Baseline inflammatory status and long-term changes in renal function after percutaneous renal artery stenting: A prospective study.
ABSTRACT OBJECTIVES: To investigate a possible independent predictive role of systemic inflammation markers on renal function after renal artery stenting. BACKGROUND: An elevated baseline serum creatinine has previously been shown to be the strongest predictor of improved renal function after percutaneous renal artery stenting. The inflammatory system is implicated in every stage of chronic kidney disease, and we hypothesized an additional value of markers of systemic inflammation in predicting response after renal artery stenting. METHODS: This single center, prospective study includes 62 consecutive patients with chronic kidney disease at stage ≥3 or resistant hypertension who underwent stent placement for 74 angiographically significant atherosclerotic renal lesions. Inflammatory markers, including serum C-reactive protein (CRP), erythrocyte sedimentation rate, and white blood cell count were determined prior to renal angioplasty and related to changes in renal function at follow-up. RESULTS: Six-month clinical follow up was completed in 57 patients. Overall, median serum creatinine concentration exhibited a non significant reduction from 1.40mg/dl (quartiles: 1.20, 1.75mg/dl) at baseline to 1.30mg/dl (quartiles: 1.1, 1.55mg/dl) at 6months (p=0.17). Significant multivariate independent predictors of decreased creatinine included higher baseline serum creatinine levels (adjusted OR per quartile increment, 2.5 [1.3 to 4.7], p=0.004) and lower C-reactive protein levels (adjusted OR per quartile increment 0.39 [0.19 to 0.82], p=0.013). CONCLUSIONS: Patients with higher serum creatinine and lower CRP derive the most benefit from renal artery stenting.
- International journal of cardiology 01/2014; · 6.18 Impact Factor
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ABSTRACT: The neutral findings of Angioplasty and Stenting for Renal Artery Lesions and Cardiovascular Outcomes in Renal Artery Lesions trials have shown that unselected revascularization does not improve outcomes in atherosclerotic renovascular disease (ARVD). This review highlights recent translational, clinical and epidemiological studies and suggests directions for future research.Current Opinion in Nephrology and Hypertension 08/2014; · 4.24 Impact Factor
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ABSTRACT: AimsThe mechanisms mediating kidney injury and repair in humans with atherosclerotic renal artery stenosis (ARAS) remain poorly understood. We hypothesized that the stenotic kidney releases inflammatory mediators and recruits progenitor cells to promote regeneration.Methods and resultsEssential hypertensive (EH) and ARAS patients (n= 24 each) were studied during controlled sodium intake and antihypertensive treatment. Inferior vena cava (IVC) and renal vein (RV) levels of CD34+/KDR+ progenitor cells, cell adhesion molecules, inflammatory biomarkers, progenitor cell homing signals, and pro-angiogenic factors were measured in EH and ARAS, and their gradient and net release compared with systemic levels in matched normotensive controls (n= 24). Blood pressure in ARAS was similar to EH, but the glomerular filtration rate was lower. Renal vein levels of soluble E-Selectin, vascular cell adhesion molecule-1, and several inflammatory markers were higher in the stenotic kidney RV vs. normal and EH RV (P< 0.05), and their net release increased. Similarly, stem-cell homing factor levels increased in the stenotic kidney RV. Systemic CD34+/KDR+ progenitor cell levels were lower in both EH and ARAS and correlated with cytokine levels. Moreover, CD34+/KDR+ progenitor cells developed a negative gradient across the ARAS kidney, suggesting progenitor cell retention. The non-stenotic kidney also showed signs of inflammatory processes, which were more subtle than in the stenotic kidney.Conclusion Renal vein blood from post-stenotic human kidneys has multiple markers reflecting active inflammation that portends kidney injury and reduced function. CD34+/KDR+ progenitor cells sequestered within these kidneys may participate in reparative processes. These inflammation-related pathways and limited circulating progenitor cells may serve as novel therapeutic targets to repair the stenotic kidney.European Heart Journal 07/2012; · 14.72 Impact Factor