Background: The prevalence of obesity is increasing globally and is associated with chronic kidney disease and premature mortality. However, the impact of recipient obesity on kidney transplant outcomes remains unclear. This study aimed to investigate the association between recipient obesity and mortality, death-censored graft loss and delayed graft function (DGF) following kidney transplantation.

Methods: A systematic review and meta-analysis was conducted using Medline, Embase and the Cochrane Library. Observational studies or randomized controlled trials investigating the association between recipient obesity at transplantation and mortality, death-censored graft loss and DGF were included. Obesity was defined as a body mass index (BMI) of ≥30 kg/m(2). Obese recipients were compared with those with a normal BMI (18.5-24.9 kg/m(2)). Pooled estimates of hazard ratios (HRs) for patient mortality or death-censored graft loss and odds ratios (ORs) for DGF were calculated.

Results: Seventeen studies including 138 081 patients were analysed. After adjustment, there was no significant difference in mortality risk in obese recipients [HR = 1.24, 95% confidence interval (CI) = 0.90-1.70, studies = 5, n = 83 416]. However, obesity was associated with an increased risk of death-censored graft loss (HR = 1.06, 95% CI = 1.01-1.12, studies = 5, n = 83 416) and an increased likelihood of DGF (OR = 1.68, 95% CI = 1.39-2.03, studies = 4, n = 28 847).

Conclusions: Despite having a much higher likelihood of DGF, obese transplant recipients have only a slightly increased risk of graft loss and experience similar survival to recipients with normal BMI.

Download full-text PDF

Source
http://dx.doi.org/10.1093/ndt/gfv214DOI Listing

Publication Analysis

Top Keywords

graft loss
20
recipient obesity
16
death-censored graft
16
mortality death-censored
12
systematic review
8
review meta-analysis
8
association recipient
8
obese recipients
8
normal bmi
8
increased risk
8

Similar Publications

Background: Growth differentiation factor (GDF)-15 is a pleiotropic cytokine that is associated with appetite-suppressing effects and weight loss in patients with malignancy.

Objectives: This study aims to investigate the relationships between GDF-15 levels, anorexia, cachexia, and clinical outcomes in patients with advanced heart failure with reduced ejection fraction (HFrEF).

Methods: In this observational, retrospective analysis, a total of 344 patients with advanced HFrEF (age 58 ± 10 years, 85% male, 67% NYHA functional class III), underwent clinical and echocardiographic examination, body composition evaluation by skinfolds and dual-energy x-ray absorptiometry, circulating metabolite assessment, Minnesota Living with Heart Failure Questionnaire, and right heart catheterization.

View Article and Find Full Text PDF

Background/objectives: Magnesium plays a crucial role in immune function, influencing immunoglobulin synthesis, antibody-dependent cytolysis, and other immune processes. In renal transplant patients, magnesium deficiency is primarily induced by calcineurin inhibitor treatment, through the reduction of magnesium transporter proteins in the renal tubules, leading to magnesium loss.

Methods: To assess the correlation between serum magnesium levels and the long-term outcomes of renal graft and transplant recipients, we conducted a retrospective study on 87 patients who have had a transplant for more than 5 years, a period considered immunologically stable.

View Article and Find Full Text PDF

Fucosidosis: A Review of a Rare Disease.

Int J Mol Sci

January 2025

Department of Molecular Biology and Genetics, Çanakkale Onsekiz Mart University, Çanakkale 17100, Turkey.

Fucosidosis is a rare lysosomal storage disease caused by α-L-fucosidase deficiency following a mutation in the gene. This enzyme is responsible for breaking down fucose-containing glycoproteins, glycolipids, and oligosaccharides within the lysosome. Mutations in result in either reduced enzyme activity or complete loss of function, leading to the accumulation of fucose-rich substrates in lysosomes.

View Article and Find Full Text PDF

Stem Cell-Based Therapies for Glaucoma Treatment: A Review Bridging the Gap in Veterinary Patients.

Int J Mol Sci

December 2024

Centro de Estudos de Ciência Animal (CECA), Instituto de Ciências, Tecnologias e Agroambiente (ICETA) da Universidade do Porto (UP), Praça Gomes Teixeira, Apartado 55142, 4051-401 Porto, Portugal.

Retinal diseases are characterized by progressive damage to retinal cells, leading to irreversible vision loss. Among these, glaucoma stands out as a multifactorial neurodegenerative disease involving elevated intraocular pressure, retinal ganglion cell apoptosis, and optic nerve damage, ultimately resulting in blindness in both humans and dogs. Stem cell-based therapies have emerged as a promising therapeutic option for such conditions due to their regenerative and neuroprotective potential.

View Article and Find Full Text PDF

Rapid Fabrication of Polyvinyl Alcohol Hydrogel Foams With Encapsulated Mesenchymal Stem Cells for Chronic Wound Treatment.

J Biomed Mater Res A

January 2025

Biomedical and Chemical Engineering and BioInspired Syracuse: Institute for Material and Living Systems, Syracuse University, Syracuse, New York, USA.

Chronic wounds present a major healthcare challenge around the world, and significant hurdles remain in their effective treatment due to limitations in accessible treatment options. Mesenchymal stem cells (MSCs) with multifunctional differentiation and modulatory properties have been delivered to chronic wounds to enhance closure but have limited engraftment when delivered without a scaffold. In this study, hybrid porous hydrogel foams composed of modified polyvinyl alcohol and gelatin were developed that are suitable for rapid and facile MSC encapsulation, fully degradable, and supportive of wound healing.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!