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1.
FASEB J ; 35(2): e21358, 2021 02.
Article in English | MEDLINE | ID: mdl-33538061

ABSTRACT

Treatment of respiratory viral infections remains a global health concern, mainly due to the inefficacy of available drugs. Therefore, the discovery of novel antiviral compounds is needed; in this context, antimicrobial peptides (AMPs) like temporins hold great promise. Here, we discovered that the harmless temporin G (TG) significantly inhibited the early life-cycle phases of influenza virus. The in vitro hemagglutinating test revealed the existence of TG interaction with the viral hemagglutinin (HA) protein. Furthermore, the hemolysis inhibition assay and the molecular docking studies confirmed a TG/HA complex formation at the level of the conserved hydrophobic stem groove of HA. Remarkably, these findings highlight the ability of TG to block the conformational rearrangements of HA2 subunit, which are essential for the viral envelope fusion with intracellular endocytic vesicles, thereby neutralizing the virus entry into the host cell. In comparison, in the case of parainfluenza virus, which penetrates host cells upon a membrane-fusion process, addition of TG to infected cells provoked ~1.2 log reduction of viral titer released in the supernatant. Nevertheless, at the same condition, an immunofluorescent assay showed that the expression of viral hemagglutinin/neuraminidase protein was not significantly reduced. This suggested a peptide-mediated block of some late steps of viral replication and therefore the impairment of the extracellular release of viral particles. Overall, our results are the first demonstration of the ability of an AMP to interfere with the replication of respiratory viruses with a different mechanism of cell entry and will open a new avenue for the development of novel therapeutic approaches against a large variety of respiratory viruses, including the recent SARS-CoV2.


Subject(s)
Antimicrobial Cationic Peptides/pharmacology , Antiviral Agents/pharmacology , Influenza A Virus, H1N1 Subtype/drug effects , Parainfluenza Virus 1, Human/drug effects , A549 Cells , Animals , Antimicrobial Cationic Peptides/chemistry , Antiviral Agents/chemistry , Binding Sites , Dogs , HN Protein/chemistry , HN Protein/metabolism , Hemagglutinin Glycoproteins, Influenza Virus/chemistry , Hemagglutinin Glycoproteins, Influenza Virus/metabolism , Humans , Influenza A Virus, H1N1 Subtype/physiology , Madin Darby Canine Kidney Cells , Molecular Docking Simulation , Parainfluenza Virus 1, Human/physiology , Protein Binding , Virus Internalization , Virus Replication
2.
Clin Nephrol ; 76(3): 201-9, 2011 Sep.
Article in English | MEDLINE | ID: mdl-21888857

ABSTRACT

AIMS: Considering the growing relevance of fibroblast growth factor-23 (FGF-23) in the pathogenesis of chronic kidney disease bone and mineral disorder (CKD-MBD), an analysis was performed to determine the relative importance of C-terminal (cFGF-23) and intact (iFGF-23) assays in assessing CKD-MBD status in the first place and the relationship between FGF-23 and mortality as a secondary aim. METHODS: In 77 patients (15 peritoneal dialysis and 62 hemodialysis), levels of calcium, phosphate, parathyroid hormone (PTH), 25-hydroxyvitamin- D (25D), 1,25D, FGF-23 (C-terminal and intact molecule) were measured and their correlations were analyzed. The relationship between FGF-23 levels and patient survival was also analyzed. RESULTS: A significant correlation was found between cFGF-23 and 1,25D, PTH and 25D while iFGF-23 was significantly correlated with phosphate, 25D and PTH. PTH and 1,25D were independent predictors of cFGF-23, while for iFGF-23 independent predictors were phosphate and 25D. No significant relationship was found between FGF-23 and mortality. CONCLUSIONS: C-terminal or intact FGF-23 levels are weakly correlated and thus not clearly indicative of FGF-23 effects on PTH, P and vitamin D metabolism in dialysis patients. Assays for cFGF-23 and iFGF-23 showed a good correlation, but the intact molecule was not superior in defining interactions with CKD-MBD molecules. Measuring FGF-23 on a regular basis with the current assays in CKD and dialysis patients does not yet seem clinically useful.


