Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality

Hu, Jiayue; Wang, Yimei; Geng, Xiwen; Chen, Rongyi; Xu, Xialian; Zhang, Xiaoyan; Lin, Jing; Teng, Jie; Ding, Xiaoqiang

doi:10.3892/etm.2017.4292

Cited by 45 publications

(40 citation statements)

References 17 publications

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“…In addition, Hu et al . noted that metabolic acidosis was an independent risk factor for development of AKI and hospital mortality in patients admitted for non‐respiratory causes . Taken together, the kidney function of preterm infants, such as those in the present study, would be more prone to insults by fluctuations in renal perfusion, if previously affected by metabolic acidosis.…”

Section: Discussionsupporting

confidence: 54%

Preoperative metabolic acidosis and acute kidney injury after open laparotomy in the neonatal intensive care unit

Yum

Seo

Youn

et al. 2019

Pediatrics International

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Background: This study evaluated potential risk factors associated with acute kidney injury (AKI) in infants undergoing bedside open laparotomy in the neonatal intensive care unit (NICU), and analyzed the association between postoperative AKI and outcomes. Methods: Retrospective data, including neonatal characteristics, perioperative findings (i.e. vital signs and fluid status), postoperative AKI incidence, and postoperative mortality rate of infants who underwent bedside open laparotomy in the NICU between May 2013 and May 2018 were collected and analyzed. Results: A total of 53 cases (26 in AKI group vs 27 in non-AKI group) were analyzed. On univariable analysis, transfusion, pre-and postoperative blood gas analysis and number of inotropic agents, cumulative postoperative percentage fluid overload (48 h), and preoperative hourly urine output were associated with the development of postoperative AKI. On multivariable logistic regression analysis, preoperative acidosis (pH <7.15 or base deficit >10; P = 0.002; OR, 11.067; 95%CI: 2.499-49.017) and preoperative urine output (P = 0.035; OR, 0.548; 95%CI: 0.314-0.959) were significant factors associated with postoperative AKI. Postoperative mortality rate 30 days after surgery was higher in the AKI group, but the difference was not significant. Conclusions: Preoperative metabolic acidosis and urine output are important factors potentially associated with the development of postoperative AKI in neonates undergoing bedside open laparotomy. Strategies such as alkali therapy, which protect the kidney from further injury, should be validated in future studies. A decreasing urine output may suggest deteriorating kidney function prior to surgery, potentially amplifying the risk of postoperative AKI.

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Section: Discussionsupporting

confidence: 54%

Preoperative metabolic acidosis and acute kidney injury after open laparotomy in the neonatal intensive care unit

Yum

Seo

Youn

et al. 2019

Pediatrics International

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“…30 Metabolic acidosis is an independent risk factor for the development of AKI. 31 Ketoacidosis is also shown to be associated with significant mortality and morbidity. 32 Therefore, higher b-OHB might worsen renal function in IR-injured mouse kidneys and optimal serum levels lower than approximately 3.0 mmol/l are required for tissue protection.…”

Section: The Effects Of Foxo3 Knockdown On B-ohb Mediated Anti-pyroptmentioning

confidence: 99%

β-hydroxybutyrate attenuates renal ischemia-reperfusion injury through its anti-pyroptotic effects

Tajima

Yoshifuji

Matsui

et al. 2019

Kidney International

115

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Ketone bodies including b-hydroxybutyrate (b-OHB) have been shown to protect against ischemic tissue injury when present at low concentrations. We evaluated the impact of b-OHB on renal ischemia/reperfusion injury (IRI). Mice were treated with a continuous infusion of b-OHB using an osmotic mini-pump before and after IRI. We also tested the effects of increasing endogenous serum b-OHB levels by fasting. Renal IRI was attenuated by b-OHB treatment compared to saline control, with similar results in the fasting condition. b-OHB treatment reduced the number of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells and increased expression of forkhead transcription factor O3 (FOXO3), an upstream regulator of pyroptosis. Although b-OHB treatment did not impact markers of apoptosis, it decreased the expression of caspase-1 and proinflammatory cytokines, indicating that b-OHB blocked pyroptosis. In a human proximal tubular cell line exposed to hypoxia and reoxygenation, b-OHB reduced cell death in a FOXO3-dependent fashion. Histone acetylation was decreased in kidneys exposed to IRI and in proximal tubular cells exposed to hypoxia and reoxygenation, and this effect was ameliorated by b-OHB through the inactivation of histone deacetylases. In vitro, b-OHB treatment restored histone acetylation at the FOXO3 promoter. Consistent with epigenetic molecular effects, the renoprotective effects of b-OHB were still observed when the continuous infusion was stopped at the time of IRI. Thus, b-OHB attenuates renal IRI through anti-pyroptotic effects, likely mediated by an epigenetic effect on FOXO3 expression.

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“…Nonvolatile organic acids are by‐products of carbohydrate and sulfur‐containing amino acid oxidation as well as metabolism of fat and phosphorus‐containing compounds (Boron & Boulpaep, 2009). A build‐up of nonvolatile organic acids in the blood, also called metabolic acidosis, can be the result of decreased acid renal excretion of these organic acids secondary to renal injury (Hu et al., 2017;Stancu, Mircescu, Mocanu, Capusa, & Stefan, 2018). Within the kidney, the proximal convoluted tubule is the primary site of acid secretion, suggesting this may be a site injured following meloxicam administration.…”

Section: Discussionmentioning

confidence: 99%

Pharmacometabolomics with a combination of PLS‐DA and random forest algorithm analyses reveal meloxicam alters feline plasma metabolite profiles

Broughton-Neiswanger

Rivera-Velez

Suarez

et al. 2020

Vet Pharm & Therapeutics

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Repeated administration of meloxicam to cats is often limited by the potential damage to multiple organ systems. Identifying molecules that predict the adverse effects of meloxicam would help to monitor and individualize its administration, maximizing meloxicam's beneficial effects. The objectives of this study were to (a) determine if the repeated administration of meloxicam to cats alters the plasma metabolome and (b) identify plasma metabolites that may serve to monitor during the administration of meloxicam in cats. Purpose bred young adult cats (n = 12) were treated with meloxicam at 0.3 mg/kg or saline subcutaneously once daily for up to 17 days. An untargeted metabolomics approach was applied to plasma samples collected prior to and at designated time points after meloxicam or saline administration. To refine the discovery of biomarkers, the machine‐learning algorithms, partial least squares discriminant analysis (PLS‐DA) and random forest (RF), were trained and validated using a separate unrelated group of meloxicam‐ and saline‐treated cats (n = 8). A total of 74 metabolites were included in the statistical analysis. Metabolomic analysis shows that the repeated administration of meloxicam alters multiple substances in plasma, including nonvolatile organic acids, aromatic amino acids, monosaccharides, and inorganic compounds as early as four days following administration of meloxicam. Seventeen plasma molecules were able to distinguish meloxicam‐treated from saline‐treated cats. The metabolomic changes discovered in this study may help to unveil unknown mechanisms of NSAID‐induced side effects. In addition, some metabolites could be valuable for individualizing the administration of meloxicam to cats to mitigate adverse effects.

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Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality

Cited by 45 publications

References 17 publications

Preoperative metabolic acidosis and acute kidney injury after open laparotomy in the neonatal intensive care unit

Preoperative metabolic acidosis and acute kidney injury after open laparotomy in the neonatal intensive care unit

β-hydroxybutyrate attenuates renal ischemia-reperfusion injury through its anti-pyroptotic effects

Pharmacometabolomics with a combination of PLS‐DA and random forest algorithm analyses reveal meloxicam alters feline plasma metabolite profiles

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