The development of clinical practice guidelines for the treatment of anemia in chronic kidney disease has been instrumental in identifying and reducing variations in the use of erythropoiesis-stimulating agents and iron replacement. Challenges to the effectiveness and safety of recommendations made in these guidelines were magnified when recent clinical trials showed no benefit or harm with respect to cardiovascular outcomes in subjects randomized to higher target hemoglobin levels. To address these concerns, Kidney Disease: Improving Global Outcomes (KDIGO) convened an international conference to examine the problems and shortcomings of existing anemia guidelines, which are a prime example of duplication of efforts to derive recommendations from a limited evidence base. The meeting was attended by representatives of the major guideline developing organizations, who agreed to avoid future duplicative efforts and to save resources in generating a common evidence report, whose recommendations could then be prioritized and implemented locally. This is a report to the international nephrology community of the recommendations for and timeline of the next anemia guidelines. It has been reviewed by the conference participants and approved as a position statement by the KDIGO Board of Directors.
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http://dx.doi.org/10.1038/ki.2008.299 | DOI Listing |
Heart Rhythm O2
December 2024
Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel.
Background: Transcatheter aortic valve replacement (TAVR) has revolutionized the management of aortic stenosis and has become the standard of care across a broad spectrum of patients with aortic stenosis. However, it is still associated with high incidence of conduction abnormalities, particularly new left bundle branch block (LBBB). Management of these patients remains a challenge.
View Article and Find Full Text PDFCalcineurin inhibitors (CNIs) are indispensable immunosuppressants for transplant recipients and patients with autoimmune diseases, but chronic use causes nephrotoxicity, including kidney fibrosis. Why inhibiting calcineurin, a serine/threonine phosphatase, causes kidney fibrosis remains unknown. We performed single-nucleus RNA sequencing of the kidney from a chronic CNI nephrotoxicity mouse model and found an increased proportion of injured proximal tubule cells, which exhibited altered expression of genes associated with oxidative phosphorylation, cellular senescence and fibrosis.
View Article and Find Full Text PDFDiabetic kidney disease (DKD) progression is often marked by early glomerular endothelial cell (GEC) dysfunction, including alterations in the fenestration size and number linked to impaired glomerular filtration. However, the cellular mechanisms regulating GEC fenestrations remain poorly understood due to limitations in existing models, challenges in imaging small fenestrations , and inconsistencies between and findings. This study used a logic-based protein-protein interaction network model with normalized Hill functions for dynamics to explore how glucose-mediated signaling dysregulation impacts fenestration dynamics in GECs.
View Article and Find Full Text PDFIntroduction: In USA, six million individuals with Sub-Saharan ancestry carry two high-risk variants, which increase the risk for kidney diseases. Whether APOL1 high-risk variants are independent risk factors for cardiovascular diseases is unclear and requires further investigation.
Methods: We characterized a mouse model to investigate the role of APOL1 in dyslipidemia and cardiovascular diseases.
The maintenance of a healthy epithelial-endothelial juxtaposition requires cross-talk within glomerular cellular niches. We sought to understand the spatially-anchored regulation and transition of endothelial and mesangial cells from health to injury in DKD. From 74 human kidney samples, an integrated multi-omics approach was leveraged to identify cellular niches, cell-cell communication, cell injury trajectories, and regulatory transcription factor (TF) networks in glomerular capillary endothelial (EC-GC) and mesangial cells.
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