A D'Angelo

National Research Council, Roma, Latium, Italy

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Publications (295)1354.47 Total impact

  • Journal of nephrology 12/2013; 26(Suppl. 22):136-138. · 2.02 Impact Factor
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    ABSTRACT: BACKGROUND: Proton pump inhibitors (PPIs) are a class of drugs that is extensively used for common gastrointestinal disorders and often prescribed long-term for years. Long-term PPI treatment is associated with an increased risk of fractures in the general population. Several studies have suggested a relationship between vascular calcification, which is a predictor of cardiovascular morbidity and mortality, impaired bone metabolism and fractures. In dialysis patients, vascular calcifications are widespread and are connected to bone health. OBJECTIVE: The aim of this study was to assess the association between the use of PPIs and vascular calcifications involving the aorta and iliac arteries in haemodialysis patients. METHODS: Between November 2008 and November 2009, 387 patients receiving long-term dialysis treatment (≥1 year) were enrolled in a multicentre (18 Dialysis Units), cross-sectional study. Overall, 76.2 % of patients were receiving long-term PPI treatment. The main outcome measure was calcification of the aorta and iliac arteries in relation to PPI use. Standardized radiographs were sent to the coordinating centre for centralized evaluation in duplicate by two physicians who were blind to PPI status. RESULTS: Arterial calcifications were significantly more common in the PPI group (p < 0.01). Also, the rates of aortic and iliac calcifications considered separately were higher (+12.2 %, p = 0.0254; and +13.6 %, p = 0.0211, respectively). After correction for the propensity score, the odds ratios [ORs] (95 % CI) related to PPI use were aorta 1.89 (1.01-3.54), p = 0.048; iliac arteries 2.27 (1.31-3.92), p = 0.003; aorta and iliac arteries 2.59 (1.48-4.53), p = 0.008. The ORs (95 % CI) related to the association of warfarin + PPI were aorta 2.19 (0.95-5.00), p = 0.06; iliac arteries 2.90 (1.07-7.86), p = 0.036; aorta and iliac arteries 2.69 (1.03-6.96), p = 0.042. CONCLUSION: In haemodialysis patients, long-term treatment with PPIs, especially in the presence of warfarin treatment, is associated with vascular calcifications.
    Drug Safety 05/2013; · 2.62 Impact Factor
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    ABSTRACT: Few studies have provided information on the prevalence of vertebral fractures (VFs) and their risk factors in hemodialysis patients. A multicenter, cross-sectional, observational study was carried out to assess the prevalence of VFs and vascular calcifications (VCs) in 387 hemodialysis patients (mean age 64.2 ± 14.1 years, 63 % males) and in a control group of 51 osteoporotic subjects. Biochemical tests included 25(OH) vitamin D, bone Gla protein (total and undercarboxylated), and total matrix Gla protein. Vertebral quantitative morphometry was carried out centrally for the detection of VF, defined as reduction by ≥20 % of one of the vertebral body dimensions. In the same radiograph, aortic and iliac VC scores were calculated. Prevalence of VF was 55.3 % in hemodialysis patients and 51.0 % in the control group. Multivariate analysis disclosed that male gender (59.8 vs. 47.6 %, p = 0.02; OR = 1.78, 95 % CI 1.15-2.75) and age (mean ± SD 66.7 ± 13.1 vs. 61.0 ± 14.7 years, p < 0.001; OR = 1.03, 95 % CI 1.01-1.05) were significantly associated with VF. The prevalence of aortic VC was significantly higher in hemodialysis patients than in controls (80.6 vs. 68.4 %, p = 0.001). The factors with the strongest association with VC, apart from atrial fibrillation, were serum 25(OH)vitamin D levels below 29 ng/mL for aortic VC (OR = 1.85, 95 % CI 1.04-3.29) and VF both for aortic (OR = 1.77, 95 % CI 1.00-3.14) and iliac (OR = 1.96, 95 % CI 1.27-3.04) VC. In conclusion, the prevalence of VF, especially in males, and VC, in both genders, is high in hemodialysis patients. VF is associated with VC. Vitamin D deficiency is also associated with VC. Further longitudinal studies are warranted to investigate fractures in renal patients.
