title: [Responsible genes for proteinuria and concept of the treatment for proteinuria].
abstract: Proteinuria has been demonstrated to be not only a representative sign of renal lesion but also a risk factor for the progression to renal failure through its injurious effects on tubulointerstitium. The responsible gene for Finnish type congenital nephrotic syndrome was identified and its product was named 'nephrin' which is located on slit membrane between foot processes of glomerular epithelial cells and is considered to be concerned also in the induction of acquired renal lesions with proteinuria. The monoclonal antibody against rat nephrin can induce proteinuria. These facts suggest that the important role for final barrier against macromolecules is played by the slit membrane. Understanding the proteinuria mechanism at molecular level is expected to lead to the establishment of appropriate treatments. Nephrin is regarded as the most promising and attractive molecule for the development of new therapeutic strategy. Many nephrologists are now much interested in the intimate relationship between nephrin and angiotensin II.
authors.affiliation: Department of Cell Biology, Institute of Nephrology, Graduate School of Medical and Dental Sciences, Niigata University.
authors.forename: Fujio
authors.initials: F
authors.lastname: Shimizu
mesh_terms: D000804:Angiotensin II / Q000502:physiology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D000911:Antibodies, Monoclonal; D004195:Disease Models, Animal; D006801:Humans; D008565:Membrane Proteins; D009404:Nephrotic Syndrome / Q000151:congenital / Q000235:genetics*; D011506:Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000502:physiology; D011507:Proteinuria / Q000235:genetics* / Q000628:therapy; D051381:Rats
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000911:Antibodies, Monoclonal; D008565:Membrane Proteins; D011506:Proteins; C113267:nephrin; D000804:Angiotensin II