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Acute coronary syndrome and acute kidney injury: role of inflammation in worsening renal function.

ABSTRACT: Acute Kidney Injury (AKI), a common complication of acute coronary syndromes (ACS), is associated with higher mortality and longer hospital stays. The role of cytokines and other mediators is unknown in AKI induced by an ACS (ACS-AKI), leading to several unanswered questions. The worsening of renal function is usually seen as a dichotomous phenomenon instead of a dynamic change, so evaluating changes of the renal function in time may provide valuable information in the ACS-AKI setting. The aim of this study was to explore inflammatory factors associated to de novo kidney injury induced by de novo cardiac injury secondary to ACS.One hundred four consecutive patients with ACS were initially included on the time of admission to the Coronary Unit of the Instituto Nacional de Cardiología in Mexico City, from February to May 2016, before any invasive procedure, imaging study, diuretic or anti-platelet therapy. White blood count, hemoglobin, NT-ProBNP, troponin I, C-reactive protein, albumin, glucose, Na+, K+, blood urea nitrogen (BUN), total cholesterol, HDL, LDL, triglycerides, creatinine (Cr), endothelin-1 (ET-1), leukotriene-B4, matrix metalloproteinase-2 and -9, tissue inhibitor of metalloproteinases-1, resolvin-D1 (RvD1), lipoxin-A4 (LXA4), interleukin-1?, -6, -8, and -10 were measured. We finally enrolled 78 patients, and subsequently we identified 15 patients with ACS-AKI. Correlations were obtained by a Spearman rank test. Low-rank regression, splines regressions, and also protein-protein/chemical interactions and pathways analyses networks were performed.Positive correlations of ?Cr were found with BUN, admission Cr, GRACE score, IL-1?, IL-6, NT-ProBNP and age, and negative correlations with systolic blood pressure, mean-BP, diastolic-BP and LxA4. In the regression analyses IL-10 and RvD1 had positive non-linear associations with ?Cr. ET-1 had also a positive association. Significant non-linear associations were seen with NT-proBNP, admission Cr, BUN, Na+, K+, WBC, age, body mass index, GRACE, SBP, mean-BP and Hb.Inflammation and its components play an important role in the worsening of renal function in ACS. IL-10, ET-1, IL-1?, TnI, RvD1 and LxA4 represent mediators that might be associated with ACS-AKI. IL-6, ET-1, NT-ProBNP might represent crossroads for several physiopathological pathways involved in "de novo cardiac injury leading to de novo kidney injury".

SUBMITTER: Ortega-Hernandez J

PROVIDER: S-EPMC5530514 | biostudies-other | 2017 Jul

REPOSITORIES: biostudies-other

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Acute coronary syndrome and acute kidney injury: role of inflammation in worsening renal function.

Ortega-Hernández Jorge J Springall Rashidi R Sánchez-Muñoz Fausto F Arana-Martinez Julio-C JC González-Pacheco Héctor H Bojalil Rafael R

BMC cardiovascular disorders 20170726 1

<h4>Background</h4>Acute Kidney Injury (AKI), a common complication of acute coronary syndromes (ACS), is associated with higher mortality and longer hospital stays. The role of cytokines and other mediators is unknown in AKI induced by an ACS (ACS-AKI), leading to several unanswered questions. The worsening of renal function is usually seen as a dichotomous phenomenon instead of a dynamic change, so evaluating changes of the renal function in time may provide valuable information in the ACS-AKI ...[more]

PMID: 28747177

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Project description:IntroductionHigh residual platelet reactivity (RPR) in patients after percutaneous coronary intervention (PCI) receiving antiplatelet agents has been associated with a high risk of developing acute kidney injury (AKI).Study aimThis study aimed at identification of independent prognostic predictors of AKI risk in patients with acute coronary syndrome (ACS) after PCI.Study design, setting and patientsThis was a prospective single-center clinical trial that included 155 patients (n = 119 without AKI, n = 36 with AKI, mean age 64.0±10.6 years, of whom 74.2% were males), who underwent PCI with stenting. We prospectively evaluated RPR using optical aggregometry. Development of AKI was the primary endpoint.ResultsAcute renal dysfunction was observed in 36 patients (23.2%) after PCI, the risk factors of which according to univariate regression analysis were: age (p = 0.040), low diastolic blood pressure (DBP) (p = 0.001), having severe heart failure (HF) according to Killip (p<0.001), low level of hemoglobin (p = 0.026) and erythrocytes (p = 0.005), increased creatinine (p<0.001), low baseline glomerular filtration rate (GFR) (p<0.001), low left ventricular ejection fraction (LV EF) (p = 0.003), high residual platelet reactivity (RPR) (p<0.001) and platelet aggregation area under the curve (AUC) with 10 μg/mL ADP (p<0.001), as well as dose of X-ray contrast medium (XCM) (p = 0.008). As a result of multivariate regression analysis the following independent predictors of AKI were established with the inclusion of the above factors: baseline creatinine level [OR 1.033 at 95% CI from 1.017 to 1.049; p<0.001], RPR with 10 μg/mL ADP [OR 1.060 at 95% CI from 1.027 to 1.094; p = 0.001], dose of an XCM [ОR 1.005 at 95% CI from 1.001 to 1.008; р = 0.014], diastolic blood pressure (DBP) [OR 0.926 at 95% CI from 0.888 to 0.965; p<0.001].ConclusionADP-induced high residual platelet reactivity, baseline creatinine level, X-ray contrast medium, low diastolic blood pressure were independent predictors of AKI in patients with ACS after PCI.

