Research - Renal Medicine
Risk factors for cardiovascular disease and malnutrition in chronic kidney disease patients.
Peter Stenvinkel, professor, MD
In close collaboration with Baxter Novum we study diagnostics, prevention and treatment of chronic kidney disease and its complications. In specifik we are interested in the metabolic effects of dialysis (hemodialysis and peritoneal dialysis) and the effects of alterations in nutritional status, inflammation, oxidative stress, sex hormones on cardiovascular health. In addition, in close collaboration with CMM we have since more than 10 years been studying the impact of genetic variations on the uremic phenotype and the effects of the toxic uremic milieu on the epigenotype. In another project we study ex vivo endothelial function in dissected arteries from uremic fat tissue. The basis for all these studies have been carefully phenotyped cohorts of chronic kidney disease patients at various stages of disease. At the moment more than 800 patients have been included. In an ongoing collaborative project with the Pharmacology Department we study the impact of genetic polymorphisms (CYP) and inflamamtion on the metabolism of different drugs in dialysis patients.
The impact of renal metabolism of peptide hormones for pathophysiology in renal failure.
Jonas Axelsson, MD, PhD
The kidney is a key organ for the metabolism of circulating peptide hormones. We are investigating the mechanisms of thismetabolism, as well as the consequences of renal dysfunction for systemic metabolism. By understanding how decreased renal function influences systemic signalling, we hope to develop novel therapies for these patients.
Dysregulation of FGF23 and Klotho in chronic kidney disease: implications for an accelerated ageing process, cardiovascular disease and mortality
Tobias Larsson, MD, PhD, Associate Professor
FGF23 and Klotho play a fundamental role in the regulation of serum phosphate, calcium and vitamin D levels. FGF23 levels are severly elevated in chronic kidney disease (CKD), leading to a reduction in the expression of its permissive FGF-receptor co-factor Klotho. Klotho was initially identified as an "ageing"-gene and reduced Klotho tissue levels confer an accelerated ageing-process and shortened life span mainly due to cardiovascular disease, a phenomenon also observed in CKD. In this translational project, we study the impact of dysregulation of FGF23 and Klotho as well as the molecular physiology of their endocrine actions employing in vitro and in vivo studies encompassing genetically engineered animal models and humans. Collectively, our studies could lead to novel treatments and improved diagnostic tools in CKD that ultimately will reduce the severely elevated mortality risk in this patient group. Patients suffering from the highest risk could be identified at an earlier stage, which should facilitate a more focused clinical management of CKD patients