CORRESPONDENCE
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mg/mL. The unused drug can be stored in polypropylene syringes at -20°C and will remain potent for 6 months. 3 Because it is uncertain whether refreezing after thawing will affect the potency of the drug, it would be prudent to refrain from using any refrozen drug. Our experience suggests that alteplase is an effective thrombolytic agent in the declotting of peritoneal dialysis catheters. The nonallergenic nature of alteplase, allowing the possibility of repetitive use. makes this agent more attractive than streptokinase. Mandeep M. Sahani, MD Kunwer N. Mukhtar, MD Rajesh Boorgu, MD David J. Leehey, MD Subhash Popli, MD Todd S. lng, MD Division of Nephrology LoyolalHines VA Medical Center Hines. Illinois
TISSUE PLASMINOGEN ACTIVATOR CAN EFFECTIVELY DECLOT PERITONEAL DIALYSIS CATHETERS To the Editor: Obstruction of the lumen by fibrin deposits is a complication of long-term, indwelling intraperitoneal catheters. Such obstruction can cause poor flow, with resultant inadequate dialysis. Urokinase, a thrombolytic agent, has been infused into clotted peritoneal dialysis catheters to achieve fibrinolysis and thus maintain patency. 1 With the recent unavailability of urokinase in the United States, declotting of these catheters has become more difficult. Indeed, the removal of catheters in which the fibrin plugs potentially could have been dissolved by thrombolytic agents is not uncommon. Tissue plasminogen activator (TPA) is being used successfully to declot central venous hemodialysis catheters. Paulsen et aF have reported that TPA given in bolus doses can reopen clotted venous catheters in most instances. Reports pertaining to the use of TPA to maintain patency of peritoneal catheters are not available. At our institution, we have instilled bolus doses of a1teplase (Activase, Genentech, South San Francisco. CA), a recombinant tissue-type plasminogen activator. into peritoneal dialysis catheters to dissolve fibrin clots successfully in four peritoneal dialysis patients. The volume of a bolus dose to be administered is the same as the volume of the affected catheter. Obstruction to both inflow and outflow occurred in all of the patients. Saline flushes administered in an attempt to dislodge the clots were unrewarding. Abdominal radiographs showed that the catheters were situated in the desired location. After the introduction of I mg/mL alteplase into the clotted catheter and allowing the drug to dwell in the lumen for an hour. relief of the obstruction was obtained in all patients. After retrieval of the TPA from the lumen, we were then able to resume dialysis. No complications attributable to the TPA therapy were observed. Alteplase is available in the United States in 50-mg and 100-mg vials. The 100-mg vial costs approximately $1,600. When using a 100-mg vial. 100 mL sterile water for injection should be added, resulting in a concentration of I
REFERENCES 1. Strippoli P, Pilolli D. Mingrone G, Dimaggio A, Coviello F, Orbello G, Querques M, Scatizzi A: A hemostasis study in CAPO patients during fibrinolytic intraperitoneal therapy with urokinase (UK). Adv Perit Dial 5:97-99, 1989 2. Paulsen 0, Reisother A, Aasen M, Fauchald P: Use of tissue plasminogen activator for reopening of clotted dialysis catheters. Nephron 64:468-470, 1993 3. Calis KA, Cullinane AM, Home MK III: Bioactivity of cryopreserved alteplase solutions. Am J Health-Syst Pharm 56:2056-2057. 1999
© 2000 by the National Kidney Foundation, Inc. doi: I O. I 053/ajkd.2000. I 62 I 2
SELECTIVE COX-2 INHIBITORS AND NEPHROTOXICITY To the Editor: With more and more reports pointing to the nephrotoxic potential of COX-2 inhibitors, selective COX-2 inhibitors clearly must be used cautiously or not at all in patients predisposed to renal failure. In addition to the acute reversible renal failure discussed recently in the Journal, 1.2 I would like to highlight instances of irreversible neonatal renal failure caused by maternal ingestion of Nimesulide. a selective COX-2 inhibitor. 3A A growing amount of experimental work is being published on the role of COX-2 in fetal development and in particular renal organogenesis. Knockout mice for the COX-2 geneS and fetal-specific inhibition of the enzyme have damaged kidneys and poor renal function because of both a direct effect and interference with renin release. 6.7 Case reports by Lizia Peruzzi et a13 and Balasubramaniam4 offer evidence for defective
American Journal of Kidney Diseases, Vol 36, No 3 (September), 2000: pp 675-676
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