Antiproliferative activity is present in bladder but not renal pelvic urine from interstitial cystitis patients

Purpose: To determine whether an antiproliferative urine factor that we pre viously discovered to be specific for urine from interstitial cystitis (IC) patients originated in the lower urinary tract or a more proximal site. Materials and Methods: Sequential catheterized urine specimens were collect ed under sterile conditions from the bladder and renal pelvis of 20 IC pati ents and one control patient (with stress incontinence). Antiproliferative activity was determined by H-3-thymidine incorporation of primary normal ad ult bladder epithelial cells cultured with pH- and osmolality-corrected bla dder or ureteral urine specimens; significant inhibition was defined as a c hange in H-3-thymidine incorporation greater than 2 standard deviations fro m the mean of control cells. Results: Bladder urine specimens from 19 of 20 IC patients significantly in hibited H-3-thymidine incorporation as compared to cell medium alone (mean change for bladder specimens = -68.7 +/- 7.5%), while a renal pelvic specim en from only 1 of 20 IC patients inhibited proliferation significantly (mea n change for renal pelvic specimens = 3.2 +/- 3.4%) (p <.001 by Fisher's ex act test). The one inhibitory IC renal pelvic specimen inhibited by 31% whi le a bladder specimen obtained during the same procedure inhibited by 94%. In comparison, neither bladder nor renal pelvic urine from the control pati ent had inhibitory activity. Conclusions: The antiproliferative factor previously found in the urine of IC patients appears to be made and/or activated in the distal ureter or uri nary bladder.