PMID- 33102961
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220417
IS  - 2468-0249 (Electronic)
IS  - 2468-0249 (Linking)
VI  - 5
IP  - 10
DP  - 2020 Oct
TI  - Clinical Use of Complement, Inflammation, and Fibrosis Biomarkers in Autoimmune 
      Glomerulonephritis.
PG  - 1690-1699
LID - 10.1016/j.ekir.2020.07.018 [doi]
AB  - INTRODUCTION: Complement activation, inflammation, and fibrosis play central 
      roles in the mechanisms of injury in autoimmune glomerulonephritis (GN) but they 
      are seldom assessed in epidemiologic studies. The measurement of urinary 
      biomarkers of these pathways of injury could parallel disease activity and add 
      clinical value beyond proteinuria. METHODS: We performed a prospective cohort 
      study of 100 patients with focal and segmental glomerulosclerosis (FSGS), 
      membranous nephropathy (MN), IgA nephropathy (IgAN), lupus nephritis (LN), 
      anti-neutrophil cytoplasmic autoantibody-associated vasculitis (AAV), and 
      membranoproliferative GN (MPGN) followed for 33 (18-54) months. Repeated urinary 
      samples were collected throughout their follow-up to determine proteinuria, 
      urinary sC5b-9, monocyte chemoattractant protein-1 (MCP-1), and transforming 
      growth factor-beta 1 (TGF-beta1), expressed as creatinine ratios. We identified 177 
      periods of active and inactive disease based on current remission definitions for 
      each disease. RESULTS: Urinary sC5b-9, MCP-1, and TGF-beta1 were present in each 
      disease. In periods leading to a remission, the reduction of urinary sC5b-9 was 
      91%, greater than for proteinuria with 76%. During inactive periods, those who 
      did not experience a relapse maintained lower levels of biomarkers compared with 
      those who relapsed. At that time, the increase in urinary sC5b-9 was 
      significantly greater than the rise in proteinuria (8.5-fold increase compared 
      with 3.2-fold) and urinary MCP-1 and TGF-beta1. Using current remission definitions 
      for each disease, thresholds for each biomarker were determined using receiver 
      operating characteristic curves. Individuals who averaged levels below these 
      cutoffs during their follow-up had better renal outcomes. CONCLUSION: In 
      autoimmune glomerular diseases, urinary sC5b-9, MCP-1, and TGF-beta1 are present and 
      parallel disease activity and outcomes. Urinary sC5b-9 appears to be a more 
      discerning marker of immunologic remissions and relapses.
CI  - (c) 2020 International Society of Nephrology. Published by Elsevier Inc.
FAU - Khalili, Myriam
AU  - Khalili M
AD  - Division of Nephrology, Hopital du Sacre-Coeur de Montreal, Quebec, Canada.
FAU - Bonnefoy, Arnaud
AU  - Bonnefoy A
AD  - Division of Hematology, Centre Hospitalier Universitaire Sainte-Justine, 
      Montreal, Quebec, Canada.
FAU - Genest, Dominique S
AU  - Genest DS
AD  - Division of Nephrology, Hopital du Sacre-Coeur de Montreal, Quebec, Canada.
FAU - Quadri, Jeremy
AU  - Quadri J
AD  - Division of Hematology, Centre Hospitalier Universitaire Sainte-Justine, 
      Montreal, Quebec, Canada.
FAU - Rioux, Jean-Philippe
AU  - Rioux JP
AD  - Division of Nephrology, Hopital du Sacre-Coeur de Montreal, Quebec, Canada.
AD  - Division of Nephrology, Hotel-Dieu de St-Jerome, Quebec, Canada.
FAU - Troyanov, Stephan
AU  - Troyanov S
AD  - Division of Nephrology, Hopital du Sacre-Coeur de Montreal, Quebec, Canada.
AD  - Division of Nephrology, Hotel-Dieu de St-Jerome, Quebec, Canada.
LA  - eng
PT  - Journal Article
DEP - 20200723
PL  - United States
TA  - Kidney Int Rep
JT  - Kidney international reports
JID - 101684752
PMC - PMC7569694
OTO - NOTNLM
OT  - MCP-1
OT  - TGF-beta1
OT  - autoimmune glomerulonephritis
OT  - complement
OT  - sC5b-9
OT  - urinary biomarkers
EDAT- 2020/10/27 06:00
MHDA- 2020/10/27 06:01
PMCR- 2020/07/23
CRDT- 2020/10/26 05:28
PHST- 2020/05/29 00:00 [received]
PHST- 2020/07/04 00:00 [revised]
PHST- 2020/07/14 00:00 [accepted]
PHST- 2020/10/26 05:28 [entrez]
PHST- 2020/10/27 06:00 [pubmed]
PHST- 2020/10/27 06:01 [medline]
PHST- 2020/07/23 00:00 [pmc-release]
AID - S2468-0249(20)31417-0 [pii]
AID - 10.1016/j.ekir.2020.07.018 [doi]
PST - epublish
SO  - Kidney Int Rep. 2020 Jul 23;5(10):1690-1699. doi: 10.1016/j.ekir.2020.07.018. 
      eCollection 2020 Oct.