Embolic protection and platelet inhibition during renal artery stenting.
BACKGROUND
Preservation of renal function is an important objective of renal artery stent procedures. Although atheroembolization can cause renal dysfunction during renal stent procedures, whether adjunctive use of embolic protection devices or glycoprotein IIb/IIIa inhibitors improves renal function is unknown.


RESULTS
One hundred patients undergoing renal artery stenting at 7 centers were randomly assigned to an open-label embolic protection device, Angioguard, or double-blind use of a platelet glycoprotein IIb/IIIa inhibitor, abciximab, in a 2x2 factorial design. The main effects of treatments and their interaction were assessed on percentage change in Modification in Diet in Renal Disease-derived glomerular filtration rate from baseline to 1 month using centrally analyzed creatinine. Filter devices were analyzed for the presence of platelet-rich thrombus. With stenting alone, stenting and embolic protection, and stenting with abciximab alone, glomerular filtration rate declined (P<0.05), but with combination therapy, it did not decline and was superior to the other allocations in the 2x2 design (P<0.01). The main effects of treatment demonstrated no overall improvement in glomerular filtration rate; although abciximab was superior to placebo (0+/-27% versus -10+/-20%; P<0.05), embolic protection was not (-1+/-28% versus -10+/-20%; P=0.08). An interaction was observed between abciximab and embolic protection (P<0.05), favoring combination treatment. Abciximab reduced the occurrence of platelet-rich emboli in the filters from 42% to 7% (P<0.01).


CONCLUSIONS
Renal artery stenting alone, stenting with embolic protection, and stenting with abciximab were associated with a decline in glomerular filtration rate. An unanticipated interaction between Angioguard and abciximab was seen, with combination therapy better than no treatment or either treatment alone.
Cooper
Christopher J
CJ
Cardiovascular Division, University of Toledo, 3000 Arlington Ave, MS 1036, Toledo, OH 43614, USA. Christopher.cooper@utoledo.edu
Haller
Steven T
ST
Colyer
William
W
Steffes
Michael
M
Burket
Mark W
MW
Thomas
William J
WJ
Safian
Robert
R
Reddy
Bhagat
B
Brewster
Pamela
P
Ankenbrandt
Mary Ann
MA
Virmani
Renu
R
Dippel
Eric
E
Rocha-Singh
Krishna
K
Murphy
Timothy P
TP
Kennedy
David J
DJ
Shapiro
Joseph I
JI
D'Agostino
Ralph D
RD
Pencina
Michael J
MJ
Khuder
Sadik
S
D000077284:Abciximab; D000368:Aged; D000369:Aged, 80 and over; D017130:Angioplasty; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D001794:Blood Pressure; D003131:Combined Modality Therapy; D004617:Embolism / Q000188:drug therapy / Q000517:prevention & control*; D005260:Female; D005919:Glomerular Filtration Rate; D006470:Hemorrhage; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000008:administration & dosage*; D007431:Intraoperative Complications / Q000517:prevention & control; D007674:Kidney Diseases / Q000517:prevention & control*; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D019736:Prostheses and Implants; D019919:Prosthesis Implantation; D012077:Renal Artery / Q000601:surgery; D012078:Renal Artery Obstruction / Q000601:surgery*; D015607:Stents; D016896:Treatment Outcome
D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D000077284:Abciximab