Renal glomerular response to the inhibition of prostaglandin E2 synthesis and protein loading after the relief of unilateral ureteropelvic junction obstruction

Purpose: We investigated glomerular filtration rate and renal function rese rve after the surgical relief of partial obstruction. Materials and Methods: We evaluated 4 boys and 1 girl 9 to 14 years old who underwent pyeloplasty because of unilateral ureteropelvic junction obstruc tion. Contralateral normal kidneys served as controls. The glomerular filtr ation rate (inulin clearance), and urinary excretion of prostaglandin E2, t hromboxane B2 and endothelin were determined at baseline and after a meal o f 4 gm./kg. cooked unsalted red meat on day 4 postoperatively. Tests were r epeated the following day 1 hour after the oral administration of 20 mg./kg . aspirin, an inhibitor of prostaglandin E2 synthesis. Urine was collected separately through a bladder catheter and another catheter placed in the up per renal pelvis at surgery. Results: Glomerular filtration rate at baseline was significantly greater i n normal than in surgically treated kidneys (77.2 ml. per minute, range 60 to 98 versus 63.6, range 43 to 78, p = 0.04). Aspirin did not change baseli ne inulin clearance in normal kidneys but it significantly decreased the gl omerular filtration rate in operated renal units (-4% versus -26.4%, p = 0. 04). The concentration of all vasoactive compounds was not significantly di fferent in the urine specimens of normal and operated kidneys. The administ ration of aspirin resulted in a significant decrease in mean urinary prosta glandin E2 excretion plus or minus standard error in operated but not in no rmal renal units (0.64+/-0.12 ng. per minute versus 0.27+/-0.06, p = 0.04). When expressed as mean versus baseline values, protein induced glomerular hyperfiltration seemed lower in operated than in contralateral intact kidne ys (6.9% and 12.4%, respectively). Conclusions: In the immediate postoperative period previously obstructed ki dneys maintain renal function via mechanisms that depend on the activation of prostaglandin, mimicking normal renal function. This effect is decreased by drugs that inhibit prostaglandin E2 production. Therefore, renal damage may be present when the glomerular filtration rate appears normal.