68 results on '"Lida Tartaglione"'
Search Results
52. Renal Diseases and Skeletal Health
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Sandro Mazzaferro, Lida Tartaglione, Cristiana Leonangeli, Natalia De Martino, Silverio Rotondi, and Marzia Pasquali
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medicine.medical_specialty ,Kidney ,Bone disease ,business.industry ,Osteoporosis ,Urology ,Renal function ,urologic and male genital diseases ,medicine.disease ,medicine.anatomical_structure ,Bone cell ,medicine ,Renal osteodystrophy ,Secondary hyperparathyroidism ,business ,Kidney disease - Abstract
Recent clinical observations underline the link between bone disease and disturbances of mineral metabolism with increased morbidity and mortality of Chronic Renal Failure (CRF). Indeed, in patients with Chronic Kidney Disease (CKD), bone disease may occur either with normal glomerular filtration rate (renal tubular disorders involving pH, Calcium or Phosphate metabolism) or with reduced glomerular filtration rate (the complex endocrine disorder of secondary hyperparathyroidism of CRF). Recently, to underline the clinical burden of this type of secondary hyperparathyroidism, a new clinical term has been introduced: CKD-MBD (chronic kidney disease-mineral and bone disorder). Besides bone disease, the endocrine derangements of mineral metabolism and the accelerated calcification processes of vessel walls are considered together in this syndrome, to highlight the pathogenetic link with cardiovascular disease and the eventual morbidity and mortality. The gold standard technique to diagnose renal osteodystrophy still remains the invasive bone biopsy. The less invasive biomarkers and radiologic techniques are less reliable to evaluate bone histology but are necessary to study the hormonal condition and the mechanical performance of the skeleton, respectively. As for therapy, it has been mostly focused on the control of secondary hyperparathyroidism, but this does not impact significantly the high fracture rate of renal patients. New drugs employed for osteoporosis and targeting specific functions of bone cells promise to open new therapeutic frontiers for renal osteodystrophy and CKD-MBD.
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- 2018
53. Calcitriol/calcifediol ratio: An indicator of vitamin D hydroxylation efficiency?
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Giusi Mandanici, Maria Luisa Muci, Silverio Rotondi, Sandro Mazzaferro, Martino Marangella, Marzia Pasquali, Alessio Farcomeni, and Lida Tartaglione
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calcitriol ,medicine.medical_specialty ,Calcitriol ,calcifediol ,vitamin D ,Pharmacology ,Pathology and Forensic Medicine ,Hydroxylation ,chemistry.chemical_compound ,chronic renal failure ,Physiology (medical) ,Internal medicine ,polycyclic compounds ,Vitamin D and neurology ,medicine ,business.industry ,Regular Article ,Serum concentration ,renal transplantation ,Endocrinology ,chemistry ,Molecular Medicine ,Chronic renal failure ,lipids (amino acids, peptides, and proteins) ,Calcifediol ,vitamin D hydroxylation ,Settore SECS-S/01 - Statistica ,business ,medicine.drug - Abstract
Background Calcifediol (25D) availability is crucial for calcitriol (1,25D) synthesis, but regulation of vitamin D hydroxylases is majorly responsible for 1,25D synthesis. The net efficiency of vitamin D hydroxylases might be informative. We assume that the ratio between calcitriol and calcifediol (25D/1,25D) serum concentrations could suggest the vitamin D hydroxylation efficiency. Methods We evaluated 25D/1,25D in different patient populations: hemodialysis (HD, n = 76), CKD stage 2–5 (n = 111), renal transplant (TX, n = 135), patients with no renal disease (No-CKD, n = 290), and primary hyperparathyroidism (PHP, n = 20). Results The geometric mean of 1,25D/25D (pg/ng) averaged 1.11 (HD), 1.36 (CKD), 1.77 (TX), 2.22 (No-CKD), and 4.11 (PHP), with a progressive increment from HD to PHP (p-value for the trend, Highlights • 1,25D/25D ratio could represent an index of vitamin D hydroxylation efficiency. • 1,25D/25D ratio progressively increases from HD to CKD, TX, No-CKD and PHP. • Each of these clinical conditions affected the value of the ratio. • In selected populations 1,25D/25D ratio could guide substitutive therapeutic choices.
