Viamonte, Argentina
Viamonte, Argentina

The Universidad del Salvador is a Jesuit university in Buenos Aires, Argentina. In addition to its main Campus, it has instructional and research facilities in Pilar, Buenos Aires; San Miguel, Buenos Aires; Santa Cruz, Misiones; and Bahía Blanca, Buenos Aires. As of 2012 it enrolled approximately 20,000 undergraduate and more than 8,000 graduate students. Wikipedia.


Time filter

Source Type

Negri A.L.,University of Salvador
Nefrologia | Year: 2016

Renal tubular calcium reabsorption is one of the principal factors that determine serum calcium concentration and calcium excretion. Calcium excretion is regulated by the distal convoluted tubule and connecting tubule, where the epithelial calcium channel TRPV5 can be found, which limits the rate of transcellular calcium transport. The dynamic presence of the TRPV5 channel on the surface of the tubular cell is mediated by an endosomal recycling process. Different intrarenal factors are involved in calcium channel fixation in the apical membrane, including the anti-ageing hormone klotho and tissue kallikrein (TK). Both proteins are synthesised in the distal tubule and secreted in the tubular fluid. TK stimulates active calcium reabsorption through the bradykinin receptor B2 that compromises TRPV5 activation through the protein kinase C pathway. TK-deficient mice show hypercalciuria of renal origin comparable to that seen in TRPV5 knockout mice. There is a polymorphism with loss of function of the human TK gene R53H (allele H) that causes a marked decrease in enzymatic activity. The presence of the allele H seems to be common at least in the Japanese population (24%). These individuals have a tendency to greater calcium and sodium excretion in urine that is more evident during furosemide infusion. Future studies should analyse if manipulating the renal kallikrein-kinin system can correct idiopathic hypercalciuria with drugs other than thiazide diuretics. © 2016 Sociedad Española de Nefrología.


Kelly C.P.,Beth Israel Deaconess Medical Center | Bai J.C.,University of Salvador | Liu E.,Childrens Hospital Colorado | Liu E.,Aurora University | Leffler D.A.,Beth Israel Deaconess Medical Center
Gastroenterology | Year: 2015

Celiac disease is an autoimmune disorder that is induced by dietary gluten in genetically predisposed individuals. It has a prevalence of approximately 1% in many populations worldwide. New diagnoses have increased substantially, owing to increased awareness, better diagnostic tools, and probable real increases in incidence. The breadth of recognized clinical presentations continues to expand, making the disorder highly relevant to all physicians. Newer diagnostic tools, including serologic tests for antibodies against tissue transglutaminase and deamidated gliadin peptide, greatly facilitate diagnosis. Tests for celiac-permissive HLA-DQ2 and HLA-DQ8 molecules are useful in defined clinical situations. Celiac disease is diagnosed by histopathologic examination of duodenal biopsy specimens. However, according to recent controversial guidelines, a diagnosis can be made without a biopsy in certain circumstances, especially in children. Symptoms, mortality, and risk for malignancy each can be reduced by adherence to a gluten-free diet. This treatment is a challenge, however, because the diet is expensive, socially isolating, and not always effective in controlling symptoms or intestinal damage. Hence, there is increasing interest in developing nondietary therapies. © 2015 AGA Institute.


Negri A.L.,University of Salvador | Torres P.A.U.,Clinique du Landy
Clinical Kidney Journal | Year: 2015

Increased cardiovascular morbidity and mortality has been associated with the hyperphosphatemia seen in patients with end-stage chronic kidney disease (CKD). Oral phosphate binders are prescribed in these patients to prevent intestinal absorption of dietary phosphate and reduce serum phosphate. In prospective observational cohorts they have shown to decrease all-cause and cardiovascular mortality risk. Different problems have been associated with currently available phosphate binders as positive calcium balance and impaired outcomes with calcium-based phosphate binders or increased costs with non-calcium-based phosphate binders. Iron-based phosphate binders represent a new class of phosphate binders. Several iron-based phosphate binders have undergone testing in clinical trials. Ferric citrate (JTT-751) and sucroferric oxyhydroxide (PA21) are the two iron-based binders that have passed to the clinical field after being found safe and effective in decreasing serum phosphate. Iron from ferric citrate is partially absorbed compared to sucroferric oxyhydroxide. Ferric citrate usage could result in an important reduction in erythropoiesis-stimulating agent (ESA) and IV iron usage, resulting in significant cost savings. Sucroferric oxyhydroxide was effective in lowering serum phosphorus in dialysis patients with similar efficacy to sevelamer carbonate, but with lower pill burden, and better adherence. Ferric citrate may be more suited for the treatment of chronic hyperphosphatemia in CKD patients requiring iron supplements but its usemay have been hampered by potential aluminum overload, as citrate facilitates its absorption; sucroferric oxyhydroxide may be more suited for hyperphosphatemic CKD patients not requiring iron supplementation, with low pill burden. © The Author 2015.


