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1.
Clin Transplant ; 34(9): e14014, 2020 09.
Article in English | MEDLINE | ID: mdl-32567723

ABSTRACT

BACKGROUND: The outcome of patients who return to dialysis after Kidney allograft failure (KAF) remains unclear. Our aim was to compare the outcome of KAF patients vs two different types of transplant naive incident dialysis (TNID) patients, those on the waiting list (WL) and those with a kidney transplant contraindication (KTC). METHODS: We performed an observational study using data from the Argentinian Dialysis Registry between 2005 and 2016. We compare mortality between KAF, WL, and KTC. RESULTS: We included 75 722 patients of which 2734 were KAF. Survival between the three cohorts (KAF vs WL (n = 14 630) vs KTC (n = 58 358) revealed a significant difference (log-rank test: P < .0001) indicating worse survival for KTC patients and best survival for WL. We found that KAF patients had as poor outcome as KTC patients after multivariate adjustment. Cox regression showed that age >65 years: HR: 1.845 (1.79-1.89) P < .0001, transient catheter: HR: 1.303 (1.26-1.34) P < .0001, diabetic: HR: 1.273 (1.22-1.31) P < .0001, hepatitis C: HR: 1.156 (1.09-1.22) P < .0001, and albumin: HR: 1.247 (1.21-1.28) P < .0001 were associated with mortality. CONCLUSION: Patients who return to dialysis after KAF have higher mortality than WL patients and similar to KTC patients.


Subject(s)
Kidney Failure, Chronic , Kidney Transplantation , Aged , Allografts , Humans , Kidney , Kidney Failure, Chronic/surgery , Renal Dialysis , Transplantation, Homologous
3.
Stem Cells Int ; 2011: 943216, 2011.
Article in English | MEDLINE | ID: mdl-21716667

ABSTRACT

One of the most important and complex diseases of modern society is metabolic syndrome. This syndrome has not been completely understood, and therefore an effective treatment is not available yet. We propose a possible stem cell mechanism involved in the development of metabolic syndrome. This way of thinking lets us consider also other significant pathologies that could have similar etiopathogenic pathways, like lipodystrophic syndromes, progeria, and aging. All these clinical situations could be the consequence of a progressive and persistent stem cell exhaustion syndrome (SCES). The main outcome of this SCES would be an irreversible loss of the effective regenerative mesenchymal stem cells (MSCs) pools. In this way, the normal repairing capacities of the organism could become inefficient. Our point of view could open the possibility for a new strategy of treatment in metabolic syndrome, lipodystrophic syndromes, progeria, and even aging: stem cell therapies.

4.
Curr Clin Pharmacol ; 5(4): 246-50, 2010 Nov.
Article in English | MEDLINE | ID: mdl-20925646

ABSTRACT

The aim of this study was to determine if Rituximab coated Biodegradable Nanoparticles (BNPs) loaded with Chlorambucil and Hydroxychloroquine could induce apoptosis of B-Chronic Lymphocytic Leukemia (B-CLL), MEC-1 and BJAB cells in vitro and evaluate their toxic and therapeutic effects on a Human/Mouse Model of Burkitt Lymphoma at an exploratory, proof of concept scale. We found that Rituximab-Chlorambucil-Hydroxychloroquine BNPs induce a decrease in cell viability of malignant B cells in a dose-dependent manner. The mediated cytotoxicity resulted from apoptosis, and was confirmed by monitoring the B-CLL cells after Annexin V/propidium iodide staining. Additional data revealed that these BNPs were non toxic for healthy animals, and had prolonged survival in this mice model of human lymphoma.


Subject(s)
Antibodies, Monoclonal, Murine-Derived/therapeutic use , Antineoplastic Agents/therapeutic use , B-Lymphocytes/drug effects , Burkitt Lymphoma/drug therapy , Chlorambucil/therapeutic use , Hydroxychloroquine/therapeutic use , Nanoparticles , Animals , Antibodies, Monoclonal, Murine-Derived/pharmacology , Antineoplastic Agents/pharmacology , B-Lymphocytes/pathology , Burkitt Lymphoma/pathology , Cell Survival/drug effects , Chlorambucil/pharmacology , Disease Models, Animal , Dose-Response Relationship, Drug , Drug Combinations , Drug Synergism , Humans , Hydroxychloroquine/pharmacology , Mice , Mice, Inbred C57BL , Rituximab , Tumor Cells, Cultured
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