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- 2015
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54. [New biomarkers of CKD-MBD]
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Marzia, Pasquali, Lida, Tartaglione, and Silverio, Rotondi
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Chronic Kidney Disease-Mineral and Bone Disorder ,Fibroblast Growth Factors ,Genetic Markers ,Fibroblast Growth Factor-23 ,Bone Morphogenetic Proteins ,Humans ,Klotho Proteins ,Biomarkers ,Adaptor Proteins, Signal Transducing ,Glucuronidase - Abstract
Chronic kidney failure involves abnormalities of mineral metabolism, skeletal and of cardiovascular system (so called CKD - MBD) that have a major impact on the survival of renal patient. Increasingly complex pathophysiological mechanisms have been discovered in recent years with evidence of new molecules involved in the development of CKD - MBD. Besides the classical PTH / Vitamin D axis, the most recent discovery of a new FGF23 / Klotho axis has expanded knowledge on the mechanisms of mineral homeostasis but also on the more complex mechanisms of cellular aging, vascular calcification and cardiac remodeling. The importance of bone as an endocrine organ has become even more evident following the discovery of molecules such as Sclerostin (involved in the regulation of osteoblastic proliferation and differentiation) and Sibling (a family of proteins that regulate both local and systemic mineral metabolism). The ability to characterize as biomarkers of CKD - MBD for these new molecules depends on their eventual ability to express a specific pathophysiological processes, identify patients at risk, highlight the response to a therapeutic treatment and to be easily identifiable and quantifiable on biological fluids. As of today, it seems that we can recognize FGF23 as a biomarker of CKD-MBD, while the remaining molecules as still waiting for a more definite settlement.
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- 2017
55. Positioning novel biologicals in CKD-mineral and bone disorders
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Silverio Rotondi, Adrian Covic, Marzia Pasquali, Maria Luisa Muci, Lida Tartaglione, and Sandro Mazzaferro
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medicine.medical_specialty ,PTH 1–34 ,Bone disease ,Osteoporosis ,030232 urology & nephrology ,Romosozumab ,030209 endocrinology & metabolism ,bone mineral density ,denosumab ,mineral bone disorders ,osteoporosis ,renal osteodystrophy ,romosozumab ,teriparatide ,Bioinformatics ,Bone and Bones ,Bone remodeling ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,Bone cell ,medicine ,Teriparatide ,Animals ,Humans ,Renal osteodystrophy ,Renal Insufficiency, Chronic ,Chronic Kidney Disease-Mineral and Bone Disorder ,Biological Products ,Bone Density Conservation Agents ,business.industry ,Antibodies, Monoclonal ,medicine.disease ,Endocrinology ,Denosumab ,Nephrology ,Parathyroid Hormone ,business ,medicine.drug - Abstract
Renal osteodystrophy (ROD), the histologic bone lesions of chronic kidney disease (CKD), is now included in a wider syndrome with laboratory abnormalities of mineral metabolism and extra-skeletal calcifications or CKD-mineral and bone disorders (CKD-MBD), to highlight the increased burden of mortality. Aging people, frequently identified as early CKD, could suffer from either the classical age-related osteoporosis (OP) or ROD. Distinguishing between these two bone diseases may not be easy without bone biopsy. In any case, besides classical therapies for ROD, nephrologists are now challenged by the possibility of using new drugs developed for OP. Importantly, while therapies for ROD mostly aim at controlling parathyroid secretion with bone effects regarded as indirect, new drugs for OP directly modulate bone cells activity. Thus, their action could be useful in specific types of ROD. Parathyroid hormone therapy, which is anabolic in OP, could be useful in renal patients with low turnover bone disease. Denosumab, the monoclonal antibody against receptor activator of NF-κB ligand (RANK-L) that inhibits osteoclast activity and proliferation, could be beneficial in cases with high turnover bone. Use of romosozumab, the monoclonal antibody against sclerostin, which both stimulates osteoblasts and inhibits osteoclasts, could allow both anabolic and anti-resorptive effects. However, we should not forget the systemic role now attributed to CKD-MBD. In fact, therapies targeting bone cells activity could also result in unpredicted extra-bone effects and affect cardiovascular outcomes. In conclusion, the new biologicals established for OP could be useful in renal patients with either OP or ROD. In addition, their potential non-bone effects warrant investigation.
