Search

Your search keyword '"Belluardo P"' showing total 3 results
Start Over Author "Belluardo P" Language undetermined
3 results on '"Belluardo P"'

1. Randomized study of traditional versus aggressive systolic blood pressure control (Cardio-Sis): rationale, design and characteristics of the study population

Author

Cardio Sis Study Group, Verdecchia, P, Staessen, Ja, Achilli, A, de Simone, G, Ganau, A, Mureddu, G, Pede, S, Porcellati, C, Fornari, G, Repaci, S, Castellani, C, Achilli, P, Jaspers, C, Cucchiara, G, Panzano, C, Angeli, F, Aillon, C, Sclavo, Mg, Scherillo, M, Raucci, D, Di Donato, M, DEI CAS, Livio, Faggiano, P, Porcu, M, Calamida, R, Pistia, L, Vancheri, F, Alletto, M, Curcio, M, Pettinati, G, Ieva, M, Muscella, A, Guerrieri, M, Denbek, C, Gulizia, M, Francese, Gm, Perticone, F, Iemma, G, Fariello, R, Sala, N, Mezzetti, A, Pierdomenico, Sd, Bucci, M, Benemio, G, Gattobigio, R, Sacchi, N, Cocchieri, M, Prosciutti, L, Battocchi, P, Garognoli, O, Arcelli, G, Pirelli, S, Emanuelli, C, Braschi, Gb, Abrignani, M, De Ferrari, G, Ponremoli, R, Igidbashian, D, Marini, R, Scarpino, L, Mandorla, S, Buccolieri, M, Picchi, L, Casolo, G, Pardini, M, Marracci, G, Strazzullo, P, Galletti, F, Barbato, A, Cavallini, C, Borgioni, C, Seghieri, G, Cipollini, F, Arcangeli, E, Boddi, W, Palermo, C, Savelli, F, Lembo, G, Vecchione, C, Malatino, L, Belluardo, P, Zoccali, C, Leonardis, D, Mallamaci, F, Lacchè, A, Gentile, C, Boccanelli, A, Mureddu, Gf, Santini, M, Colivicchi, F, Ficili, S, Uguccioni, M, Nardozi, C, Tedeschi, A, Martin, G, Zanata, G, Mos, L, Dialti, V, Martina, S, Renna, A, Farina, G, Tripodi, E, Miserrafiti, B, Scali, R, Stornello, M, Valvo, E, Bernardinangeli, M, Proietti, G, Poddighe, G, Biscottini, B, Panciarola, R, Boccali, A, Veglio, F, Rabbia, F, Caserta, M, Chiatto, M, Stefenelli, C, Cioffi, G, Bonazza, G, Scabbia, Ev, and Bottoni, D.

Published
2008

2. Hepatocyte growth factor and left ventricular geometry in end-stage renal disease

Author

Malatino, Lorenzo, Cataliotti, A., Benedetto, F. A., Stancanelli, B., Bellanuova, I., Belluardo, P., Bonaiuto, L., Tripepi, G., Mallamaci, F., Castellino, Pietro, Zoccali, C., Rapisarda, Francesco, and end Creed, i. n. v.

Subjects
Male, medicine.medical_specialty, Heart disease, medicine.medical_treatment, Population, Left ventricular hypertrophy, End stage renal disease, Muscle hypertrophy, Internal medicine, Internal Medicine, medicine, Humans, education, Ventricular remodeling, Ultrasonography, education.field_of_study, Ventricular Remodeling, business.industry, Hepatocyte Growth Factor, Middle Aged, medicine.disease, Endocrinology, Cardiology, Kidney Failure, Chronic, Female, Hypertrophy, Left Ventricular, Hemodialysis, business, Kidney disease
Abstract