    Calcified Tissue International 03/2013; · 2.75 Impact Factor
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    ABSTRACT: PurposeTo evaluate the effects of intravitreal autologous plasmin enzyme (APE) in patients with focal vitreomacular traction (VMT).MethodsAPE was obtained by incubation of patient-derived purified plasminogen with streptokinase, and intravitreally injected 5-12 days later. Twenty-four hours after injection, in case of incomplete VMT release, a pars plana vitrectomy was performed. The hyaloid internal limiting membrane adherence and removal of the posterior hyaloid were intraoperatively evaluated.ResultsThirteen patients were recruited. During preparation of APE, five patients had spontaneous release of VMT. Eight patients received APE injection (2 IU). In five patients, spontaneous resolution of VMT occurred before APE administration. Twenty-four hours after injection, persistence of VMT was detected in all the eight treated patients. Best-corrected visual acuity was 0.51±0.37 LogMAR at baseline, improving to 0.23±0.14 LogMAR at 6 months (P=0.002). Foveal thickness was 464±180 μm at baseline, reducing to 246±59 μm at 6 months (P<0.001). Hyaloid was intraoperatively judged 'partially detached' in seven cases and 'totally detached' in one case. Hyaloid peeling was evaluated 'easy' in six eyes and 'very easy' in two eyes.Conclusions In the current study, there was a large percentage of spontaneous resolution of VMT before an APE administration. A single intravitreal APE injection seems insufficient to induce a complete posterior vitreous detachment in these patients.Eye advance online publication, 14 December 2012; doi:10.1038/eye.2012.248.
    Eye (London, England) 12/2012; · 1.97 Impact Factor
  • Maria Fusaro, Angela D'Angelo, Maurizio Gallieni
    American Journal of Kidney Diseases 07/2012; 60(1):169. · 5.29 Impact Factor
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    ABSTRACT: Vitamin K (vitamin K1 or phylloquinone and vitamin K2, a series of menaquinones [MKs]) is involved in the production of bone and matrix amino acid γ-carboxy-glutamic acid (Gla) proteins, regulating bone and vascular calcification. Low vitamin K concentrations are associated with increased risks of fractures and vascular calcification, and frequent complications in hemodialysis patients. We carried out an observational study to establish the prevalence of vitamin K deficiency and to assess the relationship between vitamin K status, vertebral fractures, vascular calcification, and survival in 387 patients on hemodialysis for ≥1 year. We determined plasma levels of vitamin K compound, bone-Gla-protein, matrix-Gla-protein, and routine biochemistry. Vertebral fractures (reduction in vertebral body height by ≥20%) and aortic and iliac calcifications were also investigated in a spine (D(5) -L(4) ) radiograph. Three-year patient survival was analyzed. Important proportions of patients had deficiency of MK7 (35.4%), vitamin K1 (23.5%), and MK4 (14.5%). A total of 55.3% of patients had vertebral fractures, 80.6% had abdominal aorta calcification, and 56.1% had iliac calcification. Vitamin K1 deficiency was the strongest predictor of vertebral fractures (odds ratio [OR], 2.94; 95% confidence interval [CI], 1.38-6.26). MK4 deficiency was a predictor of aortic calcification (OR, 2.82; 95% CI, 1.14-7.01), whereas MK5 deficiency actually protected against it (OR, 0.38; 95% CI, 0.15-0.95). MK7 deficiency was a predictor of iliac calcification (OR, 1.64; 95% CI, 1.03-2.60). The presence of vertebral fractures was also a predictor of vascular calcifications (OR, 1.76; 95% CI, 1.00-3.08). Increased alkaline phosphatase and C reactive protein (CRP), age, and cerebrovascular events were predictors of mortality. Our study suggests that the vitamin K system may be important for preserving bone mass and avoiding vascular calcification in hemodialysis patients, pointing out a possible role of vitamin K in bone and vascular health. Based on our results, we suggest that the general population should also be studied for vitamin K deficiency as a possible cause of both vertebral fractures and vascular calcification. © 2012 American Society for Bone and Mineral Research.
    Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 06/2012; 27(11):2271-2278. · 6.04 Impact Factor
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    A Fattorini, L Crippa, A D'Angelo
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    ABSTRACT: we read with interest the letter by van den Besselar about ISI calibrant plasmas (1) and the ensuing exchange of correspondence with Poller et al. (2,3). We agree with the ECAA colleagues that with the FDA-approved ECAA set of artificially depleted plasmas and the PT/INR line inter-laboratory INR deviations are significantly reduced with all types of reagents, but we also suspect that, unless fresh native plasmas from patients on warfarin are used for calibration, this may not translate in better laboratory monitoring of patients on warfarin. © 2012 International Society on Thrombosis and Haemostasis.
    Journal of Thrombosis and Haemostasis 05/2012; 10(8):1715-6. · 6.08 Impact Factor
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    ABSTRACT: Glomerular protein handling mechanisms have received much attention in studies of nephrotic syndrome. Histopathological findings in renal biopsies from severely proteinuric patients support the likelihood of protein endocytosis by podocytes. ClC-5 is involved in the endocytosis of albumin in the proximal tubule. AIM: To investigate whether ClC-5 is expressed in the glomerular compartment and whether it has a role in proteinuric nephropathies. ClC-5 expression was studied using Real-time PCR in manually- and laser-microdissected biopsies from patients with type 2 diabetes (n 37) and IgA nephropathy (n 10); in biopsies of membranous glomerulopathy (MG) (n 14) immunohistochemistry for ClC-5 (with morphometric analysis) and for WT1 was done. Controls: cortical tissue (n 23) obtained from unaffected parts of tumor-related nephrectomy specimens. RESULTS: ClC-5 was expressed at glomerular level in all biopsies. Glomerular ClC-5 levels were significantly higher in diabetic nephropaty and MG at both mRNA and protein level (p<0.002; p<0.01). ClC-5 and WT1 double-staining analysis in MG showed that ClC-5 was localized in the podocytes. ClC-5 ultrastructural immunolocalization was demonstrated in podocytes foot processes. Our study is the first to demonstrate that ClC-5 is expressed in human podocytes. The ClC-5 overexpression found in biopsies of proteinuric patients suggests that proteinuria may play a part in its expression and that podocytes are likely to have a key role in albumin handling in proteinuric states.
    PLoS ONE 01/2012; 7(9):e45605. · 3.53 Impact Factor
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    ABSTRACT: Given the higher mortality rate of ICU patients with sepsis and AKI, we decided to investigate the possible correlation between serum biomarkers of organ damage, and endotoxin activity in ICU septic patients. Ninety-eight consecutive adult patients were enrolled in this study. Patients were divided in two groups depending on the presence of sepsis. Fifty-six patients had sepsis, while forty-two patients were nonseptic. Among septic patients, twenty-four subjects developed AKI, while thirty-two did not. AKI occurred in fourteen patients without sepsis as well. The levels of NGAL, BNP, and AOPP were significantly higher among septic patients compared with nonseptic subjects (P < 0.001). Among septic patients, subjects who developed AKI showed significant higher levels of NGAL and AOPP (P = 0.0425) and BNP (P = 0.0327). Among patients who developed AKI, a significant difference was found only in terms of AOPP levels between septic and nonseptic patients. The correlation between endotoxin activity and BNP in septic patients and the increase in the levels of NGAL, BNP, and AOPP in case of sepsis and AKI, in particular if they are associated, indicate a multiorgan involvement in these two conditions.
