Renal arachidonic acid metabolism and cellular changes in the rabbit renal vein constricted kidney: inflammation as a common process in renal injury models.

The process of renal inflammation was examined using the partial renal vein constricted rabbit kidney ( RVC ) as a model. Forty eight hours of partial renal vein constriction in the rabbit was associated with an increase in prostaglandin (PG) and thromboxane (Tx) production. The ex vivo perfused RVC kidney showed an enhanced time-dependent increase in PG and Tx production in response to bradykinin stimulation when compared with the unaltered contralateral ( CLK ) or normal kidney. At 6 hrs of perfusion bradykinin stimulation released 2950 +/- 350 ng PGE2, 61 +/- 15 ng TxB2 from the RVC , and 225 +/- 85 ng PGE2 and undetectable TxB2 from the CLK . Histological examination of the RVC cortex showed an increase in fibroblast-like cells, a modest increase in the interstitial space and an appearance of macrophages and lymphocytes not seen in the normal or CLK . Endotoxin has been reported to stimulate macrophages in culture to produce PGE2 and TxB2. Endotoxin (100 ng) stimulation of the perfused RVC kidney caused an immediate, followed by a chronically increasing, release of PGs and Tx. Two hours after endotoxin injection 50 ml of effluent from the RVC contained 1450 +/- 107 ng PGE2 and 15.0 +/- 4.5 ng TxB2. Other animals of renal inflammation (e.g., the hydronephrotic kidney, chronic glomerulonephritis) also show the histological appearance of macrophages. In addition, hydronephrotic kidneys undergo fibroblast proliferation and changes in arachidonic acid metabolism similar to that we observed in the RVC . This work suggests that the inflammatory process (mononuclear cell infiltration, fibroblast-like cell proliferation, and accompanying changes in arachidonate metabolism is common among different forms of renal injury.