Acute kidney injury (AKI) is independently associated with increased morbidity and mortality. Ischemia is the leading cause of AKI, and short of supportive measures, no currently available therapy can effectively treat or prevent ischemic AKI. This paper discusses recent developments in the understanding of ischemic AKI pathophysiology, the emerging relationship between ischemic AKI and develop...

Cytokines and chemokines induce the migration, activation, proliferation, and/or differentiation of inflammatory cells and resident cells, and participate in the pathogenesis of some autoimmune diseases. Some of these molecules are effective therapeutic targets. Anti-tumor necrosis factor (TNF)-α and anti-interleukin (IL)-6 therapies are effective in patients with rheumatoid arthritis, and have...

Objective(s): Renal ischemia-reperfusion injury (IRI) as a severe condition of acute kidney injury (AKI) is the most common clinical problem with high mortality rates of 35-60% deaths in hospital. Mesenchymal stem cells (MSC) due to unique regenerative characteristics are ideal candidates for the treatment of the ischemic injuries. This work is focused on the administration of MSC to IRI-induce...

PURPOSE OF REVIEW The early detection of acute kidney injury may allow for timely preventive or therapeutic measures. This review discusses the role of traditional and novel biomarkers in early acute kidney injury diagnosis. RECENT FINDINGS Detection of acute kidney injury relies on changes in serum creatinine and urea. These are not ideal and do not reflect genuine injury or real-time change...

Acute kidney injury (AKI) is a frequent clinical problem with a high mortality rate, generally caused by ischemic insults. Nevertheless, the kidney has a remarkably high capacity to regenerate after ischemic injury. Tubular cells can restore renal function by proliferation and dedifferentiation into a mesenchymal cell type, but also stem cells residing in bone marrow may contribute. We compiled...

Fatty acid-binding proteins (FABPs) bind unsaturated fatty acids and lipid peroxidation products during tissue injury from hypoxia. We evaluated the potential role of L-type FABP (L-FABP) as a biomarker of renal ischemia in both human kidney transplant patients and animal models. Urinary L-FABP levels were measured in the first urine produced from 12 living-related kidney transplant patients im...

Several adenosine receptor subtypes on endothelial, epithelial, mesangial, and inflammatory cells have been implicated in ischemic acute kidney injury, a life-threatening condition that frequently complicates the care of hospitalized patients. In this issue of the JCI, Grenz and coworkers provide novel insight into how preservation of postischemic renal perfusion by endothelial cell adenosine A...

The role of nitric oxide (NO) in ischemic renal injury is still controversial. NO release was measured in rat kidneys subjected to ischemia and reperfusion to determine whether (6R)-5,6,7,8-tetrahydro-L-biopterin (BH4), a cofactor of NO synthase (NOS), reduces ischemic injury. Twenty-four hours after bilateral renal arterial clamp for 45 min, acetylcholine-induced vasorelaxation and NO release ...

the anti-apoptotic gene bcl-2 is located in mitochondria, but it is uncertain whether its expression affects hepatocyte survival in ischemia/reperfusion (i/r) injury. this experiment was designed to evaluate the role of folic acid in expression of bcl-2 in i/r in rat liver. eighteen wister rats were divided into sham-operated controlgroup (c) (n=6), i/r group (n=6), folic acid treated group whi...

Inducible heat shock proteins (HSPs), regulated by heat shock factor-1 (HSF-1), protect against renal cell injury in vitro. To determine whether HSPs ameliorate ischemic renal injury in vivo, HSF-1 functional knockout mice (HSF-KO) were compared with wild-type mice following bilateral ischemic renal injury. Following injury, the kidneys of wild-type mice had the expected induction of HSP70 and ...