Hepatocyte growth factor is a pleiotropic cytokine with cardioprotective properties. Its serum concentration is markedly raised in end-stage renal disease. This study assessed the relation of hepatocyte growth factor (HGF) with left ventricular mass and geometry in end-stage renal disease. Serum HGF measurements and echocardiographic studies were performed in 185 patients receiving hemodialysis. Patients with serum HGF above the median (1.85 ng/mL) had more frequent cardiovascular complications. This cytokine was directly related to mean left ventricular wall thickness ( r =0.23, P =0.002) and relative wall thickness ( r =0.25, P =0.0001); a multivariate analysis showed that this relation was independent of other risk factors. Accordingly, the prevalence of left ventricular concentric geometry (either concentric left ventricular hypertrophy or remodeling) was much higher (n=49, 53%) among patients with HGF values above the median that in those with values ≤1.85 ng/mL (n=31, 34%). Furthermore, the risk for left ventricular concentric geometry was higher in patients with HGF values above the median (odds ratio, 2.57; 95% CI, 1.33 to 4.98; P =0.005), and multiple logistic regression analysis confirmed that this association was independent of other risk factors. In patients receiving hemodialysis, elevated serum HGF is associated with concentric left ventricular geometry. This is consistent with reports that link this cytokine to arterial remodeling and survival in patients with end-stage renal disease and suggests that it is part of a counterregulatory response aimed at attenuating cardiovascular damage in this high-risk population.

Published
2003

3. CNP production in the kidney and effects of protein intake restriction in nephrotic syndrome

Author

Brenda K. Huntley, Emanuela de Pascale, Pietro Castellino, Mauro Giordano, Paola Belluardo, Toshihiro Tsuruda, John C. Burnett, Shang Chiun Lee, Alessandro Cataliotti, Gelsomina Giordano, Sharon M. Sandberg, Guido Boerrigter, Lorenzo Malatino, Michihisa Jougasaki, Lisa C. Costello, Cataliotti, A, Giordano, Mauro, DE PASCALE, E, Giordano, G, Castellino, P, Jougasaki, M, Costello, Lc, Boerrigter, G, Tsuruda, T, Belluardo, P, Lee, Sc, Huntley, B, Sandberg, S, Malatino, L, and BURNETT JC, Jr

Subjects
Adult, Male, medicine.medical_specialty, Nephrotic Syndrome, Physiology, medicine.drug_class, Urinary system, medicine.medical_treatment, In situ hybridization, Biology, Kidney, Low-protein diet, Internal medicine, Diet, Protein-Restricted, medicine, Natriuretic peptide, Humans, RNA, Messenger, In Situ Hybridization, Natriuretic Peptide, C-Type, Glomerulonephritis, Middle Aged, medicine.disease, Immunohistochemistry, Lipids, Proteinuria, Endocrinology, medicine.anatomical_structure, Female, Nephrotic syndrome, Glomerular Filtration Rate, Kidney disease
Abstract

C-type natriuretic peptide (CNP) possesses well-established cardiovascular properties. Although present in the mammalian kidney, CNP production in human kidney and its modulation in human renal disease remain less defined. We investigated the presence of CNP in normal human kidney and in patients with nephrotic syndrome (NS). We also addressed whether or not a low-protein diet (LPD) alters plasma CNP and urinary CNP excretion in NS. In situ hybridization studies demonstrated CNP mRNA expression in tubular cells and glomeruli of normal human kidneys. CNP immunoreactivity was positive in proximal, distal, and medullary collecting duct tubular cells in both controls and patients with NS. The ratios of plasma CNP and urinary CNP to creatinine were significantly higher in patients with NS compared with controls. Urinary CNP, but not plasma CNP, was significantly lowered in patients with NS after an LPD. Similarly, the ratios of urinary protein to creatinine and urinary albumin to creatinine, but not urinary guanosine 3′,5′-cyclic monophosphate to creatinine, decreased significantly with an LPD. These data confirm and extend previous reports and demonstrate for the first time the presence of CNP in human kidney with NS. We also report increased plasma CNP concentration and urinary CNP excretion in NS patients and a significant reduction of CNP excretion with an LPD. Our findings demonstrate that CNP metabolism is altered in patients with NS and support the hypothesis that activation of renal CNP can be partially offset by an LPD. These results underscore that the beneficial effect of an LPD on protein excretion is paralleled by a substantial reduction in intrarenal CNP release.

Catalog

Books, media, physical & digital resources
See catalog results