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- 2017
56. Interactions of sclerostin with FGF23, soluble klotho and vitamin D in renal transplantation
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Sandro Mazzaferro, Marzia Pasquali, Maria Luisa Muci, Cristiana Leonangeli, Alessio Farcomeni, Silverio Rotondi, Valeria Fassino, and Lida Tartaglione
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Male ,Fibroblast growth factor 23 ,Fibroblast Growth Factor ,Physiology ,030232 urology & nephrology ,Organic chemistry ,lcsh:Medicine ,Biochemistry ,Bone remodeling ,chemistry.chemical_compound ,Endocrinology ,0302 clinical medicine ,FGF23 ,Chronic Kidney Disease ,Medicine and Health Sciences ,Renal Transplantation ,Sclerostin, FGF23, Transplantation, Vitamin D ,Vitamin D ,lcsh:Science ,Klotho ,Glucuronidase ,Kidney ,Multidisciplinary ,Vitamins ,Middle Aged ,Enzymes ,Physical sciences ,Chemistry ,medicine.anatomical_structure ,Nephrology ,Parathyroid Hormone ,Bone Morphogenetic Proteins ,Alkaline phosphatase ,Female ,Settore SECS-S/01 - Statistica ,Research Article ,Genetic Markers ,medicine.medical_specialty ,Sclerostin ,Transplantation ,Surgical and Invasive Medical Procedures ,030209 endocrinology & metabolism ,Urinary System Procedures ,Phosphates ,Chemical compounds ,03 medical and health sciences ,Growth Factors ,Internal medicine ,Organic compounds ,medicine ,Vitamin D and neurology ,Humans ,Klotho Proteins ,Adaptor Proteins, Signal Transducing ,Endocrine Physiology ,business.industry ,lcsh:R ,Phosphatases ,Biology and Life Sciences ,Proteins ,Organ Transplantation ,Kidney Transplantation ,Hormones ,Fibroblast Growth Factors ,Fibroblast Growth Factor-23 ,Cross-Sectional Studies ,chemistry ,Enzymology ,lcsh:Q ,business ,Biomarkers - Abstract
Relationships of Sclerostin, a bone anti-anabolic protein, with biomarkers of mineral bone disorders in chronic kidney disease are still unsettled, in particular in kidney transplant (KTR). In 80 KTR patients (31F/49M, 54.7±10.3 years) we studied the relationships of serum Sclerostin with eGFR, Calcium, Phosphate, Alkaline Phosphatase (AP), intact Parathyroid hormone (iPTH), soluble alpha-Klotho (sKlotho), intact Fibroblast Growth Factor 23 (iFGF23), 25-hydroxyvitamin D(25D) and 1,25-dihydroxyvitamin D (1,25D). Thirty healthy subjects (35.0±12.4 years, eGFR 109.1±14.1 ml /min/1,73m2) served as control for Sclerostin, iFGF23 and sKlotho. With a median eGFR of 46.3 mL/min/1.73m2 (IQR, 36.2–58.3) our KTR had median Sclerostin levels of 23.7 pmol/L (IQR: 20.8–32.8), not different from controls (26.6 pmol/L, IQR: 22.0–32.2; p = n.s). Sclerostin correlated negatively with AP (r = -.251; p = 0.023) and positively with iFGF23 (r = .227; p = 0.017) and 25D (r = .214; p = 0.025). Age-adjusted multiple regression analysis identified AP and 1,25D as negative and 25D and sKlotho as positive best predictors of Sclerostin. No correlation was evident with eGFR. The negative correlation with AP confirms the direct anti-anabolic role of Sclerostin. The associations either negative or positive with iFGF23, sKlotho, and vitamin D metabolites suggest also a modulatory role in mineral homeostasis. In particular, the associations with iFGF23 (positive) and 1,25D (negative) underline the relevant inhibitory action of Sclerostin on vitamin D activation. In conclusion, Sclerostin levels in KTR are normal and influenced more by bone turnover than by eGFR. Its involvement with other hormones of mineral homeostasis (FGF23/Klotho and Vitamin D) is part of the sophisticated cross-talk between bone and the kidney.
