INTRINSIC RENAL CELL DERIVED IL‐12 IS AN EFFECTOR OF RENAL GLOMERULAR INJURY IN CRESCENTIC GLOMERULONEPHRITIS

Nephrology ◽  
2000 ◽  
Vol 5 (3) ◽  
pp. A98-A98
Author(s):  
Timoshanko Jr ◽  
Kitching Ar ◽  
Holdsworth Sr ◽  
Tipping PG.
Nephrology ◽  
2000 ◽  
Vol 5 (3) ◽  
pp. A98-A98
Author(s):  
Timoshanko Jr ◽  
Kitching Ar ◽  
Holdsworth Sr ◽  
Tipping PG.

2018 ◽  
Vol 8 (2) ◽  
pp. 161-170
Author(s):  
Ramy M. Hanna ◽  
Naomi So ◽  
Marian Kaldas ◽  
Jean Hou ◽  
Farid Arman ◽  
...  

Hepatitis C (HCV) infection has a prevalence of 3 million infected individuals in the United States, according to recent Center for Disease Control reports, and can have various renal manifestations. Cryoglobulins, antibodies that precipitate at colder temperatures in vitro, are a relatively common cause of renal disease in HCV infection. The cryoglobulin proteins can form occlusive aggregates in small glomerular capillary lumina or deposit in other areas of the glomerulus, resulting in hypocomplementemia, proteinuria, hematuria, and renal injury. The typical biopsy pattern is that of membranoproliferative glomerulonephritis (MPGN). There are, however, other HCV-related patterns of glomerular injury. Anti-neutrophil cytoplasmic antibodies (ANCA) are known to exist in HCV-infected patients. In many reported cases, ANCA serologic testing may appear positive due to cross-reactivity of the immune assays; however, the biopsy findings do not support ANCA-associated crescentic glomerulonephritis (GN)/vasculitis as the primary cause of glomerular injury. There are rare reports of microscopic polyangiitis (MPA) p-ANCA vasculitis, in patients with HCV infection. In comparison with the MPGN pattern of cryoglobulinemic glomerular injury, biopsies from these HCV-infected patients with concomitant MPA revealed a crescentic GN, associated with normal serum complement levels. We present a case of HCV-associated glomerular disease with the surprising biopsy finding of necrotizing and crescentic p-ANCA GN, with a background, low-grade mesangial immune complex GN. Thus, p-ANCA disease should also be considered in HCV-infected patients, in addition to the more typical lesions of MPGN or cryoglobulinemic GN.


1990 ◽  
Vol 88 (2) ◽  
pp. 189-192 ◽  
Author(s):  
Lloyd P. Haskell ◽  
Mary Jean Fusco ◽  
Scott Wadler ◽  
Leonarda B. Sablay ◽  
Ralph P. Mennemeyer

1999 ◽  
Vol 10 (3) ◽  
pp. 499-506
Author(s):  
MALCOLM A. CUNNINGHAM ◽  
XIAO RU HUANG ◽  
JOHN P. DOWLING ◽  
PETER G. TIPPING ◽  
STEPHEN R. HOLDSWORTH

Abstract. The majority of patients with rapidly progressive crescentic glomerulonephritis show histologic features of extensive necrosis and focal and segmental proliferation with fibrin production, but little or absent Ig deposition in the glomerulus. This subcategory of the disease, labeled “pauci-immune” glomerulonephritis, has recently been shown to be associated with the presence of antineutrophil cytoplasmic antibody in the patient's circulation (but not within the glomerulus). The absence of the effectors of humoral immunity at the site of renal injury led to this investigation of the contribution of cell-mediated immunity to the glomerular injury in this form of glomerulonephritis. In 15 patients presenting acutely with pauci-immune glomerulonephritis, CD3-positive T cells (3.7 ± 2.5 [mean ± SD] cells per glomerular cross section, [c/gcs]), CD45RO-positive T cells (2.7 ± 1.9 c/cgs), macrophages (7.3 ± 6.1 c/gcs), fibrin (3+), and endothelial-associated tissue factor were demonstrated to be prominent in glomeruli. These mediators were absent in a group of 12 patients with thin basement membrane disease and only occasionally observed in a group of eight patients with “humorally mediated” (noncrescentic) glomerulonephritis. Thus, in pauci-immune glomerulonephritis, there is the development of significant cell-mediated immunity with activated T cells, macrophages, tissue factor, and fibrin at the site of glomerular injury, suggesting that this glomerular disease is most likely a manifestation of T cell-directed cognate immune injury.


Immunology ◽  
2009 ◽  
Vol 128 (1) ◽  
pp. 114-122 ◽  
Author(s):  
Ming Li ◽  
Kim M. O’Sullivan ◽  
Lynelle K. Jones ◽  
Cecilia Lo ◽  
Timothy Semple ◽  
...  

1997 ◽  
Vol 185 (5) ◽  
pp. 963-968 ◽  
Author(s):  
A. Richard Kitching ◽  
Stephen R. Holdsworth ◽  
Victoria A. Ploplis ◽  
Edward F. Plow ◽  
Désiré Collen ◽  
...  

The plasminogen/plasmin system has the potential to affect the outcome of inflammatory diseases by regulating accumulation of fibrin and other matrix proteins. In human and experimental crescentic glomerulonephritis (GN), fibrin is an important mediator of glomerular injury and renal impairment. Glomerular deposition of matrix proteins is a feature of progressive disease. To study the role of plasminogen and plasminogen activators in the development of inflammatory glomerular injury, GN was induced in mice in which the genes for these proteins had been disrupted by homologous recombination. Deficiency of plasminogen or combined deficiency of tissue type plasminogen activator (tPA) and urokinase type plasminogen activator (uPA) was associated with severe functional and histological exacerbation of glomerular injury. Deficiency of tPA, the predominant plasminogen activator expressed in glomeruli, also exacerbated disease. uPA deficiency reduced glomerular macrophage infiltration and did not significantly exacerbate disease. uPA receptor deficiency did not effect the expression of GN. These studies demonstrate that plasminogen plays an important role in protecting the glomerulus from acute inflammatory injury and that tPA is the major protective plasminogen activator.


Sign in / Sign up

Export Citation Format

Share Document