Research and Education

Chronic kidney disease (CKD) is associated with extensive, progressive fibrosis and inflammation to which no cure exists. A major obstacle in CKD drug development is that less than 10% of drugs entering Phase I clinical trials show clinical benefit. A main reason for this is the lack of suitable tools to predict the relevance of basic research findings for human pathophysiology. This stresses the unmet need to identify new pre-clinical models for target identification and evaluation that can bridge the translation gap. 

In collaboration with industry, we will model early stages of human CKD development using a model of precision-cut kidney slices from humans and turning these slices either fibrotic or inflammatory to identify both novel CKD biomarkers as well as targets for CKD intervention. (Introduction video of ODIN-project)

I was responsible for validating OMICs data from these tissue slices by high-resolution immunohistofluorescence staining. During this period, together with professor Lene Nejsum, developed a new method for high-resolution multiplex immunofluourescence staining (Multiplex immunofluorescence staining of coverslip-mounted paraffin-embedded tissue sections)

Sustained albuminuria is hallmark of chronic kidney disease (CKD), and the degree of albuminuria is closely associated to the outcome for patients suffering from CKD. Thus, we aimed to investigate the role of two endocytic receptors in the progression of CKD. The study was performed in a transgenic mouse model of proteinuric kidney disease in which knockout of both receptors was induced.

We found that abrogation of total protein-endocytosis accelerated the degree of kidney injury in the proteinuric mice, while more specific blockage of albumin-endocytosis protected the kidneys from early injuries.