    Critical care research and practice 01/2012; 2012:856401.
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    ABSTRACT: The epithelial-mesenchymal transition (EMT) of proximal tubular epithelial cells (PTECs) into myofibroblasts contributes to the establishment of fibrosis that leads to end stage renal disease. FGF-2 induces EMT in PTECs. Because the interaction between FGF-2 and its receptor is mediated by heparan sulfate (HS) and syndecans, we speculated that a deranged HS/syndecans regulation impairs FGF-2 activity. Heparanase is crucial for the correct turnover of HS/syndecans. The aim of the present study was to assess the role of heparanase on epithelial-mesenchymal transition induced by FGF-2 in renal tubular cells. In human kidney 2 (HK2) PTEC cultures, although FGF-2 induces EMT in the wild-type clone, it is ineffective in heparanase-silenced cells. The FGF-2 induced EMT is through a stable activation of PI3K/AKT which is only transient in heparanase-silenced cells. In PTECs, FGF-2 induces an autocrine loop which sustains its signal through multiple mechanisms (reduction in syndecan-1, increase in heparanase, and matrix metalloproteinase 9). Thus, heparanase is necessary for FGF-2 to produce EMT in PTECs and to sustain FGF-2 intracellular signaling. Heparanase contributes to a synergistic loop for handling syndecan-1, facilitating FGF-2 induced-EMT. In conclusion, heparanase plays a role in the tubular-interstitial compartment favoring the FGF-2-dependent EMT of tubular cells. Hence, heparanase is an interesting pharmacological target for the prevention of renal fibrosis.
    Journal of Biological Chemistry 11/2011; 287(2):1478-88. · 4.65 Impact Factor
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    ABSTRACT: The epithelial-mesenchymal transition (EMT) of proximal tubular epithelial cells (PTEC) into myofibroblasts contributes to the establishment of fibrosis that leads to end-stage renal disease. FGF-2 induces EMT in PTECs. Since the interaction between FGF-2 and its receptor is mediated by HS and syndecans, we speculated that a deranged HS/syndecans regulation impairs FGF-2 activity. Heparanase is crucial for the correct turn-over of HS/syndecans. The aim of the present study was to asses the role of heparanase on epithelial mesenchymal transition induced by FGF-2 in renal tubular cells. In human HK2 PTEC cultures, while FGF-2 induces EMT in the wild-type clone, it is ineffective in heparanase-silenced cells. The FGF-2 induced-EMT is through a stable activation of PI3K/AKT which is only transient in heparanase-silenced cells. In PTECs, FGF-2 induces an autocrine loop which sustains its signal through multiple mechanisms (reduction in syndecan-1, increase in heparanase and matrix metalloproteinase 9). Thus, heparanase is necessary for FGF-2 to produce EMT in PTECs and to sustain FGF-2 intracellular signaling. Heparanase contributes to a synergistic loop for handling syndecan-1, facilitating FGF-2 induced-EMT. In conclusion, heparanase plays a role in the tubular-interstitial compartment favouring the FGF-2-dependent EMT of tubular cells. Hence, heparanase is an interesting pharmacological target for the prevention of renal fibrosis.
    Journal of Biological Chemistry 11/2011; · 4.65 Impact Factor
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    ABSTRACT: The authors briefly describe the history of gout, mainly focusing their attention on the renal involvement. They report some works and theories on gout of great ancient physicians, such as Paracelsus, Sydenham, Boerhaave, Van Swieten and Morgagni.
    Reumatismo 09/2011; 54(2):165-71.
