Cellular Response to Renal Hypoxia Is Different in Adolescent and Infant Rats

Adachi, Shinsuke; Zelenin, Sergey; Matsuo, Yasutaka; Holtbäck, Ulla

doi:10.1203/01.pdr.0000106805.54926.2c

Cited by 15 publications

(6 citation statements)

References 28 publications

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“…We can assume that this pathological mechanism is universal and well proven for the kidney of adult animals, but similar phenomena have been described for the kidney damage in rat pups, for example, under hyperoxic kidney damage, leading to fibrosis and intrauterine asphyxia causing AKI . However, when comparing the effect of hypoxia on the kidney of adult and newborn rats the latter demonstrated reversible cell damage, whereas in adult rats the epithelium of the renal tubules consistently lose the reabsorption function .…”

Section: Discussionsupporting

confidence: 60%

“…These pathological mechanisms of ischemia‐induced kidney injury are universal, however, they may be different when comparing the effect of hypoxia on the kidney of adult and newborn rats. The latter were shown to undergo reversible cell damage, whereas in adult rats the epithelium of the renal tubules persistently lose the reabsorption function .…”

Section: Introductionmentioning

confidence: 99%

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The role of oxidative stress in acute renal injury of newborn rats exposed to hypoxia and endotoxin

et al. 2017

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Neonatal kidney injury is a frequent pathology, especially among premature infants. The search for effective nephroprotection requires the creation of adequate experimental models of nephropathy in newborns. In this study, we explored the development of acute kidney injury (AKI) in neonatal rats during hypoxia or administration of endotoxin. We found that 2-h hypoxia (8% O ) and the intraperitoneal injection of 4 mg·kg lipopolysaccharide (LPS) causes the appearance of AKI markers, such as kidney injury molecule-1 (КIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) in the rat urine after 24 and 72 h of exposure. On the other hand, the levels of blood urine nitrogen under the same conditions rise only slightly. The damaging effects of hypoxia and endotoxin were accompanied by histological changes in the renal tissue and a significant decrease in the proliferation marker, (proliferating cell nuclear antigen). It is revealed that 3 h after the introduction of LPS, levels of reactive oxygen species in the kidney were significantly increased, and the injection of the antioxidant N-acetylcysteine afforded protection from AKI, evaluated by urine КIM-1 and NGAL levels. Thus, the simulation of AKI in newborn rat pups can be employed in screening for potential nephroprotective drugs, particularly among antioxidative compounds to be used in neonatology.

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Section: Discussionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

The role of oxidative stress in acute renal injury of newborn rats exposed to hypoxia and endotoxin

et al. 2017

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“…In acute ischemic renal failure, loss of renal blood supply results in tissue hypoxia, leading to necrosis of renal tubular cells mediated by free radicals (35,36). Thus, urine samples collected during the first 48 h after birth revealed elevated concentrations of NAG in asphyxiated newborns.…”

Section: Discussionmentioning

confidence: 99%

Room-Air Resuscitation Causes Less Damage to Heart and Kidney than 100% Oxygen

Vento

Sastre

Asensi

et al. 2005

Am J Respir Crit Care Med

243

133

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“…Although there is no evidence that the diuresis and natriuresis of mild to moderate hypoxia arises from ion pump dysfunction due to ATP depletion, hypoxia causes a down-regulation in vivo of several membrane Na + -transporting proteins in the kidney [ 39 ]. This may be in part mediated by AMPK that decreases O 2 consumption by down-regulation and withdrawal of a number of membrane ion transporters [ 37 ] as well as by activation of the HIF pathways [ 40 ] that depress transporter gene expression.…”

Section: Tubular Functionmentioning

confidence: 99%

Renal Function and Fluid Homeostasis

Swenson

Olsen

2013

High Altitude

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Hypoxia can directly affect the kidneys, but more importantly, its effects on systemic acid-base balance, ventilation, neuroendocrine refl exes, and hemodynamics all play a far greater part in altering renal function and fl uid balance. Acute and chronic effects of hypoxia and their magnitude may differ and these will be highlighted. These changes will be related to the common diseases of high altitude and to their impact on patients with chronic renal disease. Other features of high altitude separate from hypoxia, either alone or in combination, including hypobaria, exercise, and cold may also signifi cantly perturb renal function.

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Cellular Response to Renal Hypoxia Is Different in Adolescent and Infant Rats

Cited by 15 publications

References 28 publications

The role of oxidative stress in acute renal injury of newborn rats exposed to hypoxia and endotoxin

The role of oxidative stress in acute renal injury of newborn rats exposed to hypoxia and endotoxin

Room-Air Resuscitation Causes Less Damage to Heart and Kidney than 100% Oxygen

Renal Function and Fluid Homeostasis

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