Research group Stefan Jacobson
The research group in Nephrology at Karolinska Institutet has been active for more than 20 years within a network at Danderyd University Hospital, Karolinska University Hospital, Center for Molecular Medicine and Cancer Centrum Karolinska as well as with a number of institutions and groups at the Karolinska Institutet. The clinical research groups that we mostly have collaborated with are within Clinical immunology, Cardiology, Endocrinology, Rheumatology and Tumor biology.
During recent years chronic kidney disease has been identified as a major health problem in the western world and approximately 10-15 % of the population is affected of mild to moderate to severe kidney disease. Patients with chronic kidney disease have an increased cardiovascular morbidity and mortality and are at increased risk of infections, chronic inflammation and malnutrition and renal osteodystrophy. The health care expenses in treating patients with mild to severe chronic kidney disease are very high in the western world.
Leukocyte function in chronic kidney disease
Our research group has focused on studies on the mechanisms involved in the increased risk of severe infections that occur in patients with chronic kidney disease, especially in those with severe kidney disease and in peritoneal dialysis or haemodialysis. We have a close collaboration with the Department of Clinical Immunology at Karolinska University Hospital and together we have performed a large number of clinical and experimental studies on leukocyte function in patients with chronic kidney disease and dialysis. We have analyzed soluble inflammatory markers in peripheral blood and studied leukocyte transmigration in vivo to induced inflammatory foci in the skin in these groups of patients. We have also used advanced gene technology to study intracellular activation through gene-pathways using rt-PCR, Western-blot, microRNA and performed cell surface analysis of monoclonal antibodies with flow cytometry. We have now established collaboration with colleagues at Science for Life Lab for specific studies of protein profiles in chronic kidney disease, basophil cell function at the single cell level to gain knowledge on how inflammatory processes are initiated in patients with chronic kidney disease and how they affect the immune response.
Progression of chronic kidney disease
We also study how soluble inflammatory markers and genetic factors affect the risk of progression of chronic kidney disease in different groups of patients, such as those with concomitant cardiovascular disease, glomerulonephritis and in renal patients treated with for instance statins or vitamin D analogues. Also in these studies, Science for Life Lab is involved in defining protein profiles.
We also study the pathogenesis and progression of IgA-nephropathy and have established a large cohort of patients with biopsy proven IgA-nephropathy in a biobank of more than 300 patients. A number of PhD students have defended their thesis in this field and international collaborations have been established. This is done in close collaboration with the Department of Nephrology and Rheumatology at Karolinska University Hospital.
The Cardio Renal Syndrome
The Departments of Nephrology at Danderyd University Hospital, together with the Department of Cardiology at Danderyd University Hospital, Karolinska University Hospital and Södersjukhuset study patients with acute coronary syndrome in patients with mild to severe chronic kidney disease. A biobank has been established and a number of high ranked manuscripts have been published in peer reviewed journals with high impact factor in close collaboration to SWEDEHEART. A number of different cardio-renal studies related to chronic inflammation, bone mineral metabolism and haemostasis will be performed in coming years.
|Research leader, Stefan Jacobson|
|Professor Joachim Lundahl, Department of Clinical Immunology, Karolinska University Hospital, Joachim.firstname.lastname@example.org|
|Ali Moshfegh, CancerCentrum Karolinska, email@example.com|
|Sigrid Lundberg, MD, PhD, Department of Nephrology, Karolinska University Hospital, firstname.lastname@example.org|
|Assoc professor Britta Hylander, Department of Nephrology, Karolinska University Hospital, email@example.com|
|Assoc professor Iva Gunnarsson, Department of Rheumatology, Karolinska University Hospital, firstname.lastname@example.org|
|Assoc professor Jonas Spaak, Department of Cardiology, Danderyd University Hospital, email@example.com|
|Assoc professor Tomas Jernberg, Department of Cardiology, Karolinska University Hospital, firstname.lastname@example.org|
|Karolina Szummer, MD, PhD, Department of Cardiology, Karolinska University Hospital, email@example.com|
|Professor Thomas Kahan, Department of Cardiology, Danderyd University Hospital, firstname.lastname@example.org|
|Pia Lundman, MD, PhD, Department of Cardiology, Danderyd University Hospital, email@example.com|
|Assoc professor Håkan Wallén, Department of Cardiology, Danderyd University Hospital, firstname.lastname@example.org|
|PhD student Ladan Mansouri, MD, Department of Clinical Immunology, Karolinska University Hospital, email@example.com|
|PhD student Senka Sendic, MD, Department of Nephrology, Danderyd University Hospital, firstname.lastname@example.org|
|PhD student Josefin Mörtberg, MD, Department of Nephrology, Danderyd University Hospital, email@example.com|
|PhD student Tora Almquist, MD, Department of Nephrology, Danderyd University Hospital, firstname.lastname@example.org|
|PhD student Kristina Lundwall, MD, Department of Cardiology, Danderyd University Hospital, email@example.com|
|PhD student Masih Khedri, Department of Cardiology, Danderyd University Hospital, firstname.lastname@example.org|
|PhD student Carin Wallquist, MD, Department of Nephrology, Västerås lasarett, Department of Medicine Solna, Karolinska institutet, email@example.com|
Activation of Wnt/β-catenin pathway in monocytes derived from chronic kidney disease patients.
PLoS ONE 2013 ;8(7):e68937
FGF23, albuminuria, and disease progression in patients with chronic IgA nephropathy.
Clin J Am Soc Nephrol 2012 May;7(5):727-34
Expression of neutrophil SOD2 is reduced after lipopolysaccharide stimulation: a potential cause of neutrophil dysfunction in chronic kidney disease.
Nephrol. Dial. Transplant. 2011 Jul;26(7):2195-201
Association of soluble CD89 levels with disease progression but not susceptibility in IgA nephropathy.
Kidney Int. 2010 Dec;78(12):1281-7