Zanchetta M.B.,University of Salvador | Diehl M.,Hospital Italiano Of Buenos Aires | Buttazzoni M.,Hospital Italiano Of Buenos Aires | Galich A.,Hospital Italiano Of Buenos Aires | And 3 more authors.
Journal of Bone and Mineral Research | Year: 2014

Reports of atypical femoral fractures (AFFs) in patients receiving long- term bisphosphonate therapy have raised concerns regarding the genesis of this rare event. Using high-resolution peripheral quantitative computed tomography (HR-pQCT), we conducted a study to evaluate bone microarchitecture in patients who had suffered an AFF during long-term bisphosphonate treatment. The aim of our study was to evaluate if bone microarchitecture assessment could help explain the pathophysiology of these fractures. We compared bone volumetric density and microarchitectural parameters measured by HR-pQCT in the radius and tibia in 20 patients with AFFs with 35 postmenopausal women who had also received long-term bisphosphonate treatment but had not experienced AFFs, and with 54 treatment-naive postmenopausal women. Control groups were similar in age, body mass index (BMI), and bone mineral density (BMD). Mean age of the 20 patients with AFFs was 71 years, mean lumbar spine T-score was -2.2, and mean femoral neck T-score was -2. Mean time on bisphosphonate treatment was 10.9 years (range, 5-20 years). None of the patients had other conditions associated with AFFs such as rheumatoid arthritis, diabetes or glucocorticoid use. There were no statistically significant differences in any of the parameters measured by HR-pQCT between postmenopausal women with or without treatment history and with or without history of atypical fractures. We could not find any distinctive microarchitecture features in the peripheral skeleton of women who had suffered an atypical fracture of the femur while receiving bisphosphonate treatment. This suggests that risk of developing an atypical fracture is not related to bone microarchitecture deterioration. Our results indicate that there may be other individual factors predisposing to atypical fractures in patients treated with bisphosphonates, and that those are independent of bone microarchitecture. In the future, identification of those factors could help prevent and understand the complex physiopathology of these rare events. © 2014 American Society for Bone and Mineral Research.


Negri A.L.,University of Salvador | del Valle E.E.,University of Salvador
Current Drug Safety | Year: 2011

Magnesium homeostasis is essential for many intracellular processes and depends on dynamic interplay of intestinal absorption, exchange with the bone reservoir, and renal excretion. Hypomagnesaemia may arise from various disorders. We review the case of a 59 year-old man whose only complaint was irritability with a routine analysis showing hypomagnesaemia and hypokalemia while using esomeprazole, a proton pump inhibitor (PPI). Fractional magnesium excretion was low, excluding excessive renal loss. Potassium excretion was 80 mEq/24 Hr in the presence of hypokalemia suggesting hypomagnesaemia-induced kaliuresis as its cause. Hypomagnesaemia partially resolved after oral magnesium supplementation. Esomeprazol suppression corrected hypomagnesaemia. A causal relationship with esomeprazol use was supported by the recurrence of hypomagnesaemia after rechallenge. We review the literature on hypomagnesaemia due to the use of proton pump inhibitors. In the past decade our understanding of transcellular magnesium transport was enhanced by the discovery of the magnesium channel, transient receptor potential (TR PM) 6 and 7 and other proteins that play an important role in its transport. In this light we discuss the possible etiology of proton pump inhibitor related hypomagnesaemia/hypokalemia. © 2011 Bentham Science Publishers.


Manzini J.L.,University of Salvador
Current Opinion in Supportive and Palliative Care | Year: 2011

Purpose of review Palliative sedation is a standard procedure used in palliative care especially for patients at the very end of their lives, who are enduring otherwise intractable suffering. It consists of the administration of sedatives and, when necessary, other drugs, usually by infusion, either subcutaneously or intravenously, at the necessary rate to achieve the patient's relief, by means of reducing the consciousness of the patient. If this administration is not discontinued, the usual outcome is the patient's death. So, the most frequent criticisms regarding the procedure are those that consider it as a form of euthanasia. The intention of the review is analyzing the status questionis in Europe and Latin America. Recent findings Current thinking and research about this issue refers especially to the terminology, the boundaries between palliative sedation and slow euthanasia, especially in pediatric settings, the lacking of precise definition for concepts such as refractory symptoms and unbearable suffering, and the place for existential suffering in this context; the ethical positioning of Latin-American normative and authors is similar to that of Europe. Summary It does not seem that solution to the conflicting points will come from better guidelines or more experts' meetings. Instead, efforts should be directed to reinforce moral, professional integrity, within the framework of an ethics of virtue, as inherent to palliative care. Such ethics can effectively be taught and infused, and then required to all healthcare professionals. © 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.


