Giuseppe Dalfino

Publications (2)9.23 Total impact

• Article: Pentraxin 3 and complement cascade activation in the failure of arteriovenous fistula.

  Giuseppe Castellano, Angela Di Vittorio, Giuseppe Dalfino, Antonia Loverre, Daniela Marrone, Simona Simone, Francesco Paolo Schena, Giovanni Pertosa, Giuseppe Grandaliano
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  ABSTRACT: Pentraxin-3 (PTX3) has been suggested to play a role in the development of vascular pathology. Stenosis of arteriovenous fistula (AVF) leading to its failure is the major cause of morbidity in hemodialysis patients. To date, little is known on the pathogenesis of AVF stenosis. The aim of the present study was to investigate the potential role of PTX3 in this setting. A sample of venous wall was collected at the time of AVF formation in 44 patients with end stage renal disease. Ten patients developed AVF stenosis and from these patients a second portion of the venous wall was obtained during surgical revision of the AVF. Confocal laser scanning microscopy demonstrated that PTX3 immunostaining, hardly detectable in native AVF, was significantly increased in failed AVF, showing a specific co-localization with endothelial cell markers. Circulating mononuclear cells isolated at the time of AVF revision presented a significantly higher PTX3 mRNA expression than those collected during AVF creation. Interestingly, a significant deposition of C5b-9 on endothelial cells, co-localizing with PTX3, was observed in stenotic AVF. The present study demonstrates for the first time a close association between PTX3 deposition and complement activation at the endothelial cell level in failed AVF and suggests a role for PTX3 in modulating innate immunity in the pathogenesis of AVF stenosis.
  Atherosclerosis 08/2009; 209(1):241-7. · 3.79 Impact Factor
• Source

  Available from: Alfredo Procino

  Article: Serum Fetuin A in Hemodialysis: A Link Between Derangement of Calcium-Phosphorus Homeostasis and Progression of Atherosclerosis?

  Giovanni Pertosa, Simona Simone, Marco Ciccone, Silvia Porreca, Gianluigi Zaza, Giuseppe Dalfino, Bruno Memoli, Alfredo Procino, Mario Bonomini, Vittorio Sirolli, Giuseppe Castellano, Loreto Gesualdo, Maria Ktena, Francesco Paolo Schena, Giuseppe Grandaliano
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  ABSTRACT: Background: Fetuin A, a circulating inhibitor of ectopic calcification, is downregulated in hemodialysis and has been shown to predict cardiovascular mortality in this setting. The association of altered calcium-phosphorus with serum fetuin A levels is still a matter of debate. Although carotid intima-media thickness (cIMT) is a strong predictor of major cardiovascular events, its association with serum fetuin A levels is poorly defined. Study Design: Cohort study. Participants & Settings: 174 uremic patients on long-term hemodialysis therapy enrolled in 4 university hospitals. Predictors: Serum fetuin A levels at the beginning of the study (T0) and after 12 months (T12). Outcomes: Progression of atherosclerosis assessed by means of cIMT measurements at 24 months (T24); cardiovascular morbidity and mortality at 36 months. Results: Serum fetuin A concentrations at T0 and T12 were 282.3 79.4 and 290.0 92.2 g/mL, respectively. Mean T0 and T24 cIMT values were 1.02 0.2 and 1.06 0.2 mm, respectively (P 0.001). Fatal and nonfatal cardiovascular disease occurred in 36 and 86 patients by 36 months, respectively. In multivariate logistic regression, higher calcium-phosphorus product was associated with lower serum fetuin A level (odds ratio, 0.96; 95% confidence interval [CI], 0.93 to 1.00; P 0.02). Multiple regression analysis showed that T0 serum fetuin A level was associated with T24 cIMT (P 0.01) after adjustments for age, cholesterol level, high-sensitivity C-reactive protein level, previous cardiovascular events, and T0 cIMT. In a multivariate Cox regression analysis, cardiovascular mortality was independently associated with a 1-tertile lower T0 serum fetuin A level, and a 1-tertile higher T0 cIMT value was independently associated with greater cardiovascular mortality (hazard ratio, 0.45; 95% CI, 0.15 to 0.65; P 0.007 and hazard ratio, 10.00; 95% CI, 3.16 to 31.73; P 0.001, respectively) after adjustment for age and previous cardiovascular events.
  American Journal of Kidney Diseases 01/2009; · 5.43 Impact Factor