Subject(s)
Bone Density , Fibroblast Growth Factors/blood , Kidney Failure, Chronic/blood , Renal Dialysis , Aged , Calcium/blood , Female , Fibroblast Growth Factor-23 , Humans , Kidney Failure, Chronic/metabolism , Kidney Failure, Chronic/mortality , Kidney Failure, Chronic/therapy , Male , Middle Aged , Parathyroid Hormone/blood , Peritoneal Dialysis , Phosphates/blood , Survival Analysis , Vitamin D/analogs & derivatives , Vitamin D/blood
3.
Clin Nephrol ; 75(2): 125-34, 2011 Feb.
Article in English | MEDLINE | ID: mdl-21255542

ABSTRACT

BACKGROUND: End-stage renal disease (ESRD) disrupts patients' life styles, interests and activities negatively affecting their quality of life. Social support has been previously associated with favorable health outcomes. However, no study has examined the association of social support from health care providers with perceived health and ESRD intrusiveness on patients' lives. METHODS: A self-administered questionnaire was completed by 1,238 Italian hemodialysis patients. The Self-Rated Health (SRH) and the Illness Intrusiveness Rating Scale (IIRS) assessed disease burden. 10 items assessed social support from health care providers (SS-HC). The nursing staff of each center provided patients' clinical information. Linear regression was used to assess correlates of SRH and IIRS. Mediational analysis was used to assess direct and indirect associations of SS-HC with SRH through IIRS. RESULTS: Higher SS-HC was associated with smaller IIRS and higher SRH. Further correlates of better SRH were younger age, no post-dialysis hypotension, no diabetes and cardiovascular diseases, better sleep quality, and smaller burden of oral therapy. CONCLUSIONS: Our results suggest that social support might reduce illness burden and improve patients' perceived health. Further research should assess the efficacy and cost-effectiveness of structured support programs for dialysis patients.


Subject(s)
Attitude of Health Personnel , Cost of Illness , Health Knowledge, Attitudes, Practice , Kidney Failure, Chronic/therapy , Quality of Life , Renal Dialysis , Social Support , Adolescent , Adult , Aged , Communication , Cross-Sectional Studies , Female , Humans , Italy , Kidney Failure, Chronic/psychology , Linear Models , Male , Middle Aged , Perception , Professional-Patient Relations , Renal Dialysis/psychology , Surveys and Questionnaires , Young Adult
4.
G Ital Nefrol ; 26 Suppl 49: S30-5, 2009.
Article in Italian | MEDLINE | ID: mdl-19941276

ABSTRACT

Deficiencies in vitamin D and vitamin D receptor (VDR) activation adversely affect cardiovascular health in the general population and in people at high risk of cardiovascular disease, as well as contributing to secondary hyperparathyroidism in patients with chronic kidney disease (CKD). Furthermore, epidemiological and observational data indicate that there is a close interrelationship between progressive renal dysfunction in CKD, cardiovascular disease, and mortality. The causes of death in patients even with only moderate kidney dysfunction are commonly associated with cardiovascular events. Modulation of vitamin D levels results in correlative regulatory effects on mineral homeostasis, hypertension, vascular disease, and calcification, as well as a number of other endpoints in cardiac and renal disease. The use of VDR activators to treat these and other parameters outside of cardiovascular and renal disease not only results in enhanced patient health but significantly lowers the risk of mortality in CKD and non-CKD patients with low systemic activity of vitamin D. The cardiovascular and renal systems continue to demonstrate their interrelated effects on each other, particularly when vitamin D and VDR signaling are considered.


