Deficiency of a plasma factor stimulating vascular prostacyclin generation in patients with lupus nephritis and glomerular thrombi and its correction by ancrod: in-vivo and in-vitro observations.
Glomerular thrombi occur frequently in active lupus nephritis. Their presence has been correlated with low platelet counts and with subsequent development of glomerular sclerosis. We have examined the plasma PGI2 generating capacity of 8 patients with active lupus nephritis with thrombi that were to undergo defibrination therapy with ancrod. PGI2 generation by these plasma samples was significantly decreased as compared both to normals and to 6 individuals with lupus nephritis and no glomerular thrombi. Significant improvement in the capacity to generate PGI2 was seen in the post-ancrod treatment plasma samples. the pathogenesis of this defect is discussed.
D000721:Ancrod / Q000627:therapeutic use*; D011464:Epoprostenol / Q000096:biosynthesis* / Q000097:blood; D005921:Glomerulonephritis / Q000097:blood* / Q000150:complications; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000150:complications; D011448:Prostaglandin Antagonists / Q000097:blood; D011453:Prostaglandins / Q000096:biosynthesis*; D013927:Thrombosis / Q000097:blood / Q000188:drug therapy / Q000209:etiology
D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011464:Epoprostenol; D000721:Ancrod