Proteinuria and events beyond the slit
| Autor: | Erik Ilsø Christensen, Rikke Nielsen |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
medicine.medical_specialty
Kidney Glomerulus Receptors Cell Surface Nephron 030204 cardiovascular system & hematology urologic and male genital diseases Renal protein reabsorption Kidney Tubules Proximal 03 medical and health sciences 0302 clinical medicine Risk Factors Internal medicine medicine Animals Humans 030304 developmental biology 0303 health sciences Renal oligopeptide reabsorption urogenital system business.industry Reabsorption Membrane Proteins Proteins Biological Transport Cubilin Endocytosis Molecular Weight Low Density Lipoprotein Receptor-Related Protein-2 Proteinuria Endocrinology medicine.anatomical_structure Tubule Tubular proteinuria Nephrology Renal physiology Pediatrics Perinatology and Child Health Lysosomes business Glomerular Filtration Rate |
| Zdroj: | Pediatric Nephrology; Vol 25 Pediatric Nephrology |
| ISSN: | 1432-198X 0931-041X |
| DOI: | 10.1007/s00467-009-1381-9 |
| Popis: | The origin of proteinuria is found in either the glomerular filtration device or the proximal tubular reabsorption machinery. During equilibrium, small amounts of predominantly low molecular weight proteins are filtered and reabsorbed by the receptor complex megalin/cubilin/amnionless. This results in a protein-free filtrate passing further down the tubule. During glomerular damage, the reabsorption machinery in the proximal tubule is challenged due to elevated amounts of proteins passing the glomerular filtration slits. Even though it is considered to be a high-capacity system, several conditions result in proteinuria, thus exposing the cells in the rest of the nephron to a protein-rich environment. The impact on cells in the more distal part of the nephron is uncertain, but studies support an involvement in fibrosis development. Protein accumulation in lysosomes of the proximal tubule, due to increased protein internalization, is thought to mediate inflammation and fibrosis, eventually leading to renal failure. In contrast, low molecular weight proteinuria develops when the endocytic machinery is malfunctioning either by direct or indirect causes such as in Imerslund-Gräsbeck syndrome (IGS) or Dent's disease, respectively. This review discusses the origin of proteinuria and describes the structural fundament for protein reabsorption in the proximal tubule as well as conditions resulting in low molecular weight proteinuria. |
| Databáze: | OpenAIRE |
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