Subject(s)
Bone Density Conservation Agents/therapeutic use , Calcitriol/therapeutic use , Calcium Channel Agonists/therapeutic use , Cardiovascular Diseases/prevention & control , Hyperparathyroidism, Secondary/prevention & control , Kidney Diseases/drug therapy , Receptors, Calcitriol/drug effects , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/etiology , Chronic Disease , Cinacalcet , Disease Progression , Drug Therapy, Combination , Evidence-Based Medicine , Humans , Hyperparathyroidism, Secondary/drug therapy , Hyperparathyroidism, Secondary/etiology , Kidney Diseases/complications , Kidney Diseases/diagnosis , Kidney Diseases/mortality , Naphthalenes/therapeutic use , Renal Dialysis/methods , Severity of Illness Index , Treatment Outcome
5.
G Ital Nefrol ; 26 Suppl 49: S18-22, 2009.
Article in Italian | MEDLINE | ID: mdl-19941274

ABSTRACT

Cardiovascular complications are the most common cause of death in uremic patients, especially those on chronic dialysis. One of the major findings is massive calcium deposition in the vessel walls. There is general consensus about the correlation between the distribution of vascular calcification and increased risk of death due to cardiovascular disease. An emerging issue is the possible beneficial role of vitamin D receptor (VDR) activation in reducing the morbidity and mortality rates in patients on chronic dialysis, as shown in large, although retrospective, studies. Still open is the possible role of CaSR activators in ameliorating the clinical course of patients on dialysis, although calcimimetics are able to improve the Ca-P-PTH serum profile and increase the number of patients within the international guidelines parameters. This review has been structured to give the readers an updated opinion on the possible positive impact of VDR and CaSR activators in terms of all-cause and cardiovascular morbidity and mortality in dialysis patients.


Subject(s)
Calcinosis/prevention & control , Calcitriol/therapeutic use , Calcium Channel Agonists/therapeutic use , Cardiovascular Diseases/prevention & control , Receptors, Calcitriol/metabolism , Receptors, Calcium-Sensing/metabolism , Calcinosis/complications , Calcinosis/etiology , Calcinosis/physiopathology , Cardiovascular Diseases/etiology , Cardiovascular Diseases/physiopathology , Evidence-Based Medicine , Humans , Hyperparathyroidism, Secondary/prevention & control , Renal Dialysis/adverse effects , Risk , Treatment Outcome , Uremia/complications
6.
G Ital Nefrol ; 26 Suppl 45: S20-7, 2009.
Article in Italian | MEDLINE | ID: mdl-19382090

ABSTRACT

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. In addition to abnormalities in the serum calcium and phosphate profile, CKD-MBD is characterized by abnormalities of bone turnover, mineralization, volume and growth as well as vascular calcification. Considering that the presence and extent of vascular calcification in CKD portend a poor prognosis, many efforts have been made to shed light on this complicated phenomenon to prevent vascular calcium deposition and its progression. Indeed, careful control of calcium load, serum phosphate and parathyroid hormone along with the use of calcium-free phosphate binders and vitamin D receptor activators represent a new therapeutic armamentarium to improve quality of life and reduce mortality in CKD.


Subject(s)
Calcinosis/drug therapy , Calcinosis/metabolism , Kidney Diseases/complications , Kidney Diseases/metabolism , Vascular Diseases/drug therapy , Vascular Diseases/metabolism , Biomarkers/blood , Calcinosis/blood , Calcinosis/pathology , Calcium/blood , Chelating Agents/therapeutic use , Chronic Disease , Coronary Artery Disease/metabolism , Disease Progression , Drug Therapy, Combination , Evidence-Based Medicine , Humans , Kidney Diseases/blood , Kidney Diseases/drug therapy , Kidney Diseases/pathology , Parathyroid Hormone/blood , Phosphates/blood , Practice Guidelines as Topic , Prognosis , Quality of Life , Renal Insufficiency, Chronic/metabolism , Vascular Diseases/blood , Vascular Diseases/pathology , Vitamin D/therapeutic use
7.
Int J Artif Organs ; 31(12): 1002-3, 2008 Dec.
Article in English | MEDLINE | ID: mdl-19115191

ABSTRACT

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. Together with passive deposition of calcium-phosphate in extraskeletal tissues, it has recently been demonstrated that inorganic phosphate induces arterial calcification directly through a real "ossification" of the tunica media in the vasculature of CKD patients. Therefore, control of serum phosphate in CKD patients becomes crucial in preventing increases in calcium x phosphate product, secondary hyperparathyroidism, and ultimately vascular calcification.


