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Troya M.-I.,Hospital Universitari Germans Trias i Pujol | Troya M.-I.,University of Barcelona | Troya M.-I.,Institute Investigacio Germans Trias i Pujol | Bonet J.,Hospital Universitari Germans Trias i Pujol | And 10 more authors.
Medicina Clinica | Year: 2016

Background and objective Approximately 24-40% of patients with type 2 diabetes mellitus (T2DM) develop kidney damage. Our objective was to evaluate the long-term evolution of renal function using isotopic determination of GFR and urinary albumin excretion (UAE) in patients with T2DM undergoing intensive treatment for renal and cardiovascular risk factors. Patients and methods This was a single-center, prospective study of 201 patients with T2DM and UAE who initiated intensive treatment. They were followed for 17.2 ± 6.5 years. Patients were divided into three groups, according to renal function: 167(85.6%) had stable renal function, 16(8.2%) had creatinine levels that doubled and 12(6.2%) began renal replacement therapy (RRT). We performed periodic isotopic determinations of GFR using 125I-iothalamate. Results There were significant differences between the three groups with respect to age, duration of T2DM at baseline, years of follow-up in the study and systolic blood pressure, serum creatinine, isotopic GFR, and UAE at baseline. Renal function evolution slopes were -1.55 mL/min/1.73 m2/year in patients with stable creatinine, -2.49 mL/min/1.73 m2/year in those with doubled creatinine, and -8.16 mL/min/1.73 m2/year in those requiring RRT. We also found that differences in renal events were determined by delayed initiation of intensive treatment. Conclusion Patients with glomerular hyperfiltration who were undergoing treatment with renin angiotensin aldosterone system blockers exhibited a better evolution in renal function, possibly because these patients initiated intensive treatment earlier. Although diabetic nephropathy is associated with classic risk factors, early initiation of intensive treatment should be a priority in order to prevent worsening renal function. © 2015 Elsevier España, S.L.U. Source


Bastos-Amador P.,Institute Investigacio Germans Trias i Pujol | Perez-Cabezas B.,Institute Investigacio Germans Trias i Pujol | Izquierdo-Useros N.,Irsicaixa Foundation | Puertas M.C.,Irsicaixa Foundation | And 5 more authors.
Journal of Leukocyte Biology | Year: 2012

cDCs and pDCs differ in multiple aspects. Among those, antigen capture is a recognized feature of cDCs, whereas pDCs display poor capacity to capture cell-derived antigens. However, animal models of organ transplantation suggested a role for pDCs in tolerance induction via phagocytosis of donor antigens. In a transplantation setting, microvesicles, such as apopto-tic bodies and exosomes secreted by the graft, may be potential sources of alloantigen. Here, we tested the capacity of human pDCs to capture exosomes and ap-optotic bodies from Jurkat T cells. Exosomes and apo-ptotic bodies were indeed captured by pDCs, although required longer times of incubation when compared with the highly endocytic cDCs. In cDCs and pDCs, exo-some capture was more efficient than apoptotic bodies. Endocytosis inhibitors clearly impaired exosome capture by cDCs, although this could not be verified in pDCs as a result of cellular toxicity. Functionally, capture of Jurkat-derived exosomes did not induce nor prevent pDC maturation, and exosome-loaded pDCs induced T cell proliferation, suggesting a link between capture and presentation. Thus, exosomes and apo-ptotic bodies may be sources of antigen for human pDCs. © Society for Leukocyte Biology. Source

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