作者: Vincent Fridén
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摘要: A healthy kidney produces final urine that is practically devoid of proteins and other physiologically important solutes. Tremendous amounts fluid are filtered every day through the glomerular filtration barrier which actual sieving site in kidney. Failure filtering function leads to proteinuria, a feature common nearly all disease. In spite this pivotal role, central mechanisms behind proteinuria still unexplained. The complex biological membrane composed four different structures: podocytes (epithelial cells), basement membrane, endothelium endothelial cell surface layer (ESL). During last decade focus for understanding regulation selective sieve has rested heavily on study podocytes, whereas ESL been more or less neglected as contributors permselectivity barrier. However, it fundamental importance investigate components order understand pathophysiology proteinuric molecular structure largely unexplored, available data about its constituents so far only based vitro studies. aim thesis was identify molecules located with functional significance normal vivo, examine whether disease-emulating milieu damages major structural thus increases permeability proteins. We have developed method qualitative quantitative assessment rats, includes brief injection hypertonic sodium chloride into renal artery. This displaces elutes non-covalently bound then subsequently collected further characterization liquid chromatography-mass spectrometry. Morphological well effects characterized by electron microscopy universal methods analyzing charge- size selectivity membranes. conditionally immortalized human line used hyperglycemia proteoglycans. Functional alterations were analyzed terms protein restriction measuring passage albumin across monolayer. conclusion, we identified from rats essential maintaining function. Further, found associated an alteration proteoglycans lead increased albumin. Overall, observations emphasize