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- 2017
57. Further Vitamin D Analogs
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Marzia Pasquali, Silverio Rotondi, Sandro Mazzaferro, C Leonangeli, and Lida Tartaglione
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Pharmacology ,chemistry.chemical_classification ,Bicyclic molecule ,Animals ,Bone Density ,Humans ,Hyperparathyroidism, Secondary ,Osteoporosis ,Structure-Activity Relationship ,Vitamin D ,business.industry ,Calcitriol receptor ,In vitro ,Transport protein ,Enzyme ,chemistry ,Biochemistry ,Vitamin D and neurology ,Medicine ,Structure–activity relationship ,Cardiology and Cardiovascular Medicine ,business ,Receptor - Abstract
In this brief review we point out the specificities of the vitamin D system that are necessary to understand why each change in the molecule can result in significantly different biologic effects. Vitamin D, with a specific receptor in most of the tissues, has innumerable potential therapeutic applications in many clinical fields. However, excessive pharmacologic increments of circulating natural metabolites carry the risk of significant side effects. To avoid this, natural vitamin D molecules have been modified to more selectively stimulate some tissues. Changes have been attempted on particular parts of the molecule in order to affect some specific step of the complex machinery that characterize the vitamin D system. The first modifications were those in the side chain of the molecule, which are expected to affect, either or both, the steps of binding to transfer protein or the interaction with catabolic enzymes. More recently other regions, like A-ring (involved with receptor interaction) or CD bicyclic ring (involved with molecule stability), have been modified to obtain always more selective products. Notably each modification of the molecule also affects its shape thus further and variably modifying its interaction with the VDR, with the transport proteins or the catabolic enzymes. As a consequence, the biologic effects of new molecules become less predictable and require in vitro evaluation, experimental animal studies and a complete and specific clinical validation in specific disease states. With thousands of analogs synthesized in the laboratories, only a minority are approved for clinical employment. Besides secondary hyperparathyroidism and osteoporosis, Vitamin D analogs can be employed in other clinical conditions like cancer and autoimmunity diseases. We briefly report on some new experimental or already approved analogs in their main clinical fields of employment.
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- 2014
58. Ruolo della chirurgia bariatrica nel paziente con malattia renale cronica
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Maria Luisa Muci, Silverio Rotondi, Sandro Mazzaferro, Lida Tartaglione, Rosa Grimaldi, Francesca Abbatini, Gianfranco Silecchia, and Mario Rizzello
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medicine.medical_specialty ,lcsh:Internal medicine ,Renal function ,urologic and male genital diseases ,lcsh:RC870-923 ,Internal medicine ,Diabetes mellitus ,Chronic renal failure ,Medicine ,Pharmacology (medical) ,Risk factor ,lcsh:RC31-1245 ,Contraindication ,Bariatric surgery ,Proteinuria ,business.industry ,Metabolic derangements ,medicine.disease ,lcsh:Diseases of the genitourinary system. Urology ,Transplantation ,medicine.symptom ,business ,Progression of renal failure ,Severe obesity ,Dyslipidemia ,Kidney disease - Abstract
Bariatric surgery represents the elective treatment of severe obesity (BMI≥40Kg/m2) since it results in better control of cardiovascular risk factors and comorbidities typically associated with obesity, like diabetes, hypertension and dyslipidemia. Obesity is a recognized independent risk factor for chronic kidney disease and for progression of renal insufficiency. Pathomechanisms are still incompletely known. Obesity is associated with hyper-filtration, microalbuminuria and proteinuria all of which favor renal disease and its progression. This narrative review reports on the available evidence linking bariatric surgery and renal function since this surgery may affect proteinuria, hyper-filtration and glomerular filtration rate. Although available data are limited in particular in cases with more advanced stages of renal failure, bariatric surgery associates with improved filtration and lower proteinuria in patients with mild to moderate renal insufficiency. In patients with more advanced stages of renal failure, surgery should be considered if obesity represents a relative contraindication to transplantation. Surgery seems to improve graft survival. Further, nephrologists should be informed on the metabolic and nutritional changes associated with bariatric surgery, which could be responsible for untoward effects requiring early identification and treatment. Bariatric surgery could be a valid therapeutic option in renal patients to improve the negative clinical outcomes of obese subjects.
