Significance of Glomerular Deposition of Apolipoprotein (a) in Various Glomerulopathies

Takahashi, Hiroyuki; Sato, Hírokazu; Takashima, N; Arakawa, Masaaki; Gejyo, Fumitake

doi:10.1159/000169177

Cited by 5 publications

(1 citation statement)

References 24 publications

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“…In mice, the absence of PAI-1 does not enhance renal plasmin activity after either glomerular or interstitial injury (65,79), suggesting that increased plasmin generation, facilitated by the absence of PA inhibition, remains efficiently countered in the kidney by a local or systemic plasmin inhibitor (in the mouse, other inhibitors, e.g., ␣2-macroglobulin or TAFI, might play such a role). Patients with glomerulopathies in whom plasmin-␣2-AP complexes are detected in the glomerular tuft exhibit more endothelial damage and more crescents and have more severe hematuria (80). Whether the presence of plasmin-␣2-AP complexes is a secondary phenomenon or accounts for the greater disease severity is unknown.…”

Section: Role Of Paimentioning

confidence: 99%

Role of the Coagulation/Fibrinolysis System in Fibrin-Associated Glomerular Injury

Hertig¹,

Rondeau²

2004

Journal of the American Society of Nephrology

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Abstract. In the past decade, numerous experimental studies of genetically engineered mice have confirmed the involvement of the coagulation/fibrinolysis system during glomerular inflammation and repair, revealing many unexpected biologic effects far beyond fibrin formation and clearance. Resident glomerular cells and macrophages seem to act in concert to ensure the long-term consolidation of local injury and progression toward glomerulosclerosis. These recent advances will probably pave the way to a new therapeutic approach to renal diseases. However, the balance governing glomerular permeability is very delicate, and many issues will have to be dealt with before targeting this system. Fibrin deposition is a prominent feature of crescentic glomerulonephritis and of the hemolytic uremic syndrome (HUS). Fibrin clots not only interrupt capillary blood flow, leading to irreversible ischemia and glomerular obsolescence, but also promote the influx of monocyte-macrophages and proliferation of epithelial cells in Bowman's space (Figure 1). It therefore is important to understand the mechanisms underlying fibrin formation (i.e., activation of intraglomerular coagulation) and fibrin persistence (i.e., deficiency of the fibrinolysis system). Major advances have been made during the past decade, notably by using mice in which key factors in the coagulation/ fibrinolysis pathways were genetically altered. Two principal notions have emerged. First, the glomerulus must no longer be seen as a regular capillary ball whose main function is blood ultrafiltration but as an autarchic multicellular structure finely regulating its own vascular permeability. Second, most of the mediators involved have specific, nonredundant properties that extend beyond the vascular compartment and fibrin formation per se, also controlling inflammation and lesion repair. We review the most recent findings in this field and identify the major outstanding questions.

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Section: Role Of Paimentioning

confidence: 99%