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    ABSTRACT: Epidemiological studies have shown that the burden of chronic kidney disease (CKD) is huge. CKD is a non-specific diagnosis, however, and it is hard to say which renal disorders comprise the body of CKD diagnosed on the strength of the combination of albuminuria and estimated glomerular filtration rate (eGFR) in epidemiological studies, or just how efficient such studies are in detecting chronic nephropathies. The INCIPE study identified 524 CKD cases (using the K/DOQI definition based on albuminuria and eGFR) in a random sample of 4000 Italians >40 years old, 262 of whom were randomly chosen to be investigated in order to confirm their CKD and complete a diagnostic workup. We a priori defined diagnostic algorithms for 14 renal conditions based on personal family history, medical records, urine tests, kidney ultrasound with colour-Doppler and other tests. Among the subjects whose CKD was confirmed, a diagnosis of chronic nephropathy was reached in 68% of cases recognized as having either a specific (38%) or an undetermined (30%) kidney disease. Almost 50% of subjects with a specific chronic nephropathy had a diabetic or vascular renal disease. Abnormalities consistent with a chronic nephropathy were found in 50, 68, 70 and 100% of subjects with CKD Stages 1, 2, 3 and 4, respectively. Lone low eGFR and lone microalbuminuria were observed in 20 and 12%, respectively. In Caucasians >40 years old with a confirmed CKD condition, (i) an impressive 68% of subjects have an underlying chronic nephropathy, so eGFR and albuminuria are very efficient in detecting renal diseases; (ii) in 32%, the only disclosed renal abnormalities were a glomerular filtration rate <60 mL/min/1.73 m(2) or microalbuminuria; follow-up studies are needed to clarify whether these abnormalities do really identify a chronic nephropathy or just a cardiovascular risk condition.
    Nephrology Dialysis Transplantation 07/2011; 27(2):746-51. · 3.37 Impact Factor
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    ABSTRACT: Secondary hyperparathyroidism (SHPT), known complication of chronic renal failure, in addition to effects on bone and cardiovascular systems, is associated with reduced response to erythropoietin (EPO). Calcimimetics such as cinacalcet are the latest generation of drugs used in the treatment of SHPT. Few studies have evaluated the effect of cinacalcet on anemia associated with SHPT in dialysis patients, while no study has compared this cinacalcet effect with that of vitamin D analogs such as paricalcitol. Using a retrospective chart-based review of dialysis patients' records to identify patients being treated with either cinacalcet or paricalcitol alone, matched for the same EPO treatment, which had been followed for 1 year, we have evaluated the effect of cinacalcet on anemia compared to that of paricalcitol. Ten patient records were found that fit the criteria, five treated with cinacalcet (Group 1) and five treated with paricalcitol (Group 2), all treated with the same dose of darbepoetin. Darbepoetin dosage was the only parameter that significantly changed between groups, decreasing in Group 1 (-33%, p = 0.009) while remaining unchanged in Group 2. PTH-level reduction, which was significant versus baseline in both groups, although not statistically different between groups, was higher with cinacalcet. The combination of lower EPO dose in cinacalcet-treated patients compared with paricalcitol-treated patients, along with good SHPT control is a novel information and might have considerable benefits in dialysis patients not only preventing bone (fractures) and cardiovascular system (calcifications) damages but also in terms of cost savings via a reduction of EPO dosage.
    Renal Failure 06/2011; 33(7):732-5. · 0.94 Impact Factor
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    ABSTRACT: Anticoagulant therapy in patients with atrial fibrillation requires careful evaluation because its benefits i.e. prevention of thromboembolism, must be greater than the risk of bleeding. Patients at higher risk of thrombosis are evaluated through specific scores, such as the CHA(2)DS(2)VASc, coupled with scoring systems for assessing bleeding risks, such as the HAS-BLED score. In addition to bleeding, other risks have been associated with the use of warfarin, including an increased susceptibility to vascular calcifications and fractures caused by a reduction in the levels of vitamin K dependent carboxylated enzymes, matrix Gla-protein (MGP) and bone Gla-protein or osteocalcin (BGP). In fact, while on one side warfarin is used to prevent embolism, on the other hand acting as a vitamin K antagonist it blocks the inhibitory effect of MGP on vascular calcification. Similarly, patients treated with warfarin carry a greater risk of developing osteoporosis and fractures, due to reduced BGP activity. Recently, a new generation of anticoagulant drugs has been developed, such as dabigatran, a direct thrombin inhibitor, and rivaroxaban, a direct factor-Xa inhibitor. They offer an interesting alternative to warfarin, because they do not require frequent blood tests for monitoring while offering similar results in terms of efficacy. Lacking the inhibitory effect on the vitamin K cycle, the consequent side effects can be avoided. If, compared to warfarin treated patients, a lower incidence of vascular calcifications and fractures will be demonstrated, the advantages over warfarin may be even greater, leading to further benefits in terms of morbidity and mortality.
