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Endogenous alpha2-antiplasmin does not enhance glomerular fibrin deposition or injury in glomerulonephritis

A R Kitching1, A L Turner, K-M O'Sullivan

  • 1Center for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Center, Clayton, Victoria, Australia. richard.kitching@med.monash.edu.au

Journal of Thrombosis and Haemostasis : JTH
|August 28, 2003
PubMed

Insights

Alpha-2-antiplasmin (alpha2-AP) does not significantly impact glomerular fibrin deposition or kidney damage in crescentic glomerulonephritis. Mice lacking alpha2-AP showed similar disease severity and fibrin accumulation compared to normal mice.

Area of Science:

  • Nephrology
  • Immunology
  • Coagulation and Fibrinolysis

Background:

  • Fibrin deposition is a key factor in glomerular injury during crescentic glomerulonephritis (GN).
  • The plasminogen-plasmin system regulates fibrinolysis, balancing coagulation's role in fibrin accumulation.
  • Alpha-2-antiplasmin (alpha2-AP) is a primary inhibitor of plasmin and is present in renal tissues.

Purpose of the Study:

  • To investigate the role of endogenous alpha2-AP in glomerular fibrin deposition within crescentic GN.
  • To determine if alpha2-AP deficiency influences the severity of immune-mediated renal injury.

Main Methods:

  • Induction of crescentic antiglomerular basement membrane GN in mice with and without alpha2-AP.
  • Assessment of glomerular fibrin deposition, crescent formation, and renal function (serum creatinine).
  • Analysis of related proteins (plasminogen, tPA, uPA, PAI-1) and fibrinolytic activity in kidneys.

Main Results:

  • Alpha2-AP was found in tubulointerstitium and glomeruli of affected mice.
  • Mice lacking alpha2-AP (alpha2-AP-/-) exhibited comparable glomerular fibrin deposition, crescent formation, and renal impairment to wild-type mice (alpha2-AP+/+).
  • Alpha2-AP deficiency led to enhanced renal fibrinolytic capacity without compensatory changes in key fibrinolytic proteins or activity.

Conclusions:

  • Endogenous alpha2-AP does not play a significant role in net glomerular fibrin deposition in crescentic GN.
  • Alpha2-AP is not critical for crescent formation or the development of renal impairment in this model of GN.
  • Enhanced fibrinolytic capacity in alpha2-AP deficient mice does not prevent disease progression.
Abstract

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