In chronic renal failure patients, hyperphosphatemia has been associated with vascular calcifications and increased cardiovascular morbidity and mortality. In vitro observations have shown that calcium and phosphate independently and synergistically induce calcifications in human vascular smooth muscle cells, suggesting an important role for both in the calcification process. Because non-calcium phosphate binders reduce serum phosphate without increasing the calcium load, as is the case with calcium-based phosphate binders, it has been speculated that treatment with sevelamer leads to less vascular calcification and better survival in chronic kidney disease. Although the use of sevelamer may slow the progression of vascular calcifications compared with calcium-based phosphate binders, the relationship of this surrogate marker with patients' cardiovascular mortality and survival is far from certain. To resolve this uncertainty and to determine the most cost-effective way to treat hyperphosphatemia in patients with end-stage renal disease, another randomized study analyzing mortality comparing sevelamer with calcium phosphate binders should be undertaken. © 2010 Società Italiana di Nefrologia.


Negri A.L.,University of Salvador | Spivacow F.R.,University of Salvador
Clinical Cases in Mineral and Bone Metabolism | Year: 2012

Oral bisphosphonates comprise the most widely prescribed class of antiosteoporotic drugs. Recent reports, however, suggest a link between prolonged bisphosphonate use and atypical low-energy, subtrochanteric fractures. We describe the clinical course of two patient treated for a long term with different bisphosphonates who developed subtrochanteric atypical fractures. They were treated initially with intramedullary rodding without pain disappearance or healing of the fracture. Strontium ranelate, a new orally administered agent for the treatment of osteoporosis, was given to these patients with complete closure of the fracture and pain disappearance after a few months. We conclude that based on the chronology of fracture healing and pain disappearance of our patients and published evidence that strontium ranelate can accelerate fracture healing in a rat model, that strontium ranelate had a positive anabolic effect that contributed to fracture healing that produced the secondary disappearance of pain. © CIC Edizioni Internazionali.


Negri A.L.,University of Salvador
International Urology and Nephrology | Year: 2014

Fibroblast growth factor-23 (FGF-23) has emerged as an important hormone involved in phosphorus and vitamin D homeostasis. Chronic kidney disease (CKD) is the most common clinical condition in which FGF-23 levels are persistently and markedly elevated. Abnormal phosphate homeostasis and high circulating levels of FGF-23 are early complications of CKD. Although increases in FGF-23 levels may help maintain serum phosphate levels in the normal range in CKD, the long-term effects of its sustained elevated levels are unclear. Patients with CKD have high risks of developing end-stage renal disease (ESRD), cardiovascular disease, and premature death. Recent prospective studies in populations with predialysis CKD, ESRD on hemodialysis, and kidney transplant recipients demonstrate that elevated FGF-23 levels are independently associated with cardiovascular events and mortality. It was originally thought that FGF-23 was only a biomarker of disturbed phosphate balance; however, recent studies have shown that FGF-23 can have a direct effect on the heart, inducing left ventricular hypertrophy. This suggests that elevated FGF-23 levels may be a novel mechanism that explains the poor cardiovascular outcomes in CKD patients. Interventional studies are required in order to clarify the relation of causality between FGF-23 and cardiovascular mortality in this population. © 2013 Springer Science+Business Media Dordrecht.


BACKGROUND:: We have previously shown a reduction of gastrointestinal symptoms after the oral administration of Bifidobacterium infantis Natren Life Start super strain (NLS-SS) in untreated celiac disease (CD) patients. The symptomatic improvement was not associated with changes in intestinal permeability or serum levels of cytokines, chemokines, or growth factors. Therefore, we hypothesized that the beneficial symptomatic effect observed previously in patients with CD treated with B. infantis may be related to the modulation of innate immunity. GOALS:: To investigate the potential mechanisms of a probiotic B. infantis Natren Life Start super strain on the mucosal expression of innate immune markers in adult patients with active untreated CD compared with those treated with B. infantis×6 weeks and after 1 year of gluten-free diet (GFD). METHODS:: Numbers of macrophages and Paneth cells and α-defensin-5 expression were assessed by immunohistochemistry in duodenal biopsies. RESULTS:: We showed that GFD decreases duodenal macrophage counts in CD patients more effectively than B. infantis. In contrast, B. infantis decreases Paneth cell counts and expression of α-defensin-5 in CD (P<0.001). CONCLUSIONS:: The results identify differential innate immune effects of treatment with B. infantis compared with 1 year of GFD. Further studies are needed to investigate synergistic effects of GFD and B. infantis supplementation in CD. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

Loading University of Salvador collaborators
Loading University of Salvador collaborators