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Preservation of glomerular filtration rate on dialysis when adjusted for patient dropout.
We previously reported that angiotensin-converting enzyme inhibitor (ACEi) renoprotection in Munich Wistar Frömter (MWF) rats, which develop progressive glomerular injury, was associated with podocyte repopulation and preservation of glomerular architecture.
As expected, SNX rats experienced a significant reduction in glomerular capillary density, while CMC-treated SNX rats demonstrated preservation of glomerular capillaries (Fig. 5).
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Similarly, glomerular endothelial cells, which have an important role in the preservation of the glomerular capillary network, are induced to apoptotic death in hypoxic conditions [ 17].
Conclusion: Our results suggest that intrinsic glomerular cell production of IL-8, in particular the 77-AA form, may be relevant for preservation of the glomerular architecture.
This ensures preservation of filtration pressure in glomerular capillaries at the expense of a further fall in perfusion.
In those who recover, complete resolution of glomerular disease occurs.
A stage of glomerular hyperfiltration and hypertrophy precedes the glomerular sclerosis and the deterioration of the glomerular filtration rate [22, 23].
The glomerular effects consisted of a proliferative enlargement of glomerular capillaries, followed by mesangial proliferation.
Disruption of glomerular function may be caused by primary glomerular pathology or secondary to systemic diseases.
A simple method for the determination of glomerular filtration rate.
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