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- 2016
59. Interaction Between Vitamin D and Calcimimetics in Chronic Kidney Disease
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Marzia Pasquali, Sandro Mazzaferro, Silverio Rotondi, and Lida Tartaglione
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Fibroblast growth factor 23 ,Paricalcitol ,Vitamin D analogs ,medicine.medical_specialty ,Cinacalcet ,Calcimimetic ,030232 urology & nephrology ,Parathyroid hormone ,030204 cardiovascular system & hematology ,Calcitriol receptor ,Chronic kidney disease mineral bone disorders (CKD-MBD) ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,Chronic renal failure ,Dialysis ,Secondary hyperparathyroidism ,Vitamin D ,medicine ,Vitamin D and neurology ,business.industry ,medicine.disease ,Endocrinology ,business ,medicine.drug - Abstract
For many years vitamin D has been the only available drug to suppress parathyroid hormone (PTH) hypersecretion in patients with renal insufficiency. This effect is accomplished directly through activation of the vitamin D receptor (VDR) on parathyroid cells. However, vitamin D also stimulates intestinal absorption of calcium and phosphate, thus often resulting in hypercalcemia and hyperphosphatemia, both undesirable in renal patients. For this reason vitamin D analogs with less calcemic effects have been developed, with some improvement of this problematic effect. The discovery of calcium sensing receptor (CaSR) and the subsequent production of drugs capable of stimulating it, has allowed the introduction of calcimimetics as an alternative therapy to vitamin D. Cinacalcet, the first to be available for clinical uses, has been successfully employed to reduce serum PTH levels in patients with end stage renal disease. At variance with vitamin D, calcimimetics, while decreasing PTH, also decrease serum levels of calcium and phosphate. The effect on serum calcium is of such entity that symptomatic hypocalcemia may occur. As a consequence, vitamin D is frequently associated and instead of becoming an alternative, cinacalcet is mostly prescribed together with vitamin D. Importantly, we have clear experimental evidence that vitamin D administration increases the expression of CaSR on target cells and that, reciprocally, calcimimetics increase VDR expression. This interaction allows presuming potential clinical advantages to control secondary hyperparathyroidism. Further, since both VDR and CaSR are expressed also in tissues not involved with mineral metabolism, other still unpredicted clinical effects are possible.
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- 2016
60. Distinct impact of vitamin D insufficiency on calcitriol levels in chronic renal failure and renal transplant patients: a role for FGF23
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Silverio Rotondi, Marzia Pasquali, Lida Tartaglione, Franco Citterio, Sandro Mazzaferro, Franco Taggi, Antonio R. Gargiulo, Francesco Pugliese, Giuliana Pirrò, and Carmina Conte
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Male ,calcitriol ,25- hydroxy-cholecalciferol ,Settore MED/18 - CHIRURGIA GENERALE ,Parathyroid hormone ,viamine D ,Vitamin D ,25-hydroxy-cholecalciferol ,Kidney transplantation ,renal transplantation ,Middle Aged ,Nephrology ,Regression Analysis ,Biological Markers ,Female ,Secondary hyperparathyroidism ,Glomerular Filtration Rate ,medicine.drug ,Adult ,medicine.medical_specialty ,vitamin d hydroxylation ,Calcitriol ,Renal function ,Hydroxylation ,vitamin D deficiency ,Phosphates ,chronic renal failure ,Internal medicine ,medicine ,Vitamin D and neurology ,Humans ,parathyroid hormone ,Aged ,Chi-Square Distribution ,business.industry ,fgf23 ,transplantation ,Alkaline Phosphatase ,Vitamin D Deficiency ,medicine.disease ,Kidney Transplantation ,Fibroblast Growth Factors ,Fibroblast Growth Factor-23 ,Endocrinology ,Dietary Supplements ,Kidney Failure, Chronic ,renal ,Calcium ,business ,Biomarkers ,Kidney disease - Abstract
