The effects of plasma from IgA nephropathy patients on vascular prostacyclin and platelet cyclic AMP production.
The effects of plasma from 10 IgA nephropathy patients and from ten controls were studied on vascular prostacyclin (PGI2) production, the cyclic AMP (cAMP) level and the aggregation of normal platelets. The ability of the plasma to support PGI2-like activity (PSA) was significantly lower in the group of patients (18.0 +/- 13.3%) than in the controls (52.6 +/- 12.9%). The concentration of 6-keto-PGF1 alpha in the supernatant of the vascular tissue was also lower following incubation with patient plasma than with control plasma (p less than 0.001). The reduced PGI2 released by the patient plasma led to a significantly lower platelet cAMP than that following the control plasma (p less than 0.01). There was a significantly positive correlation between the 6-keto-PGF1 alpha and the plasma PSA, and also between both the plasma PSA and 6-keto-PGF1 alpha concentrations and the platelet cAMP level. These findings suggest that a vascular PGI2 defect may cause a reduced cAMP production and an uninhibited aggregation of platelets, which might play a role in the pathogenesis of IgA nephropathy.
Túri
S
S
Department of Paediatrics, Albert Szentgyörgi University Medical School, Szeged, Hungary.
Nagy
J
J
Torday
C
C
Havass
Z
Z
Bereczky
C
C
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000328:Adult; D001792:Blood Platelets / Q000378:metabolism; D000242:Cyclic AMP / Q000097:blood*; D011464:Epoprostenol / Q000096:biosynthesis*; D005922:Glomerulonephritis, IGA / Q000097:blood*; D006801:Humans; D066298:In Vitro Techniques; D010974:Platelet Aggregation; D014469:Umbilical Arteries / Q000378:metabolism
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D000242:Cyclic AMP