Role of intraperitoneal urokinase in acute peritonitis and prevention of catheter loss in peritoneal dialysis patients.

Some studies have demonstrated the efficacy and safety of intraperitoneal (i.p.) urokinase in the resolution of recurrent or relapsing peritonitis, while others have not. Most studies were small, and they varied in methodology. Furthermore, the role of i.p. urokinase in shortening the duration of peritonitis or in preventing recurrence after initial peritonitis has not been examined. In addition, no previous studies have examined the role of i.p. urokinase in preventing, after first infection, catheter loss due to unresolving (resistant) peritonitis. Over a period of 3 years, we prospectively randomized into two groups all peritoneal dialysis (PD) patients who developed a first episode of peritonitis. Group I (n = 40) received i.p. urokinase on the first day of diagnosis (5000 IU intraluminally in the peritoneal catheter and left for 4 hours before next exchange). Group II (n = 40) received no urokinase. The duration of peritonitis was assessed by daily PD fluid white blood cell (WBC) count. Indications for catheter removal were: persistent peritonitis after four days from initiation of antibiotic therapy, or peritonitis with multiple organisms, suggesting bowel perforation. No statistically significant difference was seen between the two groups in regard to primary cause of end-stage renal disease (ESRD), age, sex, race, weight, type of dialysis [continuous ambulatory peritoneal dialysis (CAPD), automated peritoneal dialysis (APD), continuous cycling peritoneal dialysis (CCPD)], or duration of dialysis prior to first peritonitis. No statistically significant difference was seen between the two groups in the duration of peritonitis or in the severity of symptoms and signs of peritonitis. Neither was any difference seen in the peritonitis recurrence or relapse rate (10% in the urokinase group vs 7.5% in the control group). Nine patients lost their catheters (3 in the urokinase group: 1 Pseudomonas aeruginosa and 2 Candida tropicalis; 6 in the control group: 1 Klebsiella pneumonia, 1 enterococcus, 2 Pseudomonas aeruginosa, and 2 Candida tropicalis). The difference in the rate of catheter loss between the two groups was not statistically significant; it appeared to relate to the type of organism rather than to the response to urokinase. In conclusion, i.p. urokinase plays no significant role in shortening the course of peritonitis or in preventing recurrence or loss of the PD catheter. Loss of PD catheters in patients having their first peritonitis appears to be related primarily to the type of organism causing the infection.