Systemic Immune-Inflammation Index Predicts Contrast-Induced Acute Kidney Injury in Patients Undergoing Coronary Angiography: A Cross-Sectional Study

Frontiers in Medicine, Journal Year: 2022, Volume and Issue: 9

Published: March 16, 2022

Systemic immune-inflammation index (SII) is an emerging indicator and correlated to the incidence of cardiovascular diseases. This study aimed explore association between SII contrast-induced acute kidney injury (CI-AKI).In this retrospective cross-sectional study, 4,381 subjects undergoing coronary angiography (CAG) were included. defined as neutrophil count × platelet count/lymphocyte count. CI-AKI was determined by elevation serum creatinine (Scr). Multivariable linear logistic regression analysis used determine relationship with Scr CI-AKI, respectively. Receiver operator characteristic (ROC) analysis, structural equation model subgroup also performed.Overall, 786 (17.9%) patients suffered after intravascular contrast administration. The 67.1 ± 10.8 years wold, a mean 5.72 1011/L. showed that linearly increased proportion (β [95% confidence interval, CI] = 0.315 [0.206 0.424], P < 0.001). demonstrated higher associated ([≥12 vs. <3 1011/L]: odds ratio, OR 2.914 [2.121 4.003], Subgroup consistent results. ROC identified good predictive value on (area under curve CI]: 0.625 [0.602 0.647]). verified more remarkable direct effect 0.102, 0.001) compared C-reactive protein 0.070, 0.001).SII independent predictor for in CAG procedures.

Language: Английский

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Comparison of acute kidney injury of different etiology reveals in-common mechanisms of tissue damage

Physiological Genomics, Journal Year: 2018, Volume and Issue: 50(3), P. 127 - 141

Published: Jan. 8, 2018

Acute kidney injury (AKI) is a syndrome of reduced glomerular filtration rate and urine production caused by number different diseases. It associated with renal tissue damage. This damage can cause tubular atrophy interstitial fibrosis that leads to nephron loss progression chronic disease (CKD). review describes the in-common mechanisms behind in AKI underlying Comparing six high-quality microarray studies gene expression after models (gram-negative sepsis, gram-positive ischemia-reperfusion, malignant hypertension, rhabdomyolysis, cisplatin toxicity) identified 5,254 differentially expressed genes at least one models; 66% were found only model, showing there are unique features depending on disease. There form four all models, 49 five, 215 common between models. Gene ontology enrichment analysis could be broadly categorized into injurious processes hypoxia, oxidative stress, inflammation, as well cellular outcomes cell death remodeling epithelial-to-mesenchymal transition. Pathway showed MYC central connection network activated AKI, which suggests it may regulator during AKI. The outlining this molecular useful for understanding from CKD.

Language: Английский

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Pathophysiology of Contrast-Induced Acute Kidney Injury (CIAKI)

Current Pharmaceutical Design, Journal Year: 2019, Volume and Issue: 25(44), P. 4642 - 4647

Published: Dec. 11, 2019

Contrast-induced acute kidney injury (CIAKI) is a severe complication associated with the use of iodinated contrast media (CM); sudden but potentially reversible fall in glomerular filtration rate (GFR) typically occurring 48-72 hours after CM administration. Principal risk factors related presentation CIAKI are preexisting chronic disease and diabetes mellitus. Studies on present considerable complexity because differences type dose, controversies definition baseline comorbidities. Despite that, it should be noted that poses serious health problem very common cause hospitalacquired AKI, linked to increased morbidity mortality utilizing growing healthcare resources. The pathogenesis heterogeneous and, thus, incompletely understood. Three basic mechanisms appear simultaneously occur for development: Renal vasoconstriction medullary hypoxia, tubular cell toxicity reactive oxygen species formation. relative contribution each one these unknown they ultimately lead epithelial endothelial apoptosis GFR reduction. Further research needed order better clarify pathophysiology accordingly introduce effective preventive therapeutic strategies.

Language: Английский

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Reactive oxygen species in renal vascular function

Acta Physiologica, Journal Year: 2020, Volume and Issue: 229(4)

Published: April 20, 2020

Abstract Reactive oxygen species (ROS) are produced by the aerobic metabolism. The imbalance between production of ROS and antioxidant defence in any cell compartment is associated with damage may play an important role pathogenesis renal disease. NADPH oxidase (NOX) family major source vasculature modulates perfusion. Upregulation Ang II adenosine activates NOX via AT1R A1R microvessels, leading to superoxide production. Oxidative stress kidney prompts vascular remodelling increases preglomerular resistance. These key elements hypertension, acute chronic injury, as well diabetic nephropathy. Renal afferent arterioles (Af), primary resistance vessel kidney, fine tune hemodynamics impact on blood pressure. Vice versa, increase hypertension diabetes, resulting upregulation Af vasoconstriction, enhancement myogenic responses change tubuloglomerular feedback (TGF), which further promotes In following, we highlight oxidative function dysfunction hemodynamics. microcirculatory alterations brought about importantly contribute pathophysiology diabetes.

Language: Английский

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The Pathophysiology and the Management of Radiocontrast-Induced Nephropathy

Diagnostics, Journal Year: 2022, Volume and Issue: 12(1), P. 180 - 180

Published: Jan. 12, 2022

Contrast-induced nephropathy (CIN) is an impairment of renal function that occurs after the administration iodinated contrast medium (CM). Kidney dysfunction in CIN considered transient and reversible most cases. However, it third common cause hospital-acquired acute kidney injury associated with increased morbidity mortality, especially high-risk patients. Diagnostic interventional procedures require intravascular CM are being used increasing frequency, among elderly, who can be particularly susceptible to due multiple comorbidities. Therefore, identifying exact mechanisms its risk factors crucial not only provide optimal preventive management for at-risk patients, but also increase feasibility diagnostic procedure use CM. induces by impairing hemodynamics generation reactive oxygen species, addition direct cytotoxicity. Periprocedural hydration widely accepted strategy date. Here, we review latest research results on pathophysiology CIN.

Language: Английский

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