Autosomal dominant polycystic kidney disease (ADPKD) is a frequently occurring inherited condition characterised by the formation of multiple cysts and considerable enlargement of both kidneys. The presence of microalbuminuria in ADPKD may identify a subset of patients at increased risk for cardiovascular morbidity and mortality but as yet, the mechanism of microalbuminuria remains unknown.
In the February issue of American Journal of Physiology - Renal Physiology researchers from the University of Heidelberg suggest that proteinuria in these patients may be caused by a defect in the endocytic machinery.
Nicholas Obermüller and colleagues studied (cy/+) rats, a widely used model for ADPKD. Using FITC-labelled dextran as an in vivo tracer, they show that portions of cyst-lining epithelia in the proximal tubules of these rats have lost the ability to endocytose and thus cannot reabsorb low-molecular-weight proteins. Immunohistochemical examination of the expression of proteins implicated in endocytosis, such as the chloride channel ...