    Current Vascular Pharmacology 05/2011; 9(6):763-9. · 2.91 Impact Factor
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    ABSTRACT: Cardiovascular disease represents the most common cause for the excess of morbidity and mortality found in end-stage renal disease (ESRD) and has prompted the exploration of multiple approaches to improve outcomes in these patients. Cardiovascular risk factors such as increased oxidative stress (OxSt) and inflammation are found in ESRD patients. A vitamin E-coated dialyzer using polysulfone membranes has been suggested to have positive effects on these factors. This 1-year study evaluated in 25 ESRD patients under chronic dialysis, the effects of a vitamin E-coated membrane (VitabranE ViE) "ex vivo" on mononuclear cells, OxSt, and inflammation-related biochemical and molecular biology markers using a molecular biology approach. p22(phox), heme oxygenase (HO)-1, plasminogen activator inhibitor (PAI)-1 protein level, and phosphorylated extracellular signal-regulated kinase (pERK)1/2 status were evaluated at the beginning of the study, after 6 months and after 12 months by Western blot analysis and oxidized low-density lipoprotein (OxLDL) plasma level by enzyme-linked immunosorbent assay, alongside vascular remodeling assessment as measured by carotid intima-media thickness (IMT) in a subgroup of nine randomly selected patients. p22(phox), PAI-1, OxLDL, and pERK all decreased with VitabranE use, while HO-1 increased. Carotid IMT did not increase. Treatment with VitabranE significantly decreases the expression of proteins and markers relevant to OxSt and inflammation tightly associated with cardiovascular disease, and it appears highly likely that VitabranE use will provide a benefit in terms of cardiovascular protection.
    Artificial Organs 02/2011; 35(2):E33-9. · 1.96 Impact Factor
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    ABSTRACT: Introduction. Acute kidney injury (AKI) is common in the intensive care unit (ICU) and associated with poor outcome. Plasma B-type natriuretic peptide (BNP) is a biomarker related to myocardial overload, and is elevated in some ICU patients. There is a high prevalence of both cardiac and renal dysfunction in ICU patients. Aims. To investigate whether plasma BNP levels in the first 48 hours were associated with AKI in ICU patients. Methods. We studied a cohort of 34 consecutive ICU patients. Primary outcome was presence of AKI on presentation, or during ICU stay. Results. For patients with AKI on presentation, BNP was statistically higher at 24 and 48 hours than No-AKI patients (865 versus 148 pg/mL; 1380 versus 131 pg/mL). For patients developing AKI during 48 hours, BNP was statistically higher at 0, 24 and 48 hours than No-AKI patients (510 versus 197 pg/mL; 552 versus 124 pg/mL; 949 versus 104 pg/mL). Conclusion. Critically ill patients with AKI on presentation or during ICU stay have higher levels of the cardiac biomarker BNP relative to No-AKI patients. Elevated levels of plasma BNP may help identify patients with elevated risk of AKI in the ICU setting. The mechanism for this cardiorenal connection requires further investigation.
    International journal of nephrology. 01/2011; 2011:951629.
