It is well known that fibrin deposition in Bowman's space in association with crescent formation may play an important role in progressive glomerular injury in crescentic glomerulonephritis. Recent reports describe the presence of a procoagulant activity (PCA) in the glomeruli and its increased expression in human and experimental nephritis. The cells that synthesize PCA have not yet been identified. We attempted to determine if glomerular epithelial cells (GEC), one of the prominent cell populations in the crescent, can produce PCA. The PCA of cultured rat GEC was measured by clotting and amidolytic assays. The cultured GEC yielded PCA with the characteristics of a tissue factor, and this PCA was stimulated by interleukin 1, tumour necrosis factor-alpha, and lipopolysaccharide. We concluded that GEC produce tissue-factor-like PCA and thereby may contribute to fibrin deposition, which, along with macrophage or monocyte infiltration, leads to crescent formation in crescentic glomerulonephritis.
Serum secretory IgA was measured to elucidate the significance of secretory IgA in patients with IgA nephropathy. The levels of serum secretory IgA and IgA were, respectively, 6.8 ± 3.5 μg/ml and 231.0 ± 69.2 mg/dl in the controls and 11.8 ± 3.2 μg/ml and 385.3 ± 78.7 mg/dl in the patients. The levels of serum secretory IgA and IgA in the patients were significantly higher than those in controls (p < 0.01). Elevated serum secretory IgA may reflect the excessive state of the IgA-secreting system in IgA nephropathy patients.
Two patients with IgA nephropathy and a patient with Henoch-Schönlein purpura nephritis each associated with anterior uveitis are described. As anterior uveitis accompanying IgA nephropathy improved, renal manifestations were relieved. The patient with Henoch-Schönlein purpura nephritis suffered from not only anterior uveitis but also keratitis. It is suggested that immune mechanisms which induce IgA nephropathy may play a role in the development of anterior uveitis and keratitis.
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