Subject(s)
Calcinosis/etiology , Cardiovascular Diseases/etiology , Hyperphosphatemia/complications , Kidney Failure, Chronic/complications , Humans , Hyperparathyroidism, Secondary/complications , Hyperparathyroidism, Secondary/metabolism , Hyperparathyroidism, Secondary/physiopathology , Hyperphosphatemia/metabolism , Hyperphosphatemia/physiopathology , Kidney Failure, Chronic/metabolism , Kidney Failure, Chronic/physiopathology
8.
G Ital Nefrol ; 25(2): 234-7, 2008.
Article in Italian | MEDLINE | ID: mdl-18350504

ABSTRACT

Mineral metabolism disorders are well-recognized complications in patients with chronic kidney disease (CKD). Furthermore, hyperphosphatemia and secondary hyperparathyroidism are associated with both renal osteodystrophy and cardiovascular disease. During the last 5 years, new therapeutic options have become available to treat these conditions in CKD. We describe the case of a 70-year-old lady with a dialysis history of 5 years and a number of cardiovascular risk factors (hypertension, hypercholesterolemia and obesity). Unfortunately, the patient was poorly compliant with any pharmaceutical treatment. After 2 years, a pharmacological approach with a low dosage of calcium salts and sevelamer HCl, subsequently changed to lanthanum carbonate, intravenous paricalcitol, and cinacalcet HCl reached the goals suggested by the current guidelines. Every nephrologist should look at the pathogenesis and treatment of hyperphosphatemia and secondary hyperparathyroidism. New options are now available and may help the clinician to obtain satisfactory short- and long-term outcomes in the treatment of this disease.


Subject(s)
Calcium Metabolism Disorders/drug therapy , Kidney Failure, Chronic/therapy , Phosphorus Metabolism Disorders/drug therapy , Renal Dialysis , Aged , Calcium Metabolism Disorders/etiology , Female , Humans , Hyperparathyroidism/drug therapy , Hyperparathyroidism/etiology , Kidney Failure, Chronic/complications , Phosphorus Metabolism Disorders/etiology
9.
Int J Artif Organs ; 31(1): 34-42, 2008 Jan.
Article in English | MEDLINE | ID: mdl-18286452

ABSTRACT

PURPOSE: Chronic kidney disease (CKD) is associated with an impaired endothelial function, which may contribute to cardiovascular events. Whether impairment in endothelial function is involved in the circulatory response to orthostatic stress is unknown. We assessed endothelial function via brachial artery flow-mediated dilation (BAFMD), an index of endothelial-dependent vasodilation. METHODS: We measured changes in brachial artery diameter (BAD) and blood flow by Doppler ultrasound in 35 CKD patients on hemodialysis, 37 young healthy controls (HC) and 50 non-uremic matched controls (MC), in the supine position and after 60 degrees head-up tilting (HUT). RESULTS: In the supine position, endothelial flow-mediated BAD was significantly increased in HC (p<0.001) and MC (p<0.01) while no significant changes were detected in CKD. Mean percent blood flow changes were HC+323.5%, MC+195.1% and CKD+158.8% (HC vs. CKD p<0.001; HC vs. MC p<0.001; MC vs. CKD p=0.04). Similarly, during HUT mean BAD and blood flow increases were significantly impaired in CKD patients. CONCLUSION: In CKD patients, an impaired response in the physiologic vascular reactivity, suggesting endothelial dysfunction, was found in the supine position and after orthostasis by BAFMD. Our results are in favor of a possible adjunctive role of uremia in the abnormal brachial artery response.


