The urinary albumin-to-creatinine ratio is a potential predictor of target lesion revascularization after percutaneous coronary intervention with coronary stents.

The association between the urinary albumin-to-creatinine ratio (UACR) and target lesion revascularization (TLR) is unknown in patients who are implanted with drug-eluting stents (DESs) or bare metal stents (BMSs) for the treatment of coronary artery disease. Of 231 Japanese patients who were implanted with DESs and/or BMSs during percutaneous coronary intervention (PCI) between July 2009 and January 2011, 118 underwent follow-up coronary angiography at 6 to 9 months after PCI; 103 were negative for qualitative tests for urine protein: 32 (31.0%)/103 patients underwent TLR for severe in-stent restenosis (ISR) and 71 did not. On the next day after admission to the hospital, first-morning-void spot urine samples were collected to calculate UACR based on urinalysis results. Pearson's product-moment correlation coefficients indicated positive associations of UACR with late loss as assessed by quantitative coronary analysis in the overall cohort, (r = +0.515, P < 0.0001), the DES subgroup (r = +0.443, P < 0.0001), and the BMS subgroup (r = +0.652, P < 0.0001). The incidence of multivessel lesions was significantly higher (P < 0.05) in the TLR group. UACR was significantly higher (P < 0.01) in the TLR group (23.88 ± 31.8 mg/gCr) than in the control group (6.29 ± 7.46 mg/gCr). Multivariate logistic regression analysis revealed UACR (odds ratio: 1.07; 95% confidence interval: 1.02-1.12; P < 0.01) to be associated with TLR. UACR was suggested to be a potential predictor of TLR required for severe ISR after PCI with coronary stents.

Chronic kidney disease and dipstick proteinuria are risk factors for stent thrombosis in patients with myocardial infarction.

BACKGROUND: Kidney failure (stage 5 chronic kidney disease [CKD]) is an independent risk factor for stent thrombosis (ST). Moderate (stage 3-4) CKD and proteinuria are both associated with adverse cardiovascular events, including worse outcomes after myocardial infarction (MI). Whether moderate CKD and proteinuria increase the risk of ST after MI is not known. This study evaluated the risk of ST associated with moderate CKD and dipstick proteinuria. METHODS: We retrospectively analyzed clinical and laboratory data from 956 non-stage 5 CKD patients who were admitted with MI and received intracoronary stenting. Clinical follow-up was collected at 1 year for definite or probable ST, as well as for all-cause mortality, nonfatal MI or death, and target vessel revascularization or coronary artery bypass graft surgery. RESULTS: After adjustment for multiple clinical and biochemical covariates, patients with both estimated glomerular filtration rate (GFR) of 15 to 59 mL min(-1) 1.73 m(-2) and > or =30 mg/dL dipstick proteinuria had increased cumulative incidence of ST (hazard rate [HR] 3.69, 95% CI 1.54-8.89), all-cause mortality (HR 2.68, 95% CI 1.34-5.37), and nonfatal MI or death (HR 3.20, 95% CI 1.77-5.81) at 1 year. In addition, estimated GFR of 15 to 59 mL min(-1) 1.73 m(-2) was a significant independent predictor of ST (HR 2.61, 95% CI 1.33-5.10). Dipstick proteinuria > or =30 mg/dL was associated with a trend toward increased risk for all outcomes. CONCLUSIONS: In an acute MI population, moderate CKD was identified as a novel prognostic marker for ST. In addition, patients with both decreased GFR and proteinuria had higher incidences of all-cause mortality and nonfatal MI or death than patients with either condition alone.