 2014
40 Danger and damage is everywhere Hall IE, CJASN 2010
41 Donor AKI is associated with kidney discard and DGF Using AKI Network criteria quantified AKI in donors using donor information not available in UNOS database (i.e. changes in SCr) Hall, I. AJT 2015
42 Donor AKI is associated with kidney discard and DGF Donor AKI is common (25% of 1,369 kidneys) Donor AKI is associated with kidney discard and DGF 6-mo egfr was similar across AKI categories but was lower for recipients with DGF Given acceptable 6-mo allograft function, clinicians should consider cautious expansion into this donor pool Currently testing whether novel AKI biomarkers provide added decision-making value in this context Hall, I. AJT 2015
43 The reality of DGF therapeutics Lots of excellent science but Many challenges in translation bench to bedside Animal models (species/strain/gender; WIT/CIT; method of clamping, iso vs. allograft; timing of intervention relative to injury) Logistics and ethics The right timing, target cells, and duration of such therapy? Promising novel therapeutics DGF interventions need to improve long-term outcomes
44 Merci Acknowledgments Organ procurement organizations: Gift of Life Philadelphia, New York Organ Donor Network, Michigan Organ and Tissue Donation Program, New Jersey Sharing Network, New England Organ Bank. Transplant centers: Yale-New Haven (PI Chirag Parikh); University of Pennsylvania, Barnabas Health, Mount Sinai, Harper Hospital. Supported by NIH
45 Pi-GST am Ende der Perfusion ist mit DGF assoziiert Hall IE, AJT 2014
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