INTRODUCTION Vitamin D insufficiency contributes to calcitriol (1,25D) reduction in chronic kidney disease (CKD). Since CKD patients on conservative therapy (CRF) mostly develop, whereas transplant (TX) patients possibly recover from, secondary hyperparathyroidism (SH), we hypothesized a different efficiency of vitamin D hydroxylation in these 2 clinical conditions. METHODS We compared the impact of reduced 25-hydroxyvitamin D (25D) on circulating 1,25D in 111 CRF (mean age 63 ± 15 years; estimated glomerular filtration rate [eGFR] 36.4 ± 22.0 ml/min) and in 136 TX patients (mean age 50 ± 11 years; eGFR 47 ± 19.0 ml/min). RESULTS Vitamin D insufficient patients (69.1% in TX vs. 82% in CRF; p
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- 2012
61. SP439EVALUATION OF VASCULAR DAMAGE BY CARDIO-ANKLE VASCULAR INDEX (CAVI) IN TYPE 2 DIABETES PATIENTS
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Silverio Rotondi, Gaetano Leto, Daniela Mastroluca, Angela Carlone, Lida Tartaglione, Maria Luisa Muci, Marzia Pasquali, Luca D'Onofrio, Sandro Mazzaferro, and Raffaella Buzzetti
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0301 basic medicine ,Transplantation ,medicine.medical_specialty ,business.industry ,030209 endocrinology & metabolism ,Type 2 diabetes ,medicine.disease ,03 medical and health sciences ,0302 clinical medicine ,Nephrology ,Internal medicine ,medicine ,Cardiology ,030101 anatomy & morphology ,Cardio-ankle vascular index ,business - Published
- 2018
62. Soluble α-Klotho Serum Levels in Chronic Kidney Disease
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Alessio Farcomeni, Silverio Rotondi, Maria Luisa Muci, Sandro Mazzaferro, Lida Tartaglione, Giusy Mandanici, Marzia Pasquali, Silvia Sales, and Cristiana Leonangeli
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medicine.medical_specialty ,Pathology ,Article Subject ,Endocrinology, Diabetes and Metabolism ,chemistry.chemical_element ,Calcium ,urologic and male genital diseases ,lcsh:Diseases of the endocrine glands. Clinical endocrinology ,chemistry.chemical_compound ,Endocrinology ,Internal medicine ,Medicine ,Clinical significance ,lcsh:RC648-665 ,Endocrine and Autonomic Systems ,business.industry ,Serum phosphate ,α klotho ,Phosphate ,medicine.disease ,female genital diseases and pregnancy complications ,chemistry ,business ,Kidney disease ,Research Article - Abstract
Transmembraneα-Klotho (TM-Klotho), expressed in renal tubules, is a cofactor for FGF23-receptor. Circulating soluble-α-Klotho (s-Klotho) results from TM-Klotho shedding and acts on Phosphate (P) and Calcium (Ca) tubular transport. Decreased TM-Klotho, described in experimental chronic kidney disease (CKD), prevents actions of FGF23 and lessens circulating s-Klotho. Thus, levels of s-Klotho could represent a marker of CKD-MBD. To evaluate the clinical significance of s-Klotho in CKD we assayed serum s-Klotho and serum FGF23 in 68 patients (age58±15; eGFR45±21 mL/min). s-Klotho was lower than normal (519±183versus845±330 pg/mL,P<.0001) in renal patients and its reduction was detectable since CKD stage 2 (P<.01). s-Klotho correlated positively with eGFR and serum calcium (Cas) and negatively with serum phosphate (Ps), PTH and FGF23. FGF23 was higher than normal (73±51versus36±11,P<.0002) with significantly increased levels since CKD stage 2 (P<.001). Our data indicate a negative effect of renal disease on circulating s-Klotho starting very early in CKD. Assuming that s-Klotho mirrors TM-Klotho synthesis, low circulating s-Klotho seems to reflect the ensuing of tubular resistance to FGF23, which, accordingly, is increased. We endorse s-Klotho as an early marker of CKD-MBD.
