Examinando por Autor "Luis-Lima, Sergio"

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Renoprotective role of bariatric surgery in patients with established chronic kidney disease
(Oxford University Press, 2020-12-20) Morales, Enrique; Porrini, Esteban; Martin-Taboada, Marina; Luis-Lima, Sergio; Vila-Bedmar, Rocıo; Gonzalez de Pablos, Ignacio; Gomez, Pilar; Rodriguez, Elias; Torres, Lucia; Lanzon, Borja; Rodriguez, Ana Elena; Maiz, Maria; Medina-Gomez, Gema; Praga, Manuel
Background. Bariatric surgery (BS) has been postulated as the most effective measure for weight reduction. Weight loss improves metabolic parameters and exerts changes in renal function that lead to the amelioration of absolute or relative glomerular hyperfiltration, a condition that may be renoprotective in the long term. However, few studies have demonstrated the influence of BS in patients with severe obesity and chronic kidney disease (CKD). Our objective was to analyse the evolution of renal function, adipose tissue–derived molecules and inflammatory parameters in patients with CKD after BS. Methods. This is an observational and prospective study. Thirty patients were screened and 12 were included between January 2016 and January 2018 with a 24-month follow-up. Glomerular filtration rate (GFR) was determined by plasma iohexol clearance. Adipokines, cytokines, circulating hormones and fibrotic parameters were evaluated before and 12 months after BS using the Bioplex system. Results. The mean age was 50.6 years and 58.3% were males. Seven patients had a body mass index >40 kg/m2 and 66.7% were diabetic. Twenty-four months following BS there was a significant decrease in body weight (36.4%). Proteinuria decreased by 63.7628.2%. Measured GFR significantly diminished from before surgery to Month 24 after surgery (94644 to 79644 mL/min, P ¼ 0.03). There was a significant decrease in adipocyte-derived molecules (leptin and vifastin) as well as in pro-inflammatory cytokines [interleukin (IL)-1b, tumour necrosis factor a, IL-6 and monocyte chemoattractant protein-1]
Transforming growth factor β3 deficiency promotes defective lipid metabolism and fibrosis in murine kidney
(COMPANY BIOLOGISTS, 2021-09-01) Escasany, Elia; Lanzón, Borja; Garcia-Carrasco, Almudena; Izquierdo-Lahuerta, Adriuana; Torres, Lucia; Corrales, Patricia; Rodríguez Rodríguez, Ana Elena; Luis-Lima, Sergio; Martínez-Álvarez, Concepción; Ruperez, Francisco Javier; Ros, Manuel; Porrini, Esteban; Rydén, Mikael; Medina-Gomez, Gema
Glomerulosclerosis and tubulointerstitial fibrosis are pathological features of chronic kidney disease. Transforming growth factor β (TGFβ) is a key player in the development of fibrosis. However, of the three known TGFβ isoforms, only TGFβ1 has an established role in fibrosis, and the pathophysiological relevance of TGFβ2 and TGFβ3 is unknown. Because Tgfb3 deficiency in mice results in early postnatal lethality, we analyzed the kidney phenotype of heterozygous Tgfb3-knockout mice (Tgfb3+/-) and compared it with that of matched wild-type mice. Four-month-old Tgfb3+/- mice exhibited incipient renal fibrosis with epithelial-mesenchymal transition, in addition to glomerular basement membrane thickening and podocyte foot process effacement associated with albuminuria. Also evident was insulin resistance and oxidative stress at the renal level, together with aberrant renal lipid metabolism and mitochondrial function. Omics analysis revealed toxic species, such as diacylglycerides and ceramides, and dysregulated mitochondrial metabolism in Tgfb3+/- mice. Kidneys of Tgfb3+/- mice showed morphological alterations of mitochondria and overactivation of non-canonical MAPK ERK1/2 and JNK cascades. Our study indicates that renal TGFβ3 might have antifibrotic and renoprotective properties, opposing or counteracting the activity of TGFβ1. This article has an associated First Person interview with the first author of the paper.