Vasopressin is an important hormone for water regulation of the body. When dehydration occurs, vasopressin secretion leads to water reabsorption in the kidney to prevent water loss. However, vasopressin seems to have deleterious effects on the kidney as well. In autosomal dominant polycystic kidney disease (ADPKD), vasopressin increases cyst growth and disease progression. Detrimental effects of vasopressin on chronic kidney disease in general have been described as well. In the first part of this thesis, copeptin was validated as marker for vasopressin because vasopressin is difficult to measure. Copeptin was stable outside the body, easy to measure and was a reliable marker for vasopressin in patients with impaired kidney function. In the second part of this thesis vasopressin release during thirsting was investigated in ADPKD and IgA nephropathy patients. Already in an early stage of disease, ADPKD patients had an impaired urine concentrating capacity which lead to an increase in vasopressin. IgA nephropathy patients had an impaired concentrating capacity as well although less profound in comparison to ADPKD patients. Vasopressin levels were increased in IgA nephropathy patients as well. The following hypothesis was formulated: when kidney function deteriorates, urine concentrating capacity decreases leading to an increase in vasopressin. This increase in vasopressin leads to kidney damage and creates a vicious circle resulting in disease progression. Part three of this thesis showed that copeptin predicts disease progression of both ADPKD and IgA nephropathy. These results support the hypothesis that dehydration is harmful to the kidney.
|Qualification||Doctor of Philosophy|
|Place of Publication||[Groningen]|
|Publication status||Published - 2016|