Subject(s)
Brachial Artery/physiopathology , Kidney Failure, Chronic/physiopathology , Renal Dialysis/adverse effects , Uremia/physiopathology , Vasodilation/physiology , Adult , Blood Flow Velocity/physiology , Brachial Artery/diagnostic imaging , Brachial Artery/pathology , Case-Control Studies , Female , Humans , Male , Tilt-Table Test , Ultrasonography
10.
G Ital Nefrol ; 24(5): 409-14, 2007.
Article in Italian | MEDLINE | ID: mdl-17886210

ABSTRACT

It is commonly accepted that the first cause of morbidity and mortality in chronic kidney disease (CKD) is the cardiovascular (CV) disease, in which vascular calcification (VC) plays a central pathogenetic role. In CKD population, mineral metabolism disorders have been recently investigated not only as key factors on renal osteodystrophy but also as inducing players on extra-skeletal calcification. Clearly, either high phosphate (P) or high calcium (Ca) concentration induce vascular smooth muscle cells mineralization in vitro studies. In fact, VC is induced by a cell-mediated process, which actively accompanies the traditional and passive Ca-P deposition in arterial walls. Interestingly, lack of inhibitory proteins, such as fetuin-A (alpha2-HS glycoprotein, AHSG), matrix GLA protein (MGP), osteoprotegerin (OPG), and bone morphogenetic protein 7 (BMP-7) are the regulatory key factors in preventing VC in uremic conditions.


Subject(s)
Chronic Kidney Disease-Mineral and Bone Disorder , alpha-2-HS-Glycoprotein , Calcinosis/prevention & control , Cardiovascular Diseases , Renal Insufficiency, Chronic , Vascular Calcification , Vascular Diseases
11.
G Ital Nefrol ; 24(3): 230-4, 2007.
Article in Italian | MEDLINE | ID: mdl-17554735

ABSTRACT

Bisphosphonates are molecules derived from pyrophosphates,but, unlike pyrophosphates, they are resistant to enzymatic hydrolysis. Bisphosphonates are used in the treatment of Paget's disease, cancer-related osteolysis, myeloma, primary hyperparathyroidism, and osteoporosis. In dialysis patients bisphosphonates may be used to reduce bone pain due to renal osteodystrophy. We describe the case of a 60-year-old woman with a history of breast cancer who had been on dialysis for 8 years. She had been receiving clodronic acid at 100 mg per week intravenously for the last 2 years. A year ago, the patient underwent surgical extraction of the lower right second molar. Her jaw pain increased in the following days. An orthopanthograph and a CT scan of the head showed osteolysis, and a surgical osteotomy was performed. Histological examination led to a diagnosis of avascular osteonecrosis of the jaw. Avascular osteonecrosis is typically described in the jaw. In this case, prolonged bisphosphonate treatment may have worsened the osteonecrosis.


Subject(s)
Bisphosphonate-Associated Osteonecrosis of the Jaw , Renal Dialysis , Bisphosphonate-Associated Osteonecrosis of the Jaw/diagnosis , Bisphosphonate-Associated Osteonecrosis of the Jaw/surgery , Female , Humans , Middle Aged
12.
Int J Artif Organs ; 30(4): 293-300, 2007 Apr.
Article in English | MEDLINE | ID: mdl-17520565

ABSTRACT

Phosphate overload is a dramatic consequence in end-stage renal disease (ESRD) patients. Recent studies have well documented that abnormalities in mineral and bone metabolism in these patients are associated with increased cardiovascular morbidity and mortality. Elevated serum phosphate and calcium-phosphate product levels play an important role in the pathogenesis of secondary hyperparathyroidism and extra-skeletal calcification in dialysis patients. Furthermore, inorganic phosphate may cause vascular calcification directly through a real ""ossification"" of the tunica media in the vasculature of ESRD patients. The ""classical"" treatment of secondary hyperparathyroidism and hyperphosphatemia in ESRD patients consists of either calcium- or aluminum-based phosphate binders and calcitriol administration. Unfortunately, this ""old generation"" therapy is not free of complications. This review paper suggests that new calcium- and aluminum-free phosphate binders, such as lanthanum carbonate, can be used to treat hyperphosphatemia and secondary hyperparathyroidism in ESRD patients.


