Publications by authors named "Gallieni M"

In Italy, the use of arteriovenous grafts (AVGs) is limited (1-4%) due to different approaches to vascular access management compared to other countries, where guidelines that may not apply to the Italian setting have been produced. Therefore, the Vascular Access Study Group of the Italian Society of Nephrology produced this position paper, providing a list of 8 recommendations built upon current guidelines. The most controversial and innovative issues of the existing guidelines have been summed up in 12 different topics.

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The Vascular Access Study Group of the Italian Society of Nephrology has scheduled four national studies regarding the choice, implantation and use of vascular access. Study topics will include 1) utilization of vascular grafts for hemodialysis; 2) indications and use of venous catheters; 3) tunneled central venous catheter infection; 4) organization of the implantation and repair of vascular access. After examining the difficulties in implementing international guidelines on vascular access in Italy and the differences in practice patterns between our and other countries (where the most important studies were published), the Study Group set out to prepare four position papers based on discussion of controversial aspects of the international guidelines by nephrologists and surgeons experienced in the Italian practice.

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Central venous catheters (CVCs) are fundamental in the management of hemodialysis. Despite major efforts to provide arteriovenous access, their use is increasing in dialysis units worldwide. The presence of a catheter inside a vein increases the risk of thrombosis, both within the catheter and in the vein.

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Secondary prevention after acute coronary syndromes should be aimed at reducing the risk of further adverse cardiovascular events, thereby improving quality of life, and lengthening survival. Despite compelling evidence from large randomized controlled trials, secondary prevention is not fully implemented in most cases after hospitalization for acute coronary syndrome. The Lazio Region (Italy) has about 5.

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Background: Diagnostic imaging of acute pyelonephritis (APN) in renal transplanted patients is an important clinical issue. While conventional ultrasonography (US) has a limited diagnostic role, contrast-enhanced computer tomography and magnetic resonance imaging (MRI) represent the gold standard diagnostic tests. However, nephrotoxicity of either iodinated or paramagnetic contrast medium limits their use, especially in patients with kidney disease.

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The occurrence of metabolic bone disease in patients with renal dysfunction is due to the key role played by the kidney in regulating calcium-phosphate metabolism. The incidence of hip fractures in end-stage renal disease is 3- to 4-fold higher than the general population, while poor data about vertebral fractures show similar prevalence. Bone health has been mainly evaluated in the general population through bone mass density (BMD) measurements, while in Chronic Kidney Disease (CKD) patients, bone turnover (low or high turnover) has been considered the most relevant parameter.

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Introduction: A combination therapy of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers has been used to control proteinuria, following initial demonstration of its efficacy. However, recently concerns about the safety of this therapy have emerged, prompting several authors to urge for caution in its use. In the following case report, we describe the occurrence of a serious and unexpected adverse drug reaction after administration of a combination of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers to a patient with nephrotic syndrome and liver cirrhosis with severe portal hypertension.

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ACE inhibitors and angiotensin receptor blockers confer renal protection in proteinuric nephropaties, but recently worsening of renal outcomes has been reported in non-proteinuric patients treated with a combination of ramipril and telmisartan, compared to ramipril only. In view of these apparently contradictory data, the review wants to shed light on treatment modalities of patients with hypertension and chronic kidney disease.

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Vascular calcification and accelerated atherosclerosis are major causes of death in hemodialysis (HD) patients. Epigenetic mechanisms of gene regulation may be crucial determinants of cellular behavior in uremic conditions, determining an increased risk of cardiovascular morbidity and mortality. The common polymorphisms on different gene promoters have been related to increased coronary artery calcification and associated with cardiovascular outcome in HD population.

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Dialysis access, including vascular access for hemodialysis and peritoneal access for peritoneal dialysis, is critical in the clinical care of patients with end-stage renal disease. It is associated with increases in morbidity, mortality, and health care costs. A number of problematic issues are involved, some of which are addressed in this paper with reference to the most recent publications, including: the inappropriately low prevalence of peritoneal dialysis in Western countries, which is relevant to access placement in the pre-dialysis stage; the excessively high use of central venous catheters in incident and prevalent dialysis patients; the diagnosis and treatment of steal syndrome; the advantages and limitations of antiplatelet therapy; and finally, the correct pre-operative evaluation and subsequent surveillance of the vascular access.

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Renovascular disease is a complex disorder, most commonly caused by fibromuscular dysplasia and atherosclerotic diseases. It can be found in one of three forms: asymptomatic renal artery stenosis (RAS), renovascular hypertension, and ischemic nephropathy. Particularly, the atherosclerotic form is a progressive disease that may lead to gradual and silent loss of renal function.

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Energy and protein metabolism are both altered in chronic kidney disease (CKD) from its early stages. Patients undergoing peritoneal dialysis (PD) use peritoneal solutions with glucose as osmotic agent, which exposes them to an increased glucose load (40-80 g/day) and during PD there is a net loss of proteins through the peritoneum (4-8 g/day). Insulin resistance may lead to a reduction of the anabolic effects of insulin, while its proliferative effects on adipose tissue are potentially enhanced.

