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- W2068604817 endingPage "17" @default.
- W2068604817 startingPage "9" @default.
- W2068604817 abstract "There are many different glomerular disorders, including glomerulonephritis, diabetic nephropathy, and hypertensive nephrosclerosis. However, once glomerular damage reaches a certain threshold, the progression of renal disease is consistent and irreversible. Recent studies emphasized the crucial role of tubulointerstitial injury as a mediator of progression of kidney disease. One common mechanism that leads to renal failure via tubulo-interstitial injury is massive proteinuria. Accumulating evidence suggests critical effects of filtered macromolecules on tubular cells, including lysosomal rupture, energy depletion, and tubular injury directly induced by specific components such as complement components. Another common mechanism is chronic hypoxia in the tubulointerstitium. Tubulointerstitial damage results in the loss of peritubular capillaries, impairing blood flow delivery. Interstitial fibrosis also impairs oxygen diffusion and supply to tubular cells. This induces chronic hypoxia in this compartment, rendering a vicious cycle. Development of novel therapeutic approaches against these final common pathways will enable us to target any types of renal disease." @default.
- W2068604817 created "2016-06-24" @default.
- W2068604817 creator A5036113498 @default.
- W2068604817 date "2004-01-01" @default.
- W2068604817 modified "2023-10-18" @default.
- W2068604817 title "Mechanisms of Tubulointerstitial Injury in the Kidney: Final Common Pathways to End-stage Renal Failure" @default.
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- W2068604817 doi "https://doi.org/10.2169/internalmedicine.43.9" @default.
- W2068604817 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14964574" @default.
- W2068604817 hasPublicationYear "2004" @default.