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It´s a good thing that we worldwide have such great scientists making groundbreaking research in order to save lives!!
Jenny Nyström Professor, PhD. Jenny´s research aim to lead to better and more individualized treatment options for patients with renal disease (kidney failure or renal insufficiency).
Read about her interesting work!
The research projects in my group are focused on the cellular and molecular mechanisms behind kidney disease and renal transplant rejection, and how they translate into clinically observable data. Renal medicine is vastly lacking mechanistic explanations to renal disease progression and consequently also any specific therapies. Because of this, successful renal transplantations are imperative as a uremic care option. My aim is, through new and innovative approaches, to find such explanatory cellular and molecular patterns ultimately leading to better and more individualized treatment options for patients with renal disease.
BACKGROUND
Since as many as up to a tenth of the adult population in Sweden has some kind of kidney disorder, it is important to increase the possibilities of making a correct diagnosis and providing treatment. Nowadays there are very few treatments for patients with kidney failure and most patients attend dialysis, which means artificial filtering and purification of the blood. This often involves deterioration of the patient’s quality of life and is moreover expensive for the community as a whole. Kidney transplantation is a very good alternative in order to be cured of kidney disease, but unfortunately only about 25 % of patients in dialysis have this option, on account of various complications.
The kidneys function as a filter for the blood, and undesirable substances, excess water and salts are filtered out. The primary urine produced when the blood is filtered has approximately the same constitution as blood, apart from the biggest proteins that remain in the blood circulation. About 180 litres of primary urine are produced each day, but the final urine production is only between 1 and 2 litres per day. This means that most of what is filtered out must be reabsorbed before the urine is collected in the urinary bladder. This process is vital and is regulated by the body. Disturbances in the barrier function lead to proteins leaking out in the urine, ”albumen in the urine”, a typical symptom of kidney disease.
Our objective with this project is to try and develop better diagnostic techniques and treatment of patients with kidney disorders involving albumen leakage. In order to achieve this we must know more about how the normal barrier between blood and urine is structured, knowledge that is unfortunately still inadequate. The filtration process itself takes place in the vascular bundles (glomeruli) in the kidney, and the glomerular barrier consists of three layers: the endothelium, the basal membrane and specialised epithelial cells. The cells also produce negatively charged sugar-filled matrix molecules. We want to decide its functional role and how its composition is regulated at the cellular and molecular levels in different types of kidney disease. We can find out how different states of illness influence the genetic expression in the cells of the kidney in comparison with the healthy state, since we have access to small samples of tissue through biopsies of people with kidney disease. We can also make cell cultures from biopsies in order to study and compare these with healthy cells, so that we can gain knowledge about the detailed signal mechanisms in the various types of kidney cell. We are particularly interested in understanding how a certain protein works that seems to make some kidneys more liable than others to develop IgA nephritis. One might say that we are looking for the ”keyhole” that the IgA ”key” molecule fits into. Our hypothesis is that if the ”key” fits then a person becomes ill; otherwise people can have the ”key” in their blood without developing the disease.
We also want to look at background causes to the fact that certain patients who have previously rejected their transplanted kidneys tolerate them once a piece of the donor’s liver has also been transplanted. What is it in the piece of liver that allows the kidney to remain in the receiver’s body? One theory that we want to follow up is that there are special genes involved in this, and one of the candidate genes is indoleamine 2,3-dioxygenas, which has previously been shown to be important for a mother’s tolerance of her foetus during pregnancy. We also want to find out how dendrite cells (or cells in the immunological system) may be involved in the resulting tolerance. The combination of advanced molecular and functional methodology with kidney biopsies and clinical data from patients with kidney disease offer us great opportunities for achieving new and relevant research results concerning the mechanisms behind human kidney disease and transplantation.
Text by Jenny Nyström Professor, PhD.
Translated by Margaret Myers for Recycle Me