Subject(s)
Chelating Agents/therapeutic use , Lanthanum/therapeutic use , Phosphates/blood , Renal Dialysis , Humans , Hyperparathyroidism, Secondary/drug therapy , Hyperparathyroidism, Secondary/etiology , Kidney Failure, Chronic/complications , Phosphorus Metabolism Disorders/drug therapy , Phosphorus Metabolism Disorders/etiology , Polyamines/therapeutic use , Sevelamer
13.
Kidney Int ; 71(3): 190-2, 2007 Feb.
Article in English | MEDLINE | ID: mdl-17252028

ABSTRACT

Since lanthanum carbonate has become available there has been much interest in its use as a non-calcium-containing phosphate binder, but also much speculation among scientists about possible aluminum-like toxicity. This Commentary focuses on the major aspects of this scientific controversy, confirming the safety and efficacy of this new phosphate binder.


Subject(s)
Brain/drug effects , Lanthanum/adverse effects , Lanthanum/pharmacokinetics , Phosphorus Metabolism Disorders/drug therapy , Aluminum/toxicity , Animals , Bone and Bones/metabolism , Brain/metabolism , Humans , Lanthanum/toxicity , Liver/metabolism , Phosphates/blood , Rats
14.
J Vasc Access ; 7(1): 7-14, 2006.
Article in English | MEDLINE | ID: mdl-16596523

ABSTRACT

Pneumothorax is one of the most frequent complications during percutaneous central vascular cannulation. When choosing a site for central vascular access, the internal jugular vein is preferable to other vessels, for the lower frequency of related complications, including pneumothorax. This review intends to summarize the current state of the art on how to avoid and, if it occurs, to manage this rare but relevant complication. In order to prevent pneumothorax, as well as other relevant complications of central vein cannulation, it is advisable to use ultrasound guidance whenever possible. If pneumothorax occurs, it is important to recognize its signs and symptoms. To exclude the presence of asymptomatic pneumothorax, in the normal clinical routine a chest X-ray should be obtained within 4 hours from the procedure of central vein cannulation of subclavian and internal jugular veins. If promptly recognized, pneumothorax can be managed quickly and in a relatively easy way. Depending on its size and symptoms, and in particular when a tension pneumothorax is suspected, treatment can vary from simple observation to a chest tube insertion or, in the latter case, to an emergency thoracentesis needle insertion in the pleural space.


Subject(s)
Catheterization, Central Venous/adverse effects , Pneumothorax/prevention & control , Ultrasonography, Interventional , Chest Tubes , Femoral Vein/diagnostic imaging , Humans , Jugular Veins/diagnostic imaging , Paracentesis/methods , Pneumothorax/etiology , Pneumothorax/surgery , Radiography, Thoracic , Subclavian Vein/diagnostic imaging , Thoracostomy/instrumentation
15.
G Ital Nefrol ; 22(4): 329-36, 2005.
Article in Italian | MEDLINE | ID: mdl-16267793

ABSTRACT

Parathyroid gland growth is a major cause of secondary hyperparathyroidism in renal failure. It is well known that high serum phosphate levels, low serum calcium levels and vitamin D deficiency are the three promoters of parathyroid hyperplasia in renal failure. Recent studies have investigated in depth the potential role of growth factors (transforming growth factor alpha) and their receptors (epidermal growth factor receptor) in the pathogenesis of parathyroid cell hyperplasia in chronic renal failure. The identification of molecular mechanisms involved in calcium, phosphate and vitamin D manipulations in an experimental renal failure model could help design more effective therapy for secondary hyperparathyroidism in uremic patients.


Subject(s)
Hyperparathyroidism, Secondary/etiology , Kidney Failure, Chronic/complications , Parathyroid Glands/pathology , Calcium/blood , Calcium/deficiency , ErbB Receptors/blood , Humans , Hyperparathyroidism, Secondary/pathology , Hyperplasia , Kidney Failure, Chronic/pathology , Phosphates/blood , Transforming Growth Factor alpha/blood , Vitamin D Deficiency/blood
16.
Int J Artif Organs ; 28(8): 797-802, 2005 Aug.
Article in English | MEDLINE | ID: mdl-16211529

