Prognostic Value of Early Acute Kidney Injury After Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction

Kim, Jae Hee; Lee, Jang Hoon; Jang, Se Yong; Bae, Myung Hwan; Yang, Dong Heon; Park, Hun Sik; Cho, Yongkeun; Chae, Shung Chull

doi:10.1016/j.amjcard.2014.07.039

Cited by 9 publications

(6 citation statements)

References 32 publications

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“…Even though the concepts of early AKI or late AKI have been mentioned previously in acute myocardial infarction (AMI) (20,21), burn (22) and ICU (23,24) patients, definitions and time boundaries vary among them. Moriyama et al included 760 patients with AMI, and AKI was defined according to AKIN criteria.…”

Section: Discussionmentioning

confidence: 99%

“…The time boundary for early AKI and late AKI was 48h after hospital admission (20). In another AMI study of 971 patients, early AKI was defined as AKI occurred within 24h post percutaneous coronary intervention (PCI) in AKIN criteria (21). In a study of 221 burn patients, early AKI was defined as AKI occurred within 24h post hospital admission according to RIFLE criteria (22).…”

Section: Discussionmentioning

confidence: 99%

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Acute Kidney Injury in Critically Ill Patients After Noncardiac Major Surgery: Early Versus Late Onset

Wang

Priyanka

et al. 2019

Critical Care Medicine

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Objective: Acute kidney injury (AKI) is a common complication of major surgery. However, AKI occurring within the first 48h after surgery (early AKI) and therefore likely related to the surgery itself is possibly different from AKI occurring after 48h (late AKI). The aim of this study was to describe the epidemiology and identify differences in risk factors and outcomes between early and late AKI following major surgery. Design: Retrospective cohort study. Setting: Academic Medical Center. Patients: Patients admitted to ICU following non-cardiac major surgery. Interventions: None. Measurements and Main Results: We analyzed data from 3499 patients and defined AKI according to full KDIGO criteria and classified as early (48h or less) or late (>48h to 7 days) based on time from surgery. Separate multivariable logistic regression models were fit to identify risk factors of early AKI compared with no AKI and risk factors of late AKI compared with no AKI. Overall 41.7% (1459/3499) developed early AKI vs 14.4% (504/3499) late AKI. Most AKI occurred within 48h following surgery and 12h was the peak interval. Risk factors for early AKI included increased age, BMI, decreased eGFR and anemia, while late AKI cases were closely associated with postoperative factors, like sepsis, mechanical ventilation, positive fluid balance, blood transfusions and exposure to diuretics, vasopressors, and nonsteroidal anti-inflammatory drugs. After adjusting for age, BMI, eGFR, comorbidities, surgery type, both early AKI

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Acute Kidney Injury in Critically Ill Patients After Noncardiac Major Surgery: Early Versus Late Onset

Wang

Priyanka

et al. 2019

Critical Care Medicine

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“…Type 1 cardiorenal syndrome, as proposed by Ronco et al (51), is characterized by acute kidney injury (AKI) due to rapid worsening of cardiac function. Indeed, AKI often develops in patients with acute myocardial infarction (MI), and the incidence ranges from 10% to 20% (20,22,34,48). Importantly, AKI is strongly associated with short-term (20) and long-term (22,34,48) mortality in patients with MI, and even "subclinical" AKI has been shown to have a significant impact on clinical outcomes (23,47).…”

Section: Introductionmentioning

confidence: 99%

Diabetes increases the susceptibility to acute kidney injury after myocardial infarction through augmented activation of renal Toll-like receptors in rats

Ohno

Kuno

Murase

et al. 2017

American Journal of Physiology-Heart and Circulatory Physiology

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Acute kidney injury (AKI) after acute myocardial infarction (MI) worsens the prognosis of MI patients. Although type 2 diabetes mellitus (DM) is a major risk factor of AKI after MI, the underlying mechanism remains unclear. Here, we examined the roles of renal Toll-like receptors (TLRs) in the impact of DM on AKI after MI. MI was induced by coronary artery ligation in Otsuka-Long-Evans-Tokushima fatty (OLETF) rats, a rat DM model, and Long-Evans-Tokushima-Otsuka (LETO) rats, nondiabetic controls. Sham-operated rats served as no-MI controls. Renal mRNA levels of TLR2 and myeloid differentiation factor 88 (MyD88) were significantly higher in sham-operated OLETF rats than in sham-operated LETO rats, although levels of TLR1, TLR3, and TLR4 were similar. At 12 h after MI, protein levels of kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) in the kidney were elevated by 5.3- and 4.0-fold, respectively, and their mRNA levels were increased in OLETF but not LETO rats. The increased KIM-1 and NGAL expression levels after MI in the OLETF kidney were associated with upregulated expression of TLR1, TLR2, TLR4, MyD88, IL-6, TNF-α, chemokine (C-C motif) ligand 2, and transforming growth factor-β and also with activation of p38 MAPK, JNK, and NF-κB. Cu-CPT22, a TLR1/TLR2 antagonist, administered before MI significantly suppressed MI-induced upregulation of KIM-1, TLR2, TLR4, MyD88, and chemokine (C-C motif) ligand 2 levels and activation of NF-κB, whereas NGAL levels and IL-6 and TNF-α expression levels were unchanged. The results suggest that DM increases the susceptibility to AKI after acute MI by augmented activation of renal TLRs and that TLR1/TLR2-mediated signaling mediates KIM-1 upregulation after MI. This is the first report to demonstrate the involvement of Toll-like recpetors (TLRs) in diabetes-induced susceptibility to acute kidney injury after acute myocardial infarction. We propose that the TLR1/TLR2 heterodimer may be a new therapeutic target for the prevention of acute kidney injury in diabetic patients.

