BIgAN II

lgA nephropathy is a slowly progressing disease that causes kidney damage and leads to kidney failure in about 25-50% of cases. For them, dialysis or renal transplantion is the only solution. The reason why lgA nephropathy develops in some people is unclear and there is no effective treatment yet. ïhe disease is characterized by the precipitation of lgA in the kidneys. lgA is made by immune cells and helps to protect us against infection. The lgA in the blood is normally strongly bound to sugar molecules. ln lgA nephropathy patients, something appears to go wrong with the glycosylation of the lgA in the blood, causing it to precipitate in the kidneys and eventually leading to kidney damage. An important role in the development of lgA nephropathy appears to be played by immune cells that make lgA in our gastrointestinal mucosa. The lgA they secrete is naturally low in sugars and binds bacteria in the gastrointestinal tract and has a substantial influence on the composition of the bacterial ecosystem in the gastrointestinal tract. An interesting observation in this regard is that the bacterial ecosystem in the saliva and stool of lgA nephropathy patients is diÍferent from that of healthy people. This could indicate a disturbance of the immune system in the gastrointestinal tract of lgA nephropathy patients. Little is known about this at the moment.

We want to remap the entire bacterial ecosystem in the gastrointestinal tract of patients with lgA nephropathy after a period of roughy two years, in order to gain insight into the processes that may play a role in the development and progression of the disease.  Furthermore, we aim to analyse the proteome of the urine of this population again to see how specific proteins can predict disease progression. This can then lay the foundation for new forms of treatment.

This is a clinical observational study.

The participants of study 2021-13006/BIgAN I will be included again:
1. Patients with lgA nephropathy (n = 50)
2. Control individuals matched for age and kidney function (eGFR), consisting of patients with renal damage based on cystic kidney disease (ADPKD) or renovascular damage (hypertension, diabetes mellitus type 2) and healthy controls (n = 50).

The inclusion proces should take into account that participants that have reached clinical endpoints (death, transplantation, or dialysis) cannot be included again. As no new patients or controls will be included in this study, the actual number of inclusions may fall below 50.

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This is an observational study in which participants complete a questionnaire and donate body fluids (urine, sputum, faeces and blood). ln our view, there are no risks associated with this. The burden for participation in this study is minimal and consists of a 1-hour visit to our outpatient clinic.