ABSTRACT

BACKGROUND: Uremic patients on regular dialytic treatment (RDT) are often affected by a complex metabolic syndrome leading to osteodystrophy. Bone changes are primarily due to high bone turnover, often combined with a mineralization defect leading to increased bone fractures and bone deformities. Although rarely considered, the craniofacial skeleton represents one of the peculiar targets of this complex metabolic disease whose more dramatic pattern is a form of leontiasis ossea. This complication, although described, has never been evaluated in depth nor quantitatively assessed. In order to assess facial deformities in uremic conditions and to understand the possible relation with hyperparathyroidism, we undertook a quantitative evaluation of soft facial structures in a cohort of uremic patients undergoing RDT. METHODS: The three-dimensional coordinates of 50 soft-tissue facial landmarks were obtained by an electromagnetic digitizer in 10 male and 10 female patients with chronic renal insufficiency aged 53-81 years, and in 34 healthy individuals of the same age, ethnicity and sex. Uremic patients were enrolled according to hyperparathyroid status (PTH < 300 pg/mL and PTH > 500 pg/mL). From the landmarks, facial distances, angles and volumes were calculated according to a geometrical face model. RESULTS: Overall, the uremic patients had significantly larger facial volumes than the reference subjects. The effect was particularly evident in the facial middle third (maxilla), leading to an inversion of the mandibular-maxillary ratio. Facial dimensions were increased in all three spatial directions: width (skull base, mandible, nose), length (nose, mandible), and depth (mid face, mandible). The larger maxilla was accompanied by a tendency to more prominent lips (reduced interlabial angle). Some of the facial modifications (nose, lips, mandible) were significantly related to the clinical characteristics of the patients (age, duration of renal insufficiency and PTH levels). CONCLUSIONS: This report, the first in the literature, shows that facial structures of uremic patients are enlarged in comparison with matched normal subjects and that increased bone turnover could be responsible--at least in part--for facial bone changes.


Subject(s)
Facial Bones/anatomy & histology , Hyperostosis Frontalis Interna/etiology , Hyperparathyroidism, Secondary/complications , Uremia/complications , Aged , Aged, 80 and over , Bone Remodeling/physiology , Case-Control Studies , Female , Humans , Hyperostosis Frontalis Interna/physiopathology , Hyperparathyroidism, Secondary/etiology , Hyperparathyroidism, Secondary/physiopathology , Image Processing, Computer-Assisted , Imaging, Three-Dimensional , Kidney Failure, Chronic/therapy , Male , Middle Aged , Renal Dialysis , Uremia/physiopathology , Uremia/therapy
18.
G Ital Nefrol ; 22 Suppl 31: S53-5, 2005.
Article in Italian | MEDLINE | ID: mdl-15786403

ABSTRACT

Secondary hyperparathyroidism (HPTH) is a common feature in end-stage renal disease (ESRD) patients. The three main factors involved in secondary HPTH pathogenesis are high phosphate levels, hypocalcemia and vitamin D deficiency. Recently, many studies demonstrated a strong association between bone disease and cardiovascular events in chronic kidney disease patients. In addition, cardiovascular events are the most frequent cause of death in patients with chronic renal failure. Increased levels of serum phosphorus and calcium-phosphate product are directly involved in the pathogenesis of extraskeletal calcifications (blood vessels, soft tissues, etc) in dialyzed patients compared to the non-uremic population. Recent studies suggested that vascular calcification is due not only to a passive calcium-phosphate deposition on atherosclerotic arteries, but also to active mechanisms regulated by bone-associated genes. In particular, fetuin and matrix Gla-protein are two 'protective' proteins associated with reduced vascular calcification and could be the regulatory keys in preventing this process in renal failure. The limitations of calcium salts as phosphate-binders in patients with advanced renal failure have been thoroughly evaluated in the last 5 yrs. New phosphate binders, which do not contain aluminum or calcium, have been developed to reduce the risk of extraskeletal calcifications in ESRD.


