IPPB

International Pediatric Peritoneal Biobank


Within a few years of peritoneal dialysis (PD) the peritoneum undergoes major morphological and functional alterations, which ultimately result in PD failure. PD purification efficiency is limited, and PD patients suffer from rapidly progressing vascular disease.

The International Pediatric Peritoneal Biobank collects parietal peritoneal and omental specimen from patients with normal renal function, CKD, PD with different PD fluids and following renal transplantation across all age groups (0-70 years), together with blood, dialysate and clinical data. It offers unique opportunities to specifically study CKD, PD and Tx related local but also systemic pathomechanisms of tissue transformation and vasculopathy. By means of whole transcriptome and proteome analyses and omental metabolome analyses in healthy CKD, PD and post Tx samples, the biobank aims at comprehensive understanding of the molecular machineries, and provides detailed information for targeted validation studies and (experimental) therapeutic interventions aiming at improving PD efficacy and sustainability but also aiming at understanding systemic disease and identification of potential therapeutic targets.
 

Design:Open, prospective, observational
Patients included: 
  • 72 non-uremic children, 30 adults
  • 140 CKD5 children, 125 adults
  • 105 low GDP PD, 27 adults 
  • 28 high GDP PD, 0 adults
  • 28 post Tx
 
Coordinating Center:University Hospital Heidelberg
Participating Centers:

The International Pediatric Peritoneal Biobank receives samples from a variety of institutions all over the world, including from Austria (Vienna), Belgium (Ghent), Czech Republic (Prague), France (Lyon, Nantes, Strasbourg), Germany (Berlin, Cologne, Essen, Hamburg, Marburg), Greece (Thessaloniki), Hungary (Budapest), Italy (Genova, Milano), Lithuania (Vilnius), Malaysia (Kuala Lumpur), Poland (Krakow), Serbia (Belgrade), Turkey (Adana, Istanbul), Spain (Barcelona), Sweden (Stockholm), United Kingdom (Birmingham), United States (Kansas City, Columbus).

Contact Information:

betti.schaefer@med.uni-heidelberg.de
maria.bartosova@med.uni-heidelberg.de
clauspeter.schmitt@med.uni-heidelberg.de

Envisaged studies:

The International Pediatric Biobanks is open to scientific proposals requiring peritoneal and omental histomorphometric, immunohistological, untargeted and targeted molecular studies. Analysis of the impact of Tx and related medications is envisaged.

Ongoing studies: 
  • Current studies aim at an in-depth understanding of the molecular mechanisms of peritoneal solute and water transport across molecular transporters and junctions and its regulation in CKD and PD.
  • Biopsies are also being collected within the context of peritonitis. Together with PD effluents, these provide unique opportunities to obtain insight in the peritoneal inflammasome, which can be related to the systemic response.
  • Histological and experimental studies are being performed with regard to the different mechanisms of low vs. high GDP PD fluid induced peritoneal membrane transformation and with regard to molecular mechanisms of (high) GDP induced local and systemic vasculopathy
  • Omental metabolome
  • Cooperation partners use the biobank for validation of various experimental studies such as antimicrobial peptides, inhibition of glucose transporters and macrophage polarization
  • Correlation of histomorphometric findings with ultrasound imaging
 

Collaborations including tissue samples from the biobank:

 
  • MicroRNA-21 promotes fibrogenesis in peritoneal dialysis (Lopez-Anton M et al, Am J Pathol 2017) – Cardiff University
  • Thy-1+/- fibroblast subsets in the human peritoneum (Kawka E et al, Am J Physiol Renal Physiol 2017) – Poznan University
 

Finished projects:

 
  • Quantitative Histomorphometry of the Healthy Peritoneum  (Schaefer B et al, Sci Rep 2016)
  • Microvascular Density in Children with Chronic Kidney Disease (Burkhardt D et al, PLoSOne 2016)
  • Impact of PD fluid buffer on peritoneal angiogenesis (Eich G et al, PLoS One 2017)
  • Complement activation in PD induced arteriolopathy (Bartosova M et al, JASN 2018)
  • Neutral pH, low glucose degradation product content PD induced peritoneal membrane transformation (Schaefer B  et al, Kidney Int 2018)
  • Impact of peritonitis on peritoneal membrane integrity (Bartosova M el al, Front in Physiol 2019)
 


Active ESCAPE Participants:

Further Investigators:

B. Becknell, Rainer Büscher, Johan VandeWalle, R. Cerkauskiene, G. Lomic-Milosevski, Bruno Ranchin, C. Taylan, S. Testa, K. Vondrak, B. Warady, J. Yok Chin