Increased expression of TGF-beta1 but not of its receptors contributes to human obstructivenephropathy.
2
We propose that M11 is likely involved in the observed obstructivenephropathy reported in clinical studies.
3
In the presence of renal failure, these levels are elevated due to the obstructivenephropathy caused by calculi.
4
Conclusion: Lin28a attenuates renal fibrosis in obstructivenephropathy, making its mechanism a possible therapeutic target for chronic kidney disease.
5
The primary mechanism of nephrolithiasis-associated AKI is obstructivenephropathy, and factors on presentation with obstructive uropathy predict the likelihood of long-term renal recovery.
6
Summary: Obstructivenephropathy and crystalline nephropathy both contribute to nephrolithiasis-associated AKI, although the latter appears to have a worse prognosis.