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Kidney Week

Abstract: TH-PO1006

Investigating Angiotensin II-Regulated Proteins as Biomarkers of Fibrosis in Kidney Transplant Recipients

Session Information

Category: Transplantation

  • 1702 Transplantation: Clinical and Translational


  • Mohammed-Ali, Zahraa, University Health Network, Toronto, Ontario, Canada
  • Reid, Shelby, Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada
  • Tokar, Tomas, Princess Margareth Cancer Center, Toronto, Ontario, Canada
  • Yip, Paul M., University Health Network, Toronto, Ontario, Canada
  • Tavares-Brum, Alexandre, Centre Hospitalier de l'Université de Montréal, Montral, Quebec, Canada
  • Cardinal, Heloise, Centre Hospitalier de l'Université de Montréal, Montral, Quebec, Canada
  • Kim, Joseph, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada
  • Konvalinka, Ana, University Health Network, University of Toronto, Toronto, Ontario, Canada

AngiotensinII, the main effector of the renin-angiotensin system (RAS), causes kidney interstitial fibrosis/tubular atrophy (IFTA). However, specific markers of kidney AngII activity remain unknown. Here we report on the urine excretion of 6 AngII-regulated proteins (BST1, GLNA, LAMB2, LYPLA1, RHOB and TSP1), and show that 1) they reflect IFTA in kidney transplant recipients; 2) they are modified by RAS inhibition.


A previously developed mass spectrometry-based assay was used to quantify 6 AngII-regulated proteins in urine of 2 cohorts of kidney transplant recipients from a single Canadian centre: 1) 19 patients with IFTA and 19 stable controls with concomitant urine and biopsy samples; 2) 20 patients with urine and biopsy samples before and after RAS inhibition. Differences in creatinine-adjusted urine levels of AngII-regulated proteins between IFTA and control patients were assessed using two-tailed t-test. Correlations between AngII-regulated proteins and traditional markers of kidney graft function were evaluated using Spearman’s rank correlation. Fixed-effects model was used to assess changes in AngII-regulated proteins following RAS therapy.


Urine excretion of all AngII-regulated proteins was significantly higher in IFTA compared to control (In fmol/µmol of creatinine ± SD, BST1: 17.46±0.65 vs 9.76±0.20, p=0.01; GLNA: 9.73±0.52 vs 1.62±0.17, p=0.009; LAMB2: 90.22±2.99 vs 54.05±1.55, p=0.03; LYPLA1: 6.61±0.77 vs 2.13±0.05, p=0.0002; RHOB: 9.02±3.42 vs 1.10±0.13, p=0.004; TSP1: 8.05±0.81 vs 3.47±0.16; p=0.002). These proteins correctly separated IFTA and control patients in unsupervised hierarchical clustering analysis. Urine excretion of all AngII-regulated proteins correlated with each other, but not with serum creatinine and total urine protein. All AngII-regulated proteins negatively correlated with RAS inhibitor use over time (fixed effects coefficient<0); however, GLNA and TSP-1 were most significantly decreased (p<0.05).


Urine excretion of AngII-regulated proteins was significantly increased in patients with IFTA and was modified by RAS inhibition. These proteins may represent coveted markers of kidney fibrosis, and may be valuable in guiding therapy with RAS inhibitors.


  • Government Support - Non-U.S.