In the study just published by Dr. Tilman Breiderhoff, Prof. Thomas Willnow (both MDC), as well as Dr. Nina Himmerkus and Prof. Markus Bleich (both of the University of Kiel) and Dr. Dominik M-ller (Charit-) the focus is on the claudin-10 gene, which is expressed in a specific segment of the kidney, in Henle's loop. In the thick ascending limb of this loop, , a large part of the filtered sodium chloride, as well as calcium and magnesium are reabsorbed. The gene product under investigation, the claudin 10 protein, belongs to a family of proteins that connect the epithelial cells which cover the inner and outer surfaces of the body and stick them together like velcro. Claudins, however, also form pores, through which ions and substances are transported between the cells.
"If these transport processes are disturbed, this can lead to serious loss of function of the kidneys," Dr. Breiderhoff explained. As example he cited various human hereditary diseases in which either absorption of table salt (Bartter syndrome) or of calcium and magnesium (familial hypomagnesemia with hypercalciuria and nephrocalcinosis - FHHNC) is disturbed. The second disease is characterized by a lack of magnesium in the blood and an excess of calcium in the urine, which leads to calcification of the kidneys. It is caused by mutations in one of two genes (claudin 16 or claudin 19), which also belong to the gene family of the claudins.
The researchers have now demonstrated in mice that the claudin-10 gene is involved in the reabsorption of salt in the kidney. If the gene in the kidney is deactivated, the reabsorption of sodium is impaired, but the reabsorption of calcium and magnesium is increased. The consequence is that the mice have elevated magnesium levels in the blood, and excess calcium is deposited in the kidney. Simultaneously, the urine volume is increased because the kidneys of the mice cannot reabsorb enough water, a sign that the recovery of salt is disturbed.