Project description:Background: Rhabdomyolysis (RM) is a clinical syndrome characterized by breakdown of skeletal muscle fibers and release of their contents into the circulation. Myoglobin-induced acute kidney injury (AKI) is one of the most severe complications of RM. Based on our previous research, exogenous biological renal support alleviates renal ischemia-reperfusion injury in elderly mice. This study aimed to determine whether exogenous biological renal support promotes renal recovery from RM-induced AKI and to preliminarily explore the mechanisms involved. Methods: A parabiosis animal model was established to investigate the effects of exogenous biological renal support on RM-induced AKI. Mice were divided into three groups: the control group (in which mice were injected with sterile saline), the RM group (in which mice were injected with 8 mL/kg glycerol), and the parabiosis + RM group (in which recipient mice were injected with glycerol 3 weeks after parabiosis model establishment). Blood samples and kidney tissue were collected for further processing 48 h after RM induction. Bioinformatics analysis was conducted via Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes pathway analysis, functional enrichment analysis, and clustering analysis. Results: No mice died within 48 h after the procedure. Exogenous biological renal support attenuated the histological and functional deterioration in mice with RM-induced AKI. Bioinformatics analysis identified key pathways and proteins involved in this process. We further demonstrated that exogenous biological renal support ameliorated AKI through multiple mechanisms, including by suppressing the complement system; attenuating oxidative stress, inflammation, and cell death; and increasing proliferation. Conclusions: Exogenous biological renal support provided by parabiosis can improve renal function in RM-induced AKI by suppressing the complement system; decreasing oxidative stress, inflammation, and cell death; and promoting tubular cell proliferation. Our study provides basic research evidence for the use of bioartificial kidneys to treat RM-induced AKI.

Project description:BACKGROUND:We aimed to develop a nomogram based on preprocedural features for early prediction of acute kidney injury (AKI) and to assess the prognosis in patients after radical and partial nephrectomy. METHODS:The study included a development cohort of 1111 patients who were treated between June 2012 and June 2017 and an additional validation cohort of 356 patients who were treated between July 2017 and June 2018. Stepwise regression and logistic regression analyses were used to evaluate the association between predictors and AKI. Incorporating all independent predictors, a nomogram for postoperative AKI was developed and externally validated. Patients were followed up for 5 years to assess renal function, acute kidney disease (AKD), chronic kidney disease (CKD), hospital readmission and mortality were key prognosis we focused on. RESULTS:After multivariate logistic regression, radical nephrectomy (odds ratio (OR)?=?3.57, p?<?0.001), aspirin (OR?=?1.79, p?=?0.008), systolic blood pressure (OR?=?1.41, p?=?0.004), triglyceride (OR?=?1.26, p?=?0.024), and alkaline phosphatase (OR?=?1.75, p?=?0.034) were independent risk factors for postoperative AKI, while albumin (OR?=?0.72, p?=?0.031) was a protective factor for postoperative AKI. Patients with a higher estimated glomerular filtration rate (eGFR) (60-90?ml/min/1.73?m2, OR?=?0.41, p?=?0.004; ? 90?ml/min/1.73?m2, OR?=?0.37, p?<?0.001) were less prone to AKI than those with a lower eGFR (<?15?ml/min/1.73?m2). These predictors were all included in the final nomogram. The area under the receiver operating characteristics curve for the model were 0.77 (p?<?0.001) in the development cohort and 0.72 (p?<?0.001) in the validation cohort. The incidence of AKD and CKD were 27.12 and 18.64% in AKI group, which were much higher than those in no AKI group (p?<?0.001). CONCLUSIONS:The nomogram had excellent predictive ability and might have significant clinical implications for the early detection of AKI in patients undergoing nephrectomy.

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Acute coronary syndrome and acute kidney injury: role of inflammation in worsening renal function.

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Acute coronary syndrome and acute kidney injury: role of inflammation in worsening renal function.

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