ArticleExperimental and therapeutic medicine2016
Delayed kidney injury following coronary angiography.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 8 citations in OpenAlex.
- Prediction of post-PCI angina risk using machine learning-based magnetocardiography model.Frontiers in cardiovascular medicine · 2026Article
- Effect of contrast medium versus low-molecular-weight dextran for intracoronary optical coherence tomography in renal insufficiency.The international journal of cardiovascular imaging · 2021Article
- Low-molecular-weight dextran for optical coherence tomography may not be protective against kidney injury in patients with renal insufficiency.World journal of nephrology · 2021Article
- Antithrombin III expression predicts acute kidney injury in elderly patients with sepsis.Experimental and therapeutic medicine · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is occasionally observed that patients without contrast-induced nephropathy (CIN) develop kidney injury within 1-6 months after coronary angiography (CAG), termed delayed CIN or delayed kidney injury (DKI) following CAG. The present study aimed to investigate the associated risk factors of delayed CIN and its possible pathogenesis. Subjects with CAG or coronary stenting from January 2008 to December 2009 were studied. A retrospective survey on DKI after CAG was conducted and the risk factors were analyzed. There were 436 cases receiving CAG with complete medical records enrolled in the present cohort, in which the DKI incidence was 7.1% (31/436). Patients with DKI after CAG exhibited lower hemoglobin (121.2±17.3 vs. 133.8±18.6 g/l), estimated glomerular filtration rate (eGFR; 66.4±30.2 vs. 71.9±28.6 ml/min), higher serum creatinine (110.9±43.2 vs. 91.7±37.6 µmol/l), higher rate of heart failure (22.6 vs. 5.4%) and 300 mg aspirin therapy (29 vs. 5.7%) compared with non-DKI patients (all P<0.05). However, no differences were observed in morbidities of diabetes, hypertension, hyperlipidemia and proteinuria, or in the treatments with angiotensin converting enzyme (ACE) inhibitors/angiotensin II receptor-1 blockers (ARBs), diuretics, statins and other anti-platelets between the two groups (P>0.05). Logistic regression revealed that anemia, heart failure and 300 mg aspirin intake were risk factors of DKI (P<0.05), while the contrast level, isotonic contrast, diabetes, ACE inhibitors/ARBs, eGFR and other factors were not associated with DKI (P>0.05). Heart dysfunction and 300 mg aspirin therapy may contribute to DKI after CAG, and iodinated contrast media administration is not a risk factor.
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