尿蛋白
1)糸球体性蛋白尿
糸球体基底膜でのsize barrier(コラーゲン線維の網目の小孔、半径約70Åといわれている)あるいはcharge barrier(陰性荷電しているプロテオグリカンとラミニン)が障害されて尿中へ蛋白が排泄されたものが尿蛋白として認識される(。
2)selectivity indexの低下
通常は比較的分子量の小さいアルブミンとβ-グロブリンが主であるが、基底膜の破壊が強いとき(膜性増殖性糸球体腎炎、糖尿病、アミロイドーシスなど)には、γ-グロブリンなど大きな蛋白も排泄される。
3)尿細管障害
正常な糸球体からはα１-ミクログロブリンやβ２-ミクログロブリンなど低分子蛋白が排泄され、近位尿細管で再吸収されているが、尿細管障害のときにはこれらの蛋白が大量に尿中に排泄され蛋白尿となる。
この場合1日1.5g/日以上になることはほとんどない。
4)良性蛋白尿
起立性あるいは熱性などの良性蛋白尿は、1日1g以上排泄されることはない。
早朝尿で蛋白陰性で立位負荷したときにのみ陽性なら、起立性蛋白尿の可能性が大である。
http://shimonagaya.com/up.htm
http://www.hamt.or.jp/kenkyuhan/link/ippankensa/kennyo/teisei2.htm
糸球体の構造と機能
糸球体は３種類の細胞と２種類の細胞外基質から成る。
①基底膜（GBM）⇒３層構造、Ⅳ型コラーゲンを主とする細胞外基質。サイズバリアとチャージバリア。
②メサンギウム細胞と基質⇒各種サイトカインに反応して増殖・増生する。
③糸球体上皮細胞⇒foot processの形成、通常は増殖しない。
http://www.geocities.jp/study_nasubi/e/e7.html
NEPHROTIC SYNDROME is a condition resulting from increased leakage of protein into the urine (proteinuria) from the filters in the kidneys (glomeruli) that produce urine from blood. With the loss of protein in the urine, changes occur in the blood that cause fluid to accumulate in the tissues of your body. This results in tissue swelling (EDEMA). The edema may develop in your hands and feet (making shoes or rings feel tight), ankles or in your face causing puffiness around the eyes. In some instances, the fluid accumulates on your lungs making it more difficult to breathe. Nephrotic syndrome is caused by diseases that alter the function of the walls of the small vessels (capillaries) in the kidney filters (glomeruli) that filter blood to make urine.
Proteinuria results when there is a defect in the glomerular capillary wall that allows protein to leak into the urine.
http://www.unckidneycenter.org/kidneyhealthlibrary/nephroticsyndrome.html
The normal glomerular capillary wall keeps blood cells and most proteins in the blood. In patients with proteinuria, protein leaks across the wall into the urine. The barriers in the capillary wall that keep protein out of the urine are the endothelial cell lining the capillary lumen, the basement membrane under the endothelial cell and the cell on the outside surface of the capillary (epithelial cells). The epithelial cell (podocyte) normally has little “feet” (pods) that sit on the basement membrane and are connected by a thin membrane. The glomerular epithelial cells (podocytes) appear to be the most important barrier that prevents protein from leaking into the urine.
Drawn below are the barriers that keep protein and blood cells out of the urine. These are the endothelial cell, basement membrane and epithelial cell (podocyte). The epithelial cell (podocyte) seems to be most important. Injury to these barriers causes proteinuria and hematuria.
http://www.unckidneycenter.org/kidneyhealthlibrary/nephroticsyndrome.html
Schematic summary of some of the pathways and mediators that are believed to be involved in proteinuria-induced tubulointerstitial injury. RANTES, regulated upon activation, normal T cell expressed and secreted; IL-8, interleukin-8; MCP-1, monocyte chemoattractant factor-1; ET-1, endothelin-1; TGF-, transforming growth factor-; M, macrophage; L, lymphocyte; F, fibroblast; E, endothelial cell.
http://www.nature.com/ki/journal/v66/n92s/fig_tab/4494961f1.html
The tiny structures that do the work in your kidneys are called NEPHRONS.