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- 2015
63. SP657RELATIOSHIP BETWEEN VASCULAR ACCESS (VA) TRIAGE AND CLINICAL EVENTS IN HAEMODIALYSIS (HD)
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Luciano Carbone, Silverio Rotondi, Sandro Mazzaferro, Maria Luisa Muci, and Lida Tartaglione
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Transplantation ,medicine.medical_specialty ,Nephrology ,Clinical events ,business.industry ,Vascular access ,Medicine ,business ,Intensive care medicine ,Triage - Published
- 2017
64. News on Biomarkers in CKD-MBD
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Jordi Bover, Marzia Pasquali, David Goldsmith, Silverio Rotondi, Lida Tartaglione, and Sandro Mazzaferro
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medicine.medical_specialty ,Acid Phosphatase ,Osteocalcin ,Parathyroid hormone ,Bone remodeling ,Osteoprotegerin ,Internal medicine ,Matrix gla protein ,medicine ,Animals ,Humans ,Renal osteodystrophy ,Renal Insufficiency, Chronic ,Chronic Kidney Disease-Mineral and Bone Disorder ,ASARM ,BALP ,Bone collagen peptides ,Matrix Gla protein ,SIBLINGs ,TRAP-5b ,Alkaline Phosphatase ,Biological Markers ,Calcium-Binding Proteins ,Extracellular Matrix Proteins ,Hyperparathyroidism, Secondary ,Isoenzymes ,Parathyroid Hormone ,Peptide Fragments ,Procollagen ,RANK Ligand ,Receptor Activator of Nuclear Factor-kappa B ,Renal Osteodystrophy ,Nephrology ,Medicine (all) ,biology ,Tartrate-Resistant Acid Phosphatase ,medicine.disease ,Endocrinology ,biology.protein ,Secondary hyperparathyroidism ,Biomarkers ,Calcification - Abstract
The increased awareness of the potential role played by mineral and bone disorder in the appearance of cardiovascular disease in renal patients has produced research efforts aimed at discovering possible pathogenic links. Accordingly, the diagnostic significance of the classic bone markers of mineral disorders and of the new markers in the setting of chronic kidney disease-mineral and bone disorders (CKD-MBD) needs to be re-evaluated along with increasing information. In this article we include classic markers of bone metabolism and some of the noncollagenous bone proteins that are gaining experimental and clinical significance in CKD-MBD. Among classic markers of secondary hyperparathyroidism and of renal osteodystrophy, we analyzed parathyroid hormone, alkaline phosphatase, tartrate-resistant acid phosphatase, and bone collagen-derived peptides. We underlined, for each, the relevance of parent proteins (peptides or isoforms) that affect assay methods and, eventually, the diagnostic or prognostic significance. Also, we considered their relationship with cardiovascular mortality. Among the numerous noncollagenous bone proteins, we examined matrix Gla protein (MGP), osteocalcin (OC), osteoprotegerin, and the small integrin-binding ligand N-linked glycoprotein family. For MGP and OC we report the relevant involvement with the process of calcification (MGP) and with glucose and energy metabolism (OC). Both of these proteins require vitamin K to become active and this is a specific problem in renal patients who frequently are deficient of this vitamin. Finally, recent acquisitions on the fascinating family of the small integrin-binding ligand N-linked glycoprotein proteins are recapitulated briefly to underline their potential clinical interest and their complex involvement with all aspects of CKD-MBD. Their diagnostic role in clinical practice awaits further studies.
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- 2014
65. FP414SERUM SCLEROSTIN LEVELS IN HAEMODIALYSIS PATIENTS AND THEIR CORRELATION WITH THE INFLAMMATORY STATE
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Cristiana Leonangeli, Marzia Pasquali, Silverio Rotondi, Maria Luisa Muci, Sandro Mazzaferro, and Lida Tartaglione
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Correlation ,Transplantation ,medicine.medical_specialty ,chemistry.chemical_compound ,Endocrinology ,chemistry ,Nephrology ,business.industry ,Internal medicine ,medicine ,Sclerostin ,business - Published
- 2015
66. [Update on the pathogenesis and possible therapeutic approach to vascular calcifications in patients with chronic renal failure]
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Marzia, Pasquali, Lida, Tartaglione, Silverio, Rotondi, Maria Luisa, Muci, Giuliana, Pirro', and Sandro, Mazzaferro
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Osteoblasts ,Diphosphonates ,Calcinosis ,Vitamin D Deficiency ,Muscle, Smooth, Vascular ,Renal Dialysis ,Risk Factors ,Cations ,Disease Progression ,Chemical Precipitation ,Humans ,Kidney Failure, Chronic ,Hyperparathyroidism, Secondary ,Vascular Diseases ,Warfarin - Abstract
Chronic renal failure is a well-known risk condition for cardiovascular disease and in particular vascular calcifications. In fact, with respect to the normal population, where only ''classic'' risk factors have been described, kidney patients also have non-classic risk conditions. Among these, alterations in divalent ions, parathyroid hormone and vitamin D are of utmost importance. Further, several substances are recognized to have inhibitory or inductive effects in the pathogenesis of vascular calcifications, affecting either the calcium salts precipitation phenomenon or the phenotypic transformation of vascular smooth muscle cells into osteoblast-like cells (the latter phenomenon being regarded as a determinant of calcification of the tunica media). Given that vascular calcifications are irreversible, therapeutic strategies are aimed at preventing their formation or at blunting their progression (which is especially accelerated in renal patients). For this purpose it is essential to pursue optimal biochemical control of secondary hyperparathyroidism, but we must consider that in the individual patient the choice of drugs and their dosage can be essential for the development of calcifications. Given the physiological importance of inhibitory substances, we can hypothesize their future use in this setting. Finally, we must consider that by administering drugs known to interfere with inhibitors (like warfarin) or with the normal process of mineralization (like bisphosphonates), we can hypothetically favor or respectively prevent vascular calcifications.
