title: Determinants of renal function in patients with renal artery stenosis.
abstract: Renal artery stenosis (RAS) is an important cause of renal failure; however, the factors associated with loss of kidney function in patients with RAS are poorly described, as are the predictors of an improvement in kidney function after stenting. One hundred patients at seven centers undergoing renal stenting were randomly assigned to an embolic protection device or double-blind use of a platelet glycoprotein IIb/IIIa inhibitor. The glomerular filtration rate (GFR) was measured using the creatinine-derived modified Modification of Diet in Renal Disease (MDRD) equation, cystatin C, and iohexol clearance. In univariate and multivariate models, baseline MDRD and cystatin C GFR were associated with congestive heart failure (CHF) (p = 0.01), lesion length (p = 0.01), and percent stenosis (-0.27, p = 0.01). In multivariate models, MDRD-estimated GFR 1 month after stenting was associated with bilateral stenosis (p < 0.05) and lesion length (p < 0.05), whereas with cystatin C the multivariate model included angiotensin receptor blocker (ARB) (p < 0.05) and minimal luminal diameter (MLD) (p < 0.05). The improvement in GFR from baseline to 1 month, measured as percent change, was related to baseline MDRD (p = 0.009) and cystatin C (p = 0.03) GFR. For MDRD GFR combined treatment with abciximab and Angioguard(®) embolic protection (p = 0.02) remained significant in multivariate analysis as did CHF, which was also significant with cystatin C (p = 0.05). In conclusion, CHF and lesion characteristics (MLD, percent stenosis and lesion length) are determinants of renal function in patients with RAS. In contrast, the acute improvement in renal function after revascularization is most strongly influenced by baseline GFR, and to a lesser degree CHF and combined procedural treatment with abciximab and embolic protection but not lesion characteristics. Clinical Trial Registration - URL:http://www.clinicaltrials.gov. Unique identifier: NCT00234585.
authors: University of Toledo, OH, USA.
authors: Haifeng
authors: H
authors: Yu
authors: Dong
authors: D
authors: Zhang
authors: Steven
authors: S
authors: Haller
authors: Khalil
authors: K
authors: Kanjwal
authors: William
authors: W
authors: Colyer
authors: Pamela
authors: P
authors: Brewster
authors: Michael
authors: M
authors: Steffes
authors: Joseph I
authors: JI
authors: Shapiro
authors: Christopher J
authors: CJ
authors: Cooper
mesh_terms: D000077284:Abciximab; D000368:Aged; D000369:Aged, 80 and over; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D003404:Creatinine / Q000378:metabolism; D055316:Cystatin C / Q000378:metabolism; D004311:Double-Blind Method; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology*; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D007472:Iohexol; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D012078:Renal Artery Obstruction / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D015607:Stents
chemical_list: D000911:Antibodies, Monoclonal; D055316:Cystatin C; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D007472:Iohexol; D003404:Creatinine; D000077284:Abciximab