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    ABSTRACT: In end-stage renal disease (ESRD) hyperphosphatemia associates with vascular calcifications and cardiovascular events derived from endothelial dysfunction. In dialysis patients, C-reactive protein (CRP), a marker of inflammation, associates with cardiovascular mortality. Increased PO(4) concentration impairs endothelial integrity via induction of oxidative stress, and sevelamer, a phosphate binder, showed anti-inflammatory effect reducing CRP, which paralleled PO(4) reduction. To give support to a direct proinflammatory role of hyperphosphatemia "per se," we have considered previously studied dialysis patients with sevelamer-"resistant" hyperphosphatemia, who were treated with a chitosan-loaded chewing gum, as salivary phosphate binder, in addition to sevelamer, reduced serum PO(4) to normal, to retrospectively evaluate their CRP and the relationship with hyperphosphatemia and calcium × phosphate (Ca × PO(4)) product. High sensitive (hs) CRP of 13 previously studied hemodialysis patients with sevelamer-resistant hyperphosphatemia was evaluated with immunonephelometry. Chitosan chewing gum use reduced hsCRP (from 1.38 ± 0.61 to 0.39 ± 0.16 mg/L after the gum, p < 0.0002), which returned to baseline after 4 weeks from gum discontinuation (1.25 ± 0.41). hsCRP reduction paralleled serum PO(4) reduction: from 7.60 ± 0.91 mg/dL to 5.18 ± 0.73 (after the gum) (p < 0.00001), returning to baseline (7.55 ± 0.75) after gum discontinuation. hsCRP reduction directly correlated with PO(4) reduction (p = 0.029). The relationship in sevelamer-resistant dialysis patients between the reduction of serum PO(4), induced by the chitosan-loaded chewing gum, and CRP reduction supports also in humans a proinflammatory role of hyperphosphatemia "per se" derived from "in vitro" studies. This further contributes to the high cardiovascular risk of ESRD patients making their serum phosphate in the normal range of vital importance.
    Renal Failure 01/2011; 33(1):11-4. · 0.94 Impact Factor
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    Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis. 01/2011; 31(1):94-7.

Publication Stats

5k Citations
1,354.47 Total Impact Points


  • 2012–2013
    • National Research Council
      Roma, Latium, Italy
  • 2011
    • Columbus-Gemelli University Hospital
      Roma, Latium, Italy
    • San Bortolo Hospital
      Vicenza, Veneto, Italy
  • 2010
    • Azienda Ospedaliera Universitaria Integrata Verona
      Verona, Veneto, Italy
    • Università Vita-Salute San Raffaele
      Milano, Lombardy, Italy
  • 2005–2008
    • University of Verona
      • • Department of Biomedical and Surgical Sciences
      • • Section of Nephrology
      Verona, Veneto, Italy
  • 1981–2008
    • University of Padova
      • • Department of Medicine DIMED
      • • Department of Biology
      Padova, Veneto, Italy
  • 2000–2006
    • University-Hospital of Padova
      Padua, Veneto, Italy
    • University of Naples Federico II
      Napoli, Campania, Italy
  • 1989–2004
    • Ospedale di San Raffaele Istituto di Ricovero e Cura a Carattere Scientifico
      Milano, Lombardy, Italy
  • 2001
    • Sapienza University of Rome
      Roma, Latium, Italy
  • 1990–2001
    • University of Milan
      Milano, Lombardy, Italy
  • 1999
    • Ospedale Santa Maria della Misericordia, Rovigo
      Rovigo, Veneto, Italy
  • 1989–1999
    • San Raffaele Scientific Institute
      Milano, Lombardy, Italy
  • 1998
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 1997
    • Tufts University
      Georgia, United States
  • 1996
    • Università degli Studi del Sannio
      Benevento, Campania, Italy
  • 1995
    • Hannover Medical School
      Hanover, Lower Saxony, Germany
  • 1991
    • University of Washington Seattle
      • Department of Medicine
      Seattle, WA, United States
  • 1987–1988
    • Oklahoma Medical Research Foundation
      Oklahoma City, Oklahoma, United States