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“…In addition, non‐hemodynamic mechanisms, such as increased oxidative stress and chronic inflammation, contribute to type 1 CRS. Diabetes mellitus is an independent risk factor for the development of AKI in patients with MI, and we recently reported that augmented activation of Toll‐like receptors (TLRs), germline‐encoded innate immune receptors, plays roles in the susceptibility to AKI after MI in diabetic rats. However, how pharmacological treatment of hyperglycemia modifies the diabetes mellitus‐induced increase in renal susceptibility to AKI remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Canagliflozin, a sodium–glucose cotransporter 2 inhibitor, normalizes renal susceptibility to type 1 cardiorenal syndrome through reduction of renal oxidative stress in diabetic rats

Kimura

Kuno

Tanno

et al. 2019

J of Diabetes Invest

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Aims/Introduction Type 2 diabetes mellitus is a risk factor of acute kidney injury after myocardial infarction (MI), a form of cardiorenal syndrome. Recent clinical trials have shown that a sodium–glucose cotransporter 2 (SGLT2) inhibitor improved both cardiac and renal outcomes in patients with type 2 diabetes mellitus, but effects of an SGLT2 inhibitor on cardiorenal syndrome remain unclear. Materials and Methods Type 2 diabetes mellitus (Otsuka Long‐Evans Tokushima Fatty rats [OLETF]) and control (Long‐Evans Tokushima Otsuka rats [LETO]) were treated with canagliflozin, an SGLT2 inhibitor, for 2 weeks. Renal tissues were analyzed at 12 h after MI with or without preoperative fasting. Results Canagliflozin reduced blood glucose levels in OLETF, and blood β‐hydroxybutyrate levels were increased by canagliflozin only with fasting. MI increased neutrophil gelatinase‐associated lipocalin and kidney injury molecule‐1 protein levels in the kidney by 3.2‐ and 1.6‐fold, respectively, in OLETF, but not in LETO. The renal messenger ribonucleic acid level of Toll‐like receptor 4 was higher in OLETF than in LETO after MI, whereas messenger ribonucleic acid levels of cytokines/chemokines were not significantly different. Levels of lipid peroxides, nicotinamide adenine dinucleotide phosphate oxidase (NOX)2 and NOX4 proteins after MI were significantly higher in OLETF than in LETO. Canagliflozin with pre‐MI fasting suppressed MI‐induced renal expression of neutrophil gelatinase‐associated lipocalin and kidney injury molecule‐1 in OLETF, together with reductions in lipid peroxides and NOX proteins in the kidney. Blood β‐hydroxybutyrate levels before MI were inversely correlated with neutrophil gelatinase‐associated lipocalin protein levels in OLETF. Pre‐incubation with β‐hydroxybutyrate attenuated angiotensin II‐induced upregulation of NOX4 in NRK‐52E cells. Conclusions The findings suggest that SGLT2 inhibitor treatment with a fasting period protects kidneys from MI‐induced cardiorenal syndrome, possibly by β‐hydroxybutyrate‐mediated reduction of NOXs and oxidative stress, in type 2 diabetic rats.

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Prognostic Value of Early Acute Kidney Injury After Primary Percutaneous Coronary Intervention in Patients With ST-Segment Elevation Myocardial Infarction

Cited by 9 publications

References 32 publications

Acute Kidney Injury in Critically Ill Patients After Noncardiac Major Surgery: Early Versus Late Onset

Acute Kidney Injury in Critically Ill Patients After Noncardiac Major Surgery: Early Versus Late Onset

Diabetes increases the susceptibility to acute kidney injury after myocardial infarction through augmented activation of renal Toll-like receptors in rats

Canagliflozin, a sodium–glucose cotransporter 2 inhibitor, normalizes renal susceptibility to type 1 cardiorenal syndrome through reduction of renal oxidative stress in diabetic rats

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