- Published
- 2011
67. Does any therapy exist for vascular calcifications in uremia?
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Lida Tartaglione, Silverio Rotondi, Sandro Mazzaferro, and Marzia Pasquali
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medicine.medical_specialty ,Thiosulfates ,Parathyroid hormone ,Bioinformatics ,Osteoprotegerin ,Internal medicine ,Matrix gla protein ,medicine ,Animals ,Humans ,Clinical significance ,Vascular Diseases ,Osteopontin ,Uremia ,Minerals ,Diphosphonates ,biology ,business.industry ,Calcinosis ,Metabolic acidosis ,medicine.disease ,Diphosphates ,Disease Models, Animal ,Endocrinology ,Nephrology ,biology.protein ,business ,Calcification - Abstract
The pathogenesis of vascular calcifications in uremia is not completely understood, but is regarded as multifactorial, involving traditional and nontraditional risk factors. In particular, derangements in divalent ions are considered of outmost importance, but also the role of physiologic inhibitors of calcification is now claimed. The most powerful physiologic inhibitor of calcification is pyrophosphate, but its biochemical instability precludes its clinical use to date. The pharmacologic analogs of pyrophosphate, bisphosphonates, cannot be easily tested for this purpose in renal patients, given their renal clearance. The list of proteins involved in calcification is a growing one, and experimental models point to the potential clinical relevance of matrix Gla protein, fetuin, osteopontin, osteoprotegerin and bone morphogenetic protein-7. Induction of metabolic acidosis, although theoretically useful, is not recommended, while administration of sodium thiosulphate could be beneficial, but its safety awaits confirmation. Actually, the only available therapies for vascular calcifications are those directed toward achievement of the biochemical targets for calcium, phosphate and parathyroid hormone with the hope, but not the certainty, that this will be efficacious. However, to this purpose, selection of the most appropriate strategy in the individual patient seems essential.
- Published
- 2011
68. The bone and the kidney
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Sandro Mazzaferro, Silverio Rotondi, Giuliana Pirrò, Marzia Pasquali, and Lida Tartaglione
- Subjects
bmp-7 ,medicine.medical_specialty ,Calcitriol ,Bone disease ,Bone Morphogenetic Protein 7 ,klotho ,Osteoporosis ,Biophysics ,osteomalacia ,urologic and male genital diseases ,Biochemistry ,renal osteodystrophy ,Internal medicine ,rickets ,medicine ,Animals ,Humans ,Renal osteodystrophy ,Klotho Proteins ,Molecular Biology ,Klotho ,Glucuronidase ,Kidney ,Osteomalacia ,business.industry ,fgf23 ,medicine.disease ,Fibroblast Growth Factors ,Bone morphogenetic protein 7 ,Fibroblast Growth Factor-23 ,stomatognathic diseases ,Endocrinology ,medicine.anatomical_structure ,ckd-mbd ,Kidney Diseases ,Bone Diseases ,business ,medicine.drug - Abstract
Renal tubular diseases may present with osteopenia, osteoporosis or osteomalacia, as a result of significant derangements in body electrolytes. In case of insufficient synthesis of calcitriol, as in renal failure, the more complex picture of renal osteodystrophy may develop. Hypothetically, also disturbed renal production of BMP-7 and Klotho could cause bone disease. However, the acknowledgment that osteocytes are capable of producing FGF23, a phosphaturic hormone at the same time modulating renal synthesis of calcitriol, indicates that it is also bone that can influence renal function. Importantly, a feed-back mechanism exists between FGF23 and calcitriol synthesis, while Klotho, produced by the kidney, determines activity and selectivity of FGF23. Identification of human diseases linked to disturbed production of FGF23 and Klotho underlines the importance of this new bone-kidney axis. Kidney and bone communicate reciprocally to regulate the sophisticated machinery responsible for divalent ions homeostasis and for osseous or extraosseous mineralisation processes.
- Published
- 2010
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