Acute kidney injury: global health alert

Li, Philip Kam-Tao; Burdmann, Emmanuel A.; Mehta, Ravindra L.

doi:10.1038/ki.2012.427

Cited by 150 publications

(83 citation statements)

References 45 publications

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“…It is a global disease increasingly affecting people of all age groups and having a high mortality rate. The disease has no curative treatment available except renal transplantation which has its own limitations and complications [1, 2]. Thus development of new therapeutic strategies is warranted for the treatment of ARF.…”

Section: Introductionmentioning

confidence: 99%

Fetal Kidney Cells Can Ameliorate Ischemic Acute Renal Failure in Rats through Their Anti-Inflammatory, Anti-Apoptotic and Anti-Oxidative Effects

et al. 2015

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Fetal kidney cells may contain multiple populations of kidney stem cells and thus appear to be a suitable cellular therapy for the treatment of acute renal failure (ARF) but their biological characteristics and therapeutic potential have not been adequately explored. We have culture expanded fetal kidney cells derived from rat fetal kidneys, characterized them and evaluated their therapeutic effect in an ischemia reperfusion (IR) induced rat model of ARF. The fetal kidney cells grew in culture as adherent spindle shaped/polygonal cells and expressed CD29, CD44, CD73, CD90, CD105, CD24 and CD133 markers. Administration of PKH26 labeled fetal kidney cells in ARF rats resulted in a significant decrease in the levels of blood urea nitrogen, creatinine, and neutrophil gelatinase-associated lipocalin and decreased tubular necrosis in the kidney tissues (p<0.05 for all). The injected fetal kidney cells were observed to engraft around injured tubular cells, and there was increased proliferation and decreased apoptosis of tubular cells in the kidneys (p<0.05 for both). In addition, the kidney tissues of ARF rats treated with fetal kidney cells had a higher gene expression of renotropic growth factors (VEGF-A, IGF-1, BMP-7 and bFGF) and anti-inflammatory cytokine (IL10); up regulation of anti-oxidative markers (HO-1 and NQO-1); and a lower Bax/Bcl2 ratio as compared to saline treated rats (p<0.05 for all). Our data shows that culture expanded fetal kidney cells express mesenchymal and renal progenitor markers, and ameliorate ischemic ARF predominantly by their anti-apoptotic, anti-inflammatory and anti-oxidative effects.

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Section: Introductionmentioning

confidence: 99%

Fetal Kidney Cells Can Ameliorate Ischemic Acute Renal Failure in Rats through Their Anti-Inflammatory, Anti-Apoptotic and Anti-Oxidative Effects

et al. 2015

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“…Approximately 45% of critically ill patients and 20% of hospitalized patients develop AKI (2, 4). This results in increased hospital stays, infectious complications and increased mortality at significant cost (5-8).…”

Section: Introductionmentioning

confidence: 99%

Development of an Immunoassay for the Kidney-Specific Protein myo-Inositol Oxygenase, a Potential Biomarker of Acute Kidney Injury

Gaut¹,

Crimmins²,

Ohlendorf³

et al. 2014

Clinical Chemistry

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Background Acute kidney injury (AKI) affects 45% of critically ill patients resulting in increased morbidity and mortality. The diagnostic standard, serum creatinine (SCr), is non-specific and may not increase until days after injury. There is significant need for a renal specific AKI biomarker detectable early enough that there would be a potential window for therapeutic intervention. In this study, we sought to identify a renal specific biomarker of AKI. Methods Gene expression data was analyzed from normal mouse tissues to identify kidney specific genes, one of which was Miox. Monoclonal antibodies were generated to recombinant myo-inositol oxygenase (MIOX), and an immunoassay was developed to quantify MIOX in plasma. The immunoassay was tested in animals and retrospectively in patients with and without AKI. Results Kidney tissue specificity of MIOX was supported by Western blot. Immunohistochemistry localized MIOX to the proximal renal tubule. Plasma MIOX, undetectable at baseline, increased 24 hours following AKI in mice. Plasma MIOX was increased in critically ill patients with AKI (12.4 ± 4.3 ng/mL, n=42) compared with patients without AKI (0.5 ± 0.3 ng/mL, n=17) and was highest in patients with oliguric AKI (20.2 ± 7.5 ng/mL, n=23). Plasma MIOX increased 54.3 ± 3.8 hours before the increase in SCr. Conclusions MIOX is a renal specific, proximal tubule protein that is increased in plasma of animals and critically ill patients with AKI. MIOX preceded the elevation in SCr by approximately two days in human patients. Large-scale studies are warranted to further investigate MIOX as an AKI biomarker.

