Journal
TOXICOLOGIC PATHOLOGY
Volume 46, Issue 8, Pages 944-948Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0192623318796784
Keywords
tubuloglomerular cross talk; atubular glomeruli; tubuloglomerular feedback; hypoxia; renin-angiotensin-aldosterone system
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Funding
- NIH NIDDK [DK56942-09]
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Tubular injury sensitizes glomeruli to injury. We review potential mechanisms of this tubuloglomerular cross talk. In the same nephron, tubular injury can cause stenosis of the glomerulotubular junction and finally result in atubular glomeruli. Tubular injury also affects glomerular filtration function through tubuloglomerular feedback. Progenitor cells, that is, parietal epithelial cells and renin positive cells, can be involved in repair of injured glomeruli and also may be modulated by tubular injury. Loss of nephrons induces additional workload and stress on remaining nephrons. Hypoxia and activation of the renin-angiotensin-aldosterone system induced by tubular injury also modulate tubuloglomerular cross talk. Therefore, effective therapies in chronic kidney disease may need to aim to interrupt this deleterious tubuloglomerular cross talk.
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