Subject(s)
Calcinosis/etiology , Calcinosis/prevention & control , Kidney Failure, Chronic/complications , Uremia/complications , Animals , Humans
19.
J Vasc Access ; 5(2): 49-56, 2004.
Article in English | MEDLINE | ID: mdl-16596541

ABSTRACT

PURPOSE: Tunneled catheters are widely used for intermediate to long-term hemodialysis (HD) access, but are prone to several complications that can require catheter replacement. Replacing malfunctioning catheters with a new line, placed in a different access site, can lead to problems with multiple vein occlusions. This has led many nephrologists to continue using the same vein as long as possible by guidewire catheter exchanges, to preserve other veins for future use. We describe a guidewire exchange technique for the Ash-Split catheter in the internal jugular vein. METHODS: In three patients, the exchange was performed because of partial catheter removal, as evidenced by the outward dislocation of the Dacron cuff. In these patients, the guidewire was inserted through the catheter. In two additional patients, the catheter had been completely removed by accident: the replacement of the dislodged tunneled venous catheters was attempted 5 hr and 1 day after accidental removal. In these patients, the guidewire was inserted through the previous tunnel. After guidewire placement, a skin incision was made in the supraclavicular region. The metal guidewire was easily located inside the fibrous structure that had previously surrounded the catheter. The guidewire was then extracted from the subcutaneous tunnel and used to insert a new catheter safely and easily after creating a new tunnel. Patients were routinely given antibiotic prophylaxis (1 g of cefazolin) immediately before the procedure. A strict aseptic technique was used, including several sterile glove changes. RESULTS: No infections developed following this procedure, which has the potential for bacterial contamination. All procedures were successful. Only in one patient did we have to convert to a different catheter: it was not possible to replace the old Ash-Split catheter with the same dual-lumen catheter because of difficulties in inserting the peel away introducer-catheter complex. In this patient, rather than forcing it with larger dilators or trying to disrupt the fibrin sheath with balloon dilatation, a single lumen Tesio catheter was successfully placed. In both patients who completely lost the previous catheter, the guidewire was readily reinserted through the subcutaneous tunnel into the vein. Catheter function was excellent in all patients, with a test blood flow rate on the 1st catheter use >350 ml/min. CONCLUSIONS: We described a new method for catheter exchange, which allows the easy insertion of a new catheter and the creation of a new and safer subcutaneous tunnel. In addition, we demonstrated that in cases of complete catheter removal, it is possible to reinsert a catheter in the same vein through a guidewire, even when reinsertion was attempted up to 1 day later.

20.
G Ital Nefrol ; 20 Suppl 22: S12-6, 2003.
Article in Italian | MEDLINE | ID: mdl-12851915

ABSTRACT

The management of secondary hyperparathyroidism is of crucial importance in the treatment of end stage renal disease (ESRD) patients. In particular, hypercalcemia, hyperphosphatemia, and elevated calcium x phosphate (Ca x P) product should be taken into consideration during administration of vitamin D metabolites for the control of PTH secretion. During the last 10 years, many authors have been studying the efficacy of new non-calcemic vitamin D analogs on suppressing secondary hyperparathyroidism in ESRD patients. In this brief review, we analyzed three new vitamin D analogs: 22-oxacalcitriol (Maxacalcitriol), 19-nor-1a, 25(OH)2D2 (Paracalcitriol), and 1a (OH)2D2 (Doxacalciferol). In addition, calcimimetic agents may represent a new pharmacologic choice to the treatment of secondary hyperparathyroidism, binding parathyroid calcium sensing receptors (CaSR) and reducing PTH secretion. These compounds may represent an important tool for the treatment of both secondary hyperparathyroidism and soft tissue calcifications in ESRD patients. In conclusion, a combined use of non calcemic phosphate binders, new vitamin D analogs and calcimimetics should be seriously considered to further improve the already known therapy of secondary hyperparathyroidism in ESRD patients.


Subject(s)
Chronic Kidney Disease-Mineral and Bone Disorder/physiopathology , Hyperparathyroidism, Secondary/prevention & control , Kidney Failure, Chronic/complications , Calcitriol/analogs & derivatives , Calcitriol/therapeutic use , Calcium/blood , Chronic Kidney Disease-Mineral and Bone Disorder/metabolism , Ergocalciferols/therapeutic use , Humans , Hyperparathyroidism, Secondary/drug therapy , Hyperparathyroidism, Secondary/etiology , Kidney Failure, Chronic/metabolism , Kidney Failure, Chronic/therapy , Phosphorus/blood
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