Cellular adaptive changes in AKI: mitigating renal hypoxic injury

Heyman, Samuel N.; Evans, Roger G.; Rosen, Seymour; Rosenberger, Christian

doi:10.1093/ndt/gfs100

Cited by 55 publications

(50 citation statements)

References 56 publications

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“…Zorov et al (161) believe that it is the immune system involved in mitochondrial signaling, and not kidney failure itself, that leads to an organism's senescence and death. Recent reviews have highlighted the critical role of sublethal hypoxic tubular cell injury and microcirculation disturbance in the pathogenesis of AKI (2,57).…”

Section: Acquired Mitochondrial Dysfunction In Kidney Diseasementioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial dysfunction in the pathophysiology of renal diseases

Che

Yuan

Huang

et al. 2014

American Journal of Physiology-Renal Physiology

329

272

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Mitochondrial dysfunction has gained recognition as a contributing factor in many diseases. The kidney is a kind of organ with high energy demand, rich in mitochondria. As such, mitochondrial dysfunction in the kidney plays a critical role in the pathogenesis of kidney diseases. Despite the recognized importance mitochondria play in the pathogenesis of the diseases, there is limited understanding of various aspects of mitochondrial biology. This review examines the physiology and pathophysiology of mitochondria. It begins by discussing mitochondrial structure, mitochondrial DNA, mitochondrial reactive oxygen species production, mitochondrial dynamics, and mitophagy, before turning to inherited mitochondrial cytopathies in kidneys (inherited or sporadic mitochondrial DNA or nuclear DNA mutations in genes that affect mitochondrial function). Glomerular diseases, tubular defects, and other renal diseases are then discussed. Next, acquired mitochondrial dysfunction in kidney diseases is discussed, emphasizing the role of mitochondrial dysfunction in the pathogenesis of chronic kidney disease and acute kidney injury, as their prevalence is increasing. Finally, it summarizes the possible beneficial effects of mitochondrial-targeted therapeutic agents for treatment of mitochondrial dysfunction-mediated kidney injury-genetic therapies, antioxidants, thiazolidinediones, sirtuins, and resveratrol-as mitochondrial-based drugs may offer potential treatments for renal diseases.

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Section: Acquired Mitochondrial Dysfunction In Kidney Diseasementioning

confidence: 99%

“…This represents a renoprotective mechanism that decreases oxygen expenditure and maintains the medullary blood flow (57). Therefore, tubular cells undergo a sublethal state, with characteristics of brush border loss, mitochondrial swelling, and nuclear pyknosis (14).…”

Section: Acquired Mitochondrial Dysfunction In Kidney Diseasementioning

confidence: 99%

Mitochondrial dysfunction in the pathophysiology of renal diseases

Che

Yuan

Huang

et al. 2014

American Journal of Physiology-Renal Physiology

329

272

View full text Add to dashboard Cite

show abstract

“…Furthermore, the relationship bet-but also reinforce these effect by feed-forward loop [21,22]. Enhanced reparative processes, such as poly ADP-ribose polymerase-mediated DNA repair or autophagy, may intensify oxygen consumption [8].…”

Section: Discussionmentioning

confidence: 96%

“…Multiple regulators such as nitric oxide (NO) and prostaglandins have been recognized as main regulators of renal regional perfusion and tubular transport activity [8]. Serum levels of these regulators will be changed in lupus nephritis patients, which were proven by previous investigations [9,10].…”

Section: Introductionmentioning

confidence: 98%

Detection of Renal Hypoxia in Lupus Nephritis Using Blood Oxygen Level-Dependent MR Imaging: A Multiple Correspondence Analysis

Shi¹,

Yan

Liu

et al. 2017

Kidney Blood Press Res

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Background/Aims: Nephrologists have pursued ideal, dynamic and noninvasive methods for assessing renal function and disease progression. Blood oxygen level dependent (BOLD) imaging is a useful technique for assessing renal disease. This current study was performed to explore the correlation between the hypoxia iconographical index and renal pathological features in lupus nephritis. Methods: Adult patients with lupus nephritis (LN) and healthy volunteers were recruited for this study. Renal biopsy tissues were characterized based on the LNISN/RPS 2003 classification. R2* values of functional magnetic resonance parameters were acquired using the BOLD technique. The data characteristics of R2* values of different pathological patterns were calculated. Multiple correspondence analysis (MCA) was performed to explore the correlation between R2* values and clinical or pathological features. Results: A total of twenty-three patients and eighteen healthy volunteers were examined with BOLD MRI. Renal pathological patterns included five class III (including 3 class III+V), eight class IV (including 4 class IV+V) and five class IV. The mean renal R2* values in LN patients were higher than those in healthy volunteers. R2* values in class V patients were higher than those in class IV and class III. The MCA showed that higher R2* values were associated with pathological features in class V patients. Conclusions: The extent of renal hypoxia in patients with LN was more serious compared with the healthy volunteers. Differentiated mechanisms of renal oxygenation are possibly involved in proliferative and non-proliferative LN patients. R2* values may be linked with multiple clinical and pathological indexes.

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“…Tissue hypoxia in the kidney during sepsis may be defined by inflammation, changes in intrarenal nitric oxide, nitrosative stress or oxygen radical homeostasis, and dysregulation. Downregulation of mediators of oxidative phosphorylation occurs during sepsis and protection of mitochondrial respiration may mitigate renal injury during sepsis [14,17,18].…”

Section: Sepsis-associated Atnmentioning

confidence: 99%

Acute Kidney Injury in the Intensive Care Unit

Zaragoza¹,

Renteria²

2017

Intensive Care

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Acute kidney injury (AKI) is defined as an abrupt decrease in glomerular filtration rate (GFR). Incidence varies from 20% to as high as 70% in critically ill patients. Classically, AKI has been divided into three broad pathophysiologic categories: prerenal AKI, intrinsic AKI, and postrenal (obstructive) AKI. The clinical manifestations of AKI vary among a wide range of symptoms and metabolic abnormalities. A sudden decrease in GFR will result in rising concentrations of solutes in the blood, which are normally excreted by the kidneys. Recently, new urinary and serum biomarkers have gained a place in the diagnosis, classification, and prognosis prediction of AKI. The best treatment for AKI is prevention. Patients with prerenal azotemia should have intravascular volume deficits corrected and cardiac function optimized. Obstructive (postrenal) kidney disease is treated by mechanical relief of the block. The primary management of acute interstitial nephritis is discontinuation of the inciting agent. Renal replacement therapy (RRT) has emerged as a supportive mechanism rather than just as a lifesaving measure. Continuous techniques are preferable in treating critically ill patients, although every modality has its benefits, indications, and contraindications.

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Cellular adaptive changes in AKI: mitigating renal hypoxic injury

Cited by 55 publications

References 56 publications

Mitochondrial dysfunction in the pathophysiology of renal diseases

Mitochondrial dysfunction in the pathophysiology of renal diseases

Detection of Renal Hypoxia in Lupus Nephritis Using Blood Oxygen Level-Dependent MR Imaging: A Multiple Correspondence Analysis

Acute Kidney Injury in the Intensive Care Unit

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