Renal prostaglandins in systemic lupus erythematosus.
Inhibition of prostaglandin synthesis at the prostaglandin synthetase and phospholipase steps could account for acute changes in renal function which are sometimes induced in patients with systemic lupus erythematosus (S.L.E.) by nonsteroidal anti-inflammatory drugs and high-dose corticosteriids, respectively. Renal function in S.L.E. patients seems to be more susceptible to inhibition of prostaglandin synthesis than in normal subjects. This susceptibility, in conjunction with increased urinary excretion of prostaglandin compounds, indicates that renal function in  S.L.E. patients may depend on enhanced renal prostaglandin production for the maintenance of renal haemodynamics.
D001241:Aspirin / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D008180:Lupus Erythematosus, Systemic / Q000503:physiopathology*; D008775:Methylprednisolone / Q000494:pharmacology; D009393:Nephritis / Q000503:physiopathology*; D010740:Phospholipases / Q000037:antagonists & inhibitors; D011448:Prostaglandin Antagonists; D011458:Prostaglandins E / Q000096:biosynthesis*
D016861:Cyclooxygenase Inhibitors; D011448:Prostaglandin Antagonists; D011458:Prostaglandins E; D010740:Phospholipases; D001241:Aspirin; D008775:Methylprednisolone