Topographically-patterned porous membranes in a microfluidic device as an in vitro model of renal reabsorptive barriers.
Arvaniti, E. et al. Whole-transcriptome analysis of UUO mouse model of renal fibrosis reveals new molecular players in kidney diseases.
The remnant kidney model of renal failure is associated with normal or suppressed plasma renin and angiotensin (Ang) II levels when hypertension is established.
Whereas angiotensin converting enzyme inhibitors and angiotensin type 1 receptor antagonists have beneficial effects in the remnant model of renal failure, calcium channel blockers do not consistently improve renal disease in this model.
This study was designed to further clarify the potential reno-protective effect of brain natriuretic peptide (BNP) using an established rat model of renal I/R injury.
We designed an experimental model of renal ischemia-reperfusion to evaluate the preemptive effect of intravenous sildenafil according to the dose administered (0.7 vs 1.4 mg/kg) and the time of administration (30 minutes before ischemia or during ischemia).
Treatment strategies that increase NO bioavailability, or reduce levels of reactive oxygen species, were proven beneficial in this model of renal and cardiovascular disease.
In a sheep model of renal I-R, BH4 pre-treatment can prevent microvascular injury and dysfunction.
In a recent study by our group, ANP pre-treatment prevented kidney-lung crosstalk in a rat model of renal IRI [18].
In the preclinical model of renal ischemia-reperfusion injury, functional data based on standard biochemical parameters can only be obtained in the acute phase of injury [1, 2].
The objective of the present study was to elucidate whether ANP post-treatment attenuates kidney-lung-heart crosstalk in a rat model of renal IRI.
