Investigating the risk of progressive kidney disease
Study code
NBR144
Lead researcher
Jonathan Barratt
Study type
Participant re-contact
Institution or company
University of Leicester
Researcher type
Academic
Speciality area
Kidney Disorders, Genomics and Rare Diseases
Summary
3 million people in the UK suffer from poor kidney function, the severest form of which is end stage kidney disease (ESKD). When ESKD develops, only a kidney transplant or treatment with an artificial kidney (dialysis) can prolong life.
IgA nephropathy (IgAN) is an important cause of poor kidney function and ESKD. It occurs when the body's immune system produces an abnormal form of a defence protein called 'IgA', which gets trapped in the kidney's filtration system.
IgAN produces a number of microscopic changes in the filters of the kidneys, one of which is the accumulation of cells called macrophages. These cells are part of the immune system and normally defend us against infections. Inappropriate accumulation of macrophages can damage the kidneys, and this is likely occurring in IgAN. Macrophages in the kidneys evolve from cells in the bloodstream called monocytes.
This project will investigate which genes are switched on in blood monocytes and how this relates to macrophage accumulation in the kidneys in IgAN. A better understanding of why these monocytes move into the kidneys will hopefully allow us to identify new ways to prevent these cells from entering the kidneys and turning into kidney-damaging macrophages in IgAN.
The patients were recalled from the IgA Nephropathy (IAN) cohort at the Rare Diseases BioResource.
This study is part of our Rare Diseases RNA Phenotyping Project. Each participating study in the project is included in a collection hosted on our main studies page.