Each nephron has a small blood vessel (arteriole) that brings in unfiltered blood, a GLOMERULUS that filters the blood and a small blood vessel that returns filtered blood to the body.
The earliest detectable change in glomeruli (pleural for glomerulus) is thickening of the thin membrane (basement membrane) that is part of the filter that separates the blood from the urine.
Damage to this membrane and the cells next to it in the capillary walls causes proteins (such a albumin) to leak from the blood into the urine.
This is called proteinuria and albuminuria.
Damage to the membrane can be identified in a kidney using electron microscopy to show thickening of the membrane.
Diabetic Glomerulosclerosis
Diabetes also can cause progressive scarring (SCLEROSIS) of glomeruli that is called GLOMERULOSCLEROSIS. This scarring (sclerosis) often produces nodules of scar in the glomeruli and thus is called NODULAR DIABETIC GLOERULOSCLEROSIS in a renal biopsy report.
http://www.unckidneycenter.org/kidneyhealthlibrary/diabetes.html
Proteinuria in diabetic kidney disease: A mechanistic viewpoint
http://www.nature.com/ki/journal/v74/n1/fig_tab/ki2008128f3.html
Podocyte abnormalities in DKD. (a) Normal podocyte architecture. (b) Some podocytes undergo apoptosis, resulting in reduced cell number. Albumin can then leak through areas denuded of podocytes. (c) The normal architecture of the slit diaphragm is disrupted (by either reduced levels of specific proteins and/or relocalization of these proteins) leading to a loss of size barrier. Podocytes also undergo changes in shape due to effacement. (d) The normal function of podocytes is also limited by individual cells increasing in size (hypertrophy) and detachment leads to reduced overall podocyte number.
Proteinuria in diabetic kidney disease: A mechanistic viewpoint
http://www.nature.com/ki/journal/v74/n1/fig_tab/ki2008128f4.html
1)糸球体性蛋白尿
糸球体基底膜でのsize barrier(コラーゲン線維の網目の小孔、半径約70Åといわれている)あるいはcharge barrier(陰性荷電しているプロテオグリカンとラミニン)が障害されて尿中へ蛋白が排泄されたものが尿蛋白として認識される(。
2)selectivity indexの低下
通常は比較的分子量の小さいアルブミンとβ-グロブリンが主であるが、基底膜の破壊が強いとき(膜性増殖性糸球体腎炎、糖尿病、アミロイドーシスなど)には、γ-グロブリンなど大きな蛋白も排泄される。
3)尿細管障害
正常な糸球体からはα１-ミクログロブリンやβ２-ミクログロブリンなど低分子蛋白が排泄され、近位尿細管で再吸収されているが、尿細管障害のときにはこれらの蛋白が大量に尿中に排泄され蛋白尿となる。
この場合1日1.5g/日以上になることはほとんどない。
4)良性蛋白尿
起立性あるいは熱性などの良性蛋白尿は、1日1g以上排泄されることはない。
早朝尿で蛋白陰性で立位負荷したときにのみ陽性なら、起立性蛋白尿の可能性が大である。
http://shimonagaya.com/up.htm
http://www.hamt.or.jp/kenkyuhan/link/ippankensa/kennyo/teisei2.htm
糸球体の構造と機能
糸球体は３種類の細胞と２種類の細胞外基質から成る。
①基底膜（GBM）⇒３層構造、Ⅳ型コラーゲンを主とする細胞外基質。サイズバリアとチャージバリア。
②メサンギウム細胞と基質⇒各種サイトカインに反応して増殖・増生する。
③糸球体上皮細胞⇒foot processの形成、通常は増殖しない。
http://www.geocities.jp/study_nasubi/e/e7.html
NEPHROTIC SYNDROME is a condition resulting from increased leakage of protein into the urine (proteinuria) from the filters in the kidneys (glomeruli) that produce urine from blood. With the loss of protein in the urine, changes occur in the blood that cause fluid to accumulate in the tissues of your body. This results in tissue swelling (EDEMA). The edema may develop in your hands and feet (making shoes or rings feel tight), ankles or in your face causing puffiness around the eyes. In some instances, the fluid accumulates on your lungs making it more difficult to breathe. Nephrotic syndrome is caused by diseases that alter the function of the walls of the small vessels (capillaries) in the kidney filters (glomeruli) that filter blood to make urine.
