Research group Kidney physiology

The development of next-generation diagnostics and innovative functional methods to measure magnesium transport are essential to diagnose and to understand magnesium-wasting tubulopathies. We envision that patient-specific models are the future of pathophysiological research. Personalized drug screening to identify therapeutics that fit the needs of individual patients will become the new standard for treatment of rare diseases

Cardiovascular complications are the main cause of death for patients with chronic kidney disease (CKD). Our research on magnesium in vascular calcification demonstrates that novel interventions can contribute to prevent cardiovascular disease in CKD. In our vision, better understanding of mechanisms of vascular calcification is essential to develop dietary and pharmacological approaches to reduce cardiovascular mortality and morbidity in CKD.

Our recent findings demonstrate that disturbed metabolic process result in urinary electrolyte wasting. We aim understand how metabolism and ion transport are related in the distal convoluted tubule of the kidney.

Our mission is to decipher the pathophysiological mechanisms of magnesium disorders. By identification of genes involved in hereditary hypomagnesemia, we aim to increase our understanding of the molecular mechanisms of magnesium reabsorption in the kidney.

We develop patient-specific models for genetic tubulopathies and perform drug screening to identify therapeutics that fit the needs of individual patients

We introduce state-of-the-art technology to measure ion transport in vitro and in vivo, using multiphoton microscopy and radio-labeled and stable isotopes

We have identified of novel magnesium-wasting and salt-losing tubulopathies caused by mutations in CNNM2, PCBD1, KCNJ16, RRAGD and TRPM7. By linking genetic screening to functional studies, we have provided insights into the mechanisms of magnesium reabsorption in the kidney and improved diagnostics of patients with genetic kidney diseases.

We have shown that magnesium prevents vascular calcification in vitro and in vivo. In vascular smooth muscle cells (VSMC), magnesium effectively prevented high phosphate-induced mineralization, as well as in mouse models of CKD. Currently, clinical trials are in progress to determine the clinical relevance of magnesium supplements in CKD.

We have demonstrated that 10-30% of all people with diabetes suffers from hypomagnesemia. Our work shows that magnesium affects insulin sensitivity and lipid metabolism. In clinical trials, we have evaluated benefits of magnesium for insulin sensitivity and immune function.