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“…1 Although estimates of AKI incidence in the general population are sparse, AKI occurs in 3.2%–9.6% of hospital admissions 2,3 and 2.1%–22.1% of prevalent intensive care unit patients 4 worldwide. Furthermore, AKI is associated with substantial morbidity, including prolonged hospital stay, end-stage renal disease (ESRD), earlier stages of chronic kidney disease (CKD), and short- and long-term mortality.…”

mentioning

confidence: 99%

A Meta-analysis of the Association of Estimated GFR, Albuminuria, Age, Race, and Sex With Acute Kidney Injury

Tonelli

Hemmelgarn²,

James³

et al. 2015

American Journal of Kidney Diseases

158

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Background Acute kidney injury (AKI) is a serious global public health problem. We aimed to quantify the risk of AKI associated with estimated glomerular filtration rate (eGFR), albuminuria (albumin-creatinine ratio [ACR]), age, sex, and race (African American and Caucasian). Study Design Collaborative meta-analysis. Setting & Population 8 general population cohorts (1,285,049 participants) and 5 chronic kidney disease (CKD) cohorts (79,519 participants). Selection Criteria for Studies Available eGFR, ACR, and ≥50 AKI events. Predictors Age, sex, race, eGFR, urine ACR, and interactions. Outcome Hospitalized with or for AKI, using Cox proportional hazards models to estimate HRs of AKI and random effects meta-analysis to pool results. Results 16,480 (1.3%) general population cohort participants had AKI over a mean follow-up of 4 years; 2,087 (2.6%) CKD participants had AKI over mean follow-up of 1 year. Lower eGFR and higher ACR were strongly associated with AKI. Compared with eGFR 80 ml/min/1.73 m2, the adjusted HR of AKI at eGFR 45 ml/min/1.73 m2 was 3.35 (95% CI, 2.75–4.07). Compared with ACR 5 mg/g, the risk of AKI at ACR 300 mg/g was 2.73 (95% CI, 2.18–3.43). Older age was associated with higher risk of AKI, but this effect was attenuated in lower eGFR or higher ACR. Male sex was associated with higher risk of AKI, with a slight attenuation in lower eGFR but not in higher ACR. African Americans had higher AKI risk at higher levels of eGFR and most levels of ACR. Limitations Only 2 general population cohorts could contribute to analyses by race; AKI identified by diagnostic code. Conclusions Reduced eGFR and increased ACR are consistent, strong risk factors for AKI whereas the associations of AKI with age, sex, and race may be weaker in more advanced stages of CKD.

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Acute kidney injury: global health alert

Cited by 150 publications

References 45 publications

Fetal Kidney Cells Can Ameliorate Ischemic Acute Renal Failure in Rats through Their Anti-Inflammatory, Anti-Apoptotic and Anti-Oxidative Effects

Fetal Kidney Cells Can Ameliorate Ischemic Acute Renal Failure in Rats through Their Anti-Inflammatory, Anti-Apoptotic and Anti-Oxidative Effects

Development of an Immunoassay for the Kidney-Specific Protein myo-Inositol Oxygenase, a Potential Biomarker of Acute Kidney Injury

A Meta-analysis of the Association of Estimated GFR, Albuminuria, Age, Race, and Sex With Acute Kidney Injury

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