Renal ischaemia/reperfusion injury: possible role of aquaporins

Hussein, Abdelaziz M.; El-Dken, Z. H.; Barakat, Nashwa; Abol‐Enein, Hassan

doi:10.1111/j.1748-1716.2011.02372.x

Cited by 31 publications

(20 citation statements)

References 53 publications

(57 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…We found that VDD-induced urinary concentrating defect. Ischemia/reperfusion is associated with a marked reduction in the renal protein expression of AQP1, AQP2, and AQP3 (Hussein et al 2012). However, the mechanism by which vitamin D downregulates AQP2 (Figs.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D deficiency aggravates ischemic acute kidney injury in rats

et al. 2015

View full text Add to dashboard Cite

Vitamin D deficiency (VDD) increases the risk of death in hospitalized patients. Renal ischemia/reperfusion injury (IRI) induces acute kidney injury (AKI), which activates cell cycle inhibitors, including p21, a cyclin-dependent kinase inhibitor and genomic target of 25-hydroxyvitamin D, which is in turn a potent immunomodulator with antiproliferative effects. In this study, we assess the impact of VDD in renal IRI. Wistar rats were divided into groups, each evaluated for 30 days: control (receiving a standard diet); VDD (receiving a vitamin D-free diet); IRI (receiving a standard diet and subjected to 45-min bilateral renal ischemia on day 28); and VDD + IRI (receiving a vitamin D-free diet and subjected to 45-min bilateral renal ischemia on day 28). At 48 h after IRI, animals were euthanized; blood, urine, and kidney tissue samples were collected. Compared with IRI rats, VDD + IRI rats showed a more severe decrease in glomerular filtration rate, greater urinary protein excretion, a higher kidney/body weight ratio and lower renal aquaporin 2 expression, as well as greater morphological damage, characterized by increased interstitial area and tubular necrosis. Our results suggest that the severity of tubular damage in IRI may be associated with downregulation of vitamin D receptors and p21. VDD increases renal inflammation, cell proliferation and cell injury in ischemic AKI.

show abstract

Section: Discussionmentioning

confidence: 99%

Vitamin D deficiency aggravates ischemic acute kidney injury in rats

et al. 2015

View full text Add to dashboard Cite

show abstract

“…The molecular mechanisms underlying IR-induced AKI are not fully understood, but it has been suggested that the mechanisms are most likely multifactorial and interdependent, including endothelial and epithelial cell death, intratubular obstruction, changes in local microvascular blood flow, as well as immunological and inflammatory processes [28], [48], [49]. It is not excluded that LMWF may prevent kidney injury and promote kidney repair after IR by other mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Low Molecular Weight Fucoidan against Renal Ischemia–Reperfusion Injury via Inhibition of the MAPK Signaling Pathway

et al. 2013

View full text Add to dashboard Cite

BackgroundIschemia reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI) in both native and transplanted kidneys. The objective of the present study was to evaluate whether low-molecular-weight fucoidan (LMWF) could attenuate renal IRI in an animal model and in vitro cell models and study the mechanisms in which LMWF protected from IRI.Methodology/Principal FindingsMale mice were subjected to right renal ischemia for 30 min and reperfusion for 24 h, or to a sham operation with left kidney removed. Kidneys undergone IR showed characteristic morphological changes, such as tubular dilatation, and brush border loss. However, LMWF significantly corrected the renal dysfunction and the abnormal levels of MPO, MDA and SOD induced by IR. LMWF also inhibited the activation of MAPK pathways, which consequently resulted in a significant decrease in the release of cytochrome c from mitochondria, ratios of Bax/Bcl-2 and cleaved caspase-3/caspase-3, and phosphorylation of p53. LMWF alleviated hypoxia-reoxygenation or CoCl2 induced cell viability loss and ΔΨm dissipation in HK2 renal tubular epithelial cells, which indicates LMWF may result in an inhibition of the apoptosis pathway through reducing activity of MAPK pathways in a dose-dependent manner.Conclusions/SignificanceOur in vivo and in vitro studies show that LMWF ameliorates acute renal IRI via inhibiting MAPK signaling pathways. The data provide evidence that LMWF may serve as a potential therapeutic agent for acute renal IRI.

show abstract

“…Renal I/R injury results in down-regulation of aquaporins and sodium transporters [29], [33]. Aquaporins and sodium transporters are important for the renal reabsorptive capacity of water and sodium.…”

Section: Discussionmentioning

confidence: 99%

α-Melanocyte Stimulating Hormone Treatment in Pigs Does Not Improve Early Graft Function in Kidney Transplants from Brain Dead Donors

et al. 2014

View full text Add to dashboard Cite

Delayed graft function and primary non-function are serious complications following transplantation of kidneys derived from deceased brain dead (DBD) donors. α-melanocyte stimulating hormone (α-MSH) is a pleiotropic neuropeptide and its renoprotective effects have been demonstrated in models of acute kidney injury. We hypothesized that α-MSH treatment of the recipient improves early graft function and reduces inflammation following DBD kidney transplantation. Eight Danish landrace pigs served as DBD donors. After four hours of brain death both kidneys were removed and stored for 18 hours at 4°C in Custodiol preservation solution. Sixteen recipients were randomized in a paired design into two treatment groups, transplanted simultaneously. α-MSH or a vehicle was administered at start of surgery, during reperfusion and two hours post-reperfusion. The recipients were observed for ten hours following reperfusion. Blood, urine and kidney tissue samples were collected during and at the end of follow-up. α-MSH treatment reduced urine flow and impaired recovery of glomerular filtration rate (GFR) compared to controls. After each dose of α-MSH, a trend towards reduced mean arterial blood pressure and increased heart rate was observed. α-MSH did not affect expression of inflammatory markers. Surprisingly, α-MSH impaired recovery of renal function in the first ten hours following DBD kidney transplantation possibly due to hemodynamic changes. Thus, in a porcine experimental model α-MSH did not reduce renal inflammation and did not improve short-term graft function following DBD kidney transplantation.

show abstract

Renal ischaemia/reperfusion injury: possible role of aquaporins

Cited by 31 publications

References 53 publications

Vitamin D deficiency aggravates ischemic acute kidney injury in rats

Vitamin D deficiency aggravates ischemic acute kidney injury in rats

Low Molecular Weight Fucoidan against Renal Ischemia–Reperfusion Injury via Inhibition of the MAPK Signaling Pathway

α-Melanocyte Stimulating Hormone Treatment in Pigs Does Not Improve Early Graft Function in Kidney Transplants from Brain Dead Donors

Contact Info

Product

Resources

About