Proteinuria results when there is a defect in the glomerular capillary wall that allows protein to leak into the urine.
http://www.unckidneycenter.org/kidneyhealthlibrary/nephroticsyndrome.html
The normal glomerular capillary wall keeps blood cells and most proteins in the blood. In patients with proteinuria, protein leaks across the wall into the urine. The barriers in the capillary wall that keep protein out of the urine are the endothelial cell lining the capillary lumen, the basement membrane under the endothelial cell and the cell on the outside surface of the capillary (epithelial cells). The epithelial cell (podocyte) normally has little “feet” (pods) that sit on the basement membrane and are connected by a thin membrane. The glomerular epithelial cells (podocytes) appear to be the most important barrier that prevents protein from leaking into the urine.
Drawn below are the barriers that keep protein and blood cells out of the urine. These are the endothelial cell, basement membrane and epithelial cell (podocyte). The epithelial cell (podocyte) seems to be most important. Injury to these barriers causes proteinuria and hematuria.
http://www.unckidneycenter.org/kidneyhealthlibrary/nephroticsyndrome.html
Schematic summary of some of the pathways and mediators that are believed to be involved in proteinuria-induced tubulointerstitial injury. RANTES, regulated upon activation, normal T cell expressed and secreted; IL-8, interleukin-8; MCP-1, monocyte chemoattractant factor-1; ET-1, endothelin-1; TGF-, transforming growth factor-; M, macrophage; L, lymphocyte; F, fibroblast; E, endothelial cell.
http://www.nature.com/ki/journal/v66/n92s/fig_tab/4494961f1.html
The tiny structures that do the work in your kidneys are called NEPHRONS.
Each nephron has a small blood vessel (arteriole) that brings in unfiltered blood, a GLOMERULUS that filters the blood and a small blood vessel that returns filtered blood to the body.
The earliest detectable change in glomeruli (pleural for glomerulus) is thickening of the thin membrane (basement membrane) that is part of the filter that separates the blood from the urine.
Damage to this membrane and the cells next to it in the capillary walls causes proteins (such a albumin) to leak from the blood into the urine.
This is called proteinuria and albuminuria.
Damage to the membrane can be identified in a kidney using electron microscopy to show thickening of the membrane.
Diabetic Glomerulosclerosis
Diabetes also can cause progressive scarring (SCLEROSIS) of glomeruli that is called GLOMERULOSCLEROSIS. This scarring (sclerosis) often produces nodules of scar in the glomeruli and thus is called NODULAR DIABETIC GLOERULOSCLEROSIS in a renal biopsy report.
http://www.unckidneycenter.org/kidneyhealthlibrary/diabetes.html
Proteinuria in diabetic kidney disease: A mechanistic viewpoint
http://www.nature.com/ki/journal/v74/n1/fig_tab/ki2008128f3.html
Podocyte abnormalities in DKD. (a) Normal podocyte architecture. (b) Some podocytes undergo apoptosis, resulting in reduced cell number. Albumin can then leak through areas denuded of podocytes. (c) The normal architecture of the slit diaphragm is disrupted (by either reduced levels of specific proteins and/or relocalization of these proteins) leading to a loss of size barrier. Podocytes also undergo changes in shape due to effacement. (d) The normal function of podocytes is also limited by individual cells increasing in size (hypertrophy) and detachment leads to reduced overall podocyte number.
Proteinuria in diabetic kidney disease: A mechanistic viewpoint
http://www.nature.com/ki/journal/v74/n1/fig_tab/ki2008128f4.html
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