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Chronic Kidney Disease Mineral and Bone Disorder (CKD-MBD) is a systemic disorder of mineral and bone metabolism that occurs in Chronic Kidney Disease (CKD). In addition to abnormalities in serum calcium (Ca) and phosphate (P) profile, CKD-MBD is characterized by abnormalities of bone turnover, mineralization, volume and growth as well as vascular calcification (VC). Indeed, the co-localization of bone markers such as Osteopontin, Alkaline Phosphatase and Osteocalcin along with osteoblast-like cells in the contest of the arterial wall of uremic patients, indicate that VC is an active biological process with peculiar analogies with bone mineralization.

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Patients with chronic kidney disease (CKD) are generally affected by secondary hyperparathyroidism (SHPT). High phosphate, low calcium and vitamin D deficiency represent the classical 'triad' involved into the pathogenesis of SHPT in renal insufficiency, in which downregulation of the parathyroid vitamin D receptor and calcium-sensing receptor represents a critical step. Recently, new studies indicate that fibroblast growth factor 23 may play a central role in the regulation of phosphate-vitamin D metabolism in patients with CKD.

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Background: About 300,000 patients in the United States with Chronic Kidney Failure (CKF) are of working age, but up to 70% lose their job within the first year of renal replacement therapy .No study has examined how work ability and perceived health are influenced by the subjects' adjustment to their job. We assessed the association of occupational stress (Effort-Reward Imbalance, ERI),work ability (WAI) and health-related quality of life (QoL) in hemodialysis.

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Secondary hyperparathyroidism is a serious complication of chronic renal disease when function decline and is characterized by abnormalities in serum calcium and phosphate profile, along with a decline in calcitriol synthesis. A reduced density of specific receptors for vitamin D and calcium in several tissues and organs are also present, thus contributing to parathyroid hyperplasia and abnormal parathyroid hormone synthesis and secretion. This metabolic derangement is observable early in the course of chronic renal failure (stages 3 and 4) and on this basis it should also be treated early in order to avoid important clinical consequences.

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Continuously emerging evidence indicates that defi ciencies in 25-hydroxyvitamin D and consequently vitamin D receptor (VDR) activation play crucial roles in adversely affecting cardiovascular (CV) health in the general population and those at high risk of CV disease, as well as in patients with chronic kidney disease (CKD). In CKD patients, a lack of VDR activation is one of the main pathophysiological factors contributing to secondary hyperparathyroidism (SHPT). However, this lack of VDR activation has numerous additional implications on CV and renal function, with SHPT being only one symptom of a much more extensive disorder.

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Large differences in dialysis access exist between Europe, Canada, and the United States, even after adjustment for patient characteristics. Vascular access care is characterized by similar issues, but with a different magnitude. Obesity, type 2 diabetes, and peripheral vascular disease, independent predictors of central venous catheter use, are growing problems globally, which could lead to more difficulties in native arteriovenous fistula placement and survival.

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Increased vascular calcification is a major cause of cardiovascular events in patients with chronic kidney disease (CKD). It is the result of an active ossification process counteracted by ''bone'' proteins such as osteopontin, alkaline phosphatase, osteoprotegerin, and osteocalcin. Chronic kidney disease - mineral and bone disorder (CKD-MBD) is a systemic disorder of mineral and bone metabolism that occurs in CKD.

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Although vitamin D was initially considered a nutrient, it has been recognized that the molecules derived from vitamin D metabolism are best considered as a complex endocrine system. In this review article we summarize the basic concepts regarding vitamin D metabolism, transport, and genomic activity through the vitamin D receptor, facilitating activation or suppression of target genes. We also examine non-genomic actions, biological responses to vitamin D in classic target organs (intestine, bone, kidneys, and parathyroid glands), and in organs and tissues not related to mineral homeostasis.

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Chronic renal failure is the primary cause of secondary hyperparathyroidism (SHPT). Patients with mineral metabolism disorders commonly present with low serum calcium levels, hyperphosphatemia, and calcitriol deficiency. In normal renal function subjects, parathyroid cells have a low turnover and rarely undergo mitoses.

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Background: Vascular calcification and accelerated atherosclerosis are major causes of death in haemodialysis (HD) patients. Matrix metalloproteinases (MMPs) are a family of enzymes, involved in the biology of extracellular matrix and in atherogenesis. MMP1 and MMP3 contribute to the enlargement and instability of atherosclerotic plaque, respectively.

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Extensive calcification of the arterial wall and soft tissues is a frequent feature of patients with end-stage chronic kidney disease (CKD stage 5). Hyperphosphatemia and secondary hyperparathyroidism have been extensively investigated as inducing factors in cardiovascular calcification. In fact, cardiovascular disease in renal failure is associated with bone metabolism alterations.

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