Pathophysiology of contrast medium–induced nephropathy

Persson, Pontus B.; Hansell, Peter; Liss, Per

doi:10.1111/j.1523-1755.2005.00377.x

Cited by 485 publications

(404 citation statements)

References 95 publications

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“…Animal models generally require that additional insults to the kidney be combined with contrast exposure to reliably induce AKI 16. Similarly, in clinical studies including elective procedures performed on stable patients, the development of CI‐AKI largely depends on coexisting risk factors such as intravascular volume depletion, baseline renal dysfunction, heart failure, and diabetes mellitus 9…”

Section: Discussionmentioning

confidence: 99%

Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?

Caspi

Habib

Cohen

et al. 2017

JAHA

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BackgroundAcute kidney injury (AKI) following primary percutaneous coronary intervention (pPCI) is frequently interpreted as contrast‐induced AKI but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following pPCI using a control group of propensity score–matched patients with ST‐segment–elevation myocardial infarction who were not exposed to contrast material.Methods and ResultsWe studied 2025 patients with ST‐segment–elevation myocardial infarction who underwent pPCI and 1025 patients receiving fibrinolysis or no reperfusion who were not exposed to contrast material during the first 72 hours of hospital stay (control group). AKI was defined as creatinine of ≥0.5 mg/dL or >25% rise within 72 hours. AKI rates were similar in the pPCI and control groups (10.3% versus 12.1%, respectively; P=0.38). Propensity score matching resulted in 931 matched pairs with PCI and no PCI, with balanced baseline covariates (standardized difference <0.1). Among propensity score–matched patients, AKI rates were not significantly different with and without PCI (8.6% versus 10.9%, P=0.12). In the pPCI cohort, independent predictors of AKI included age ≥70 years, insulin‐treated diabetes mellitus, diuretic therapy, anterior infarction, baseline estimated glomerular filtration rate, and variables related to the presence of pump failure (higher Killip class, intra‐aortic balloon pump use) and reduced left ventricular ejection fraction but not contrast material dose. A risk score based on the PCI cohort had similar discriminatory capacity for AKI in the control group (C statistic 0.81±0.02 and 0.78±0.02, respectively; P=0.26).ConclusionsThe development of AKI in patients with ST‐segment–elevation myocardial infarction undergoing pPCI is mainly related to older age, baseline estimated glomerular filtration rate, heart failure, and hemodynamic instability. Risk for AKI is similar among ST‐segment–elevation myocardial infarction patients with and without contrast material exposure.

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Section: Discussionmentioning

confidence: 99%

Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?

Caspi

Habib

Cohen

et al. 2017

JAHA

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“…In addition, oxygen free radicals contribute at least in part to the renal tubular cellular injury. 47 Various treatment strategies have been investigated in an effort to decrease CI-AKI incidence in patients undergoing cardiac catheterization. Dopamine, fenoldopam, furosemide, mannitol, aminophylline, atrial natriuretic peptide, captopril, calcium channel blockers, alprostadil, and N-acetylcysteine were not effective in preventing contrast-induced nephropathy.…”

Section: Signal Transduction Pathwaysmentioning

confidence: 99%

Remote Ischemic Preconditioning and Renoprotection

Gassanov¹,

Nia

Caglayan³

et al. 2014

Journal of the American Society of Nephrology

123

106

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There is currently no effective prophylactic regimen available to prevent contrastinduced AKI (CI-AKI), a frequent and life-threatening complication after cardiac catheterization. Therefore, novel treatment strategies are required to decrease CI-AKI incidence and to improve clinical outcomes in these patients. Remote ischemic preconditioning (rIPC), defined as transient brief episodes of ischemia at a remote site before a subsequent prolonged ischemia/reperfusion injury of the target organ, is an adaptational response that protects against ischemic and reperfusion insult. Indeed, several studies demonstrated the tissue-protective effects of rIPC in various target organs, including the kidneys. In this regard, rIPC may offer a novel noninvasive and virtually cost-free treatment strategy for decreasing CI-AKI incidence. This review evaluates the current experimental and clinical evidence for rIPC as a potential renoprotective strategy, and discusses the underlying mechanisms and key areas for future research.

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“…[15][16][17] Elevated CRP prior to exposure to CM is a significant and independent predictor of CIN; inflammation is a pro-thrombotic state and elevated levels of inflammatory markers may contribute to increased plasma viscosity and subsequent tubular damage. 10,11 Consequences of administration of contrast medium Our study supports previous findings that people with co-existing diabetes and renal dysfunction are at increased risk of CIN 7,18,19 : all five of our patients who developed CIN had pre-existing CKD.…”

Section: Discussionmentioning

confidence: 99%

The effect of radiological contrast media on renal function and inflammatory markers in people with diabetes – a clinical study and review

2015

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Aim: To assess the association of inflammatory markers and the risk of developing contrast-induced nephropathy (CIN) in patients with diabetes undergoing lower limb angiography.Methods: This was a retrospective study of 77 patients undergoing lower limb angiography. We measured renal function and markers of inflammation, in particular neutrophil and lymphocyte count and C-reactive protein (CRP) levels, before and at 24, 48 and 72 hours after administration of contrast medium. Results: Those with pre-existing renal disease were at increased risk of CIN. We found no relationship between baseline renal function and CRP. There was a reduction in haemoglobin and lymphocyte count that is currently unexplained. Conclusions: While several traditional risk factors for CIN have been identified, further work is needed to determine the significance of changes in other haematological parameters. Br J Diabetes Vasc Dis 2015;15:187-191

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Pathophysiology of contrast medium–induced nephropathy

Abstract: Many experimental studies provide evidence for a greater perturbation in renal functions by dimeric contrast media in comparison to nonionic monomeric contrast media. Clinical trials have yielded conflicting results.

Cited by 485 publications

References 95 publications

Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?

Acute Kidney Injury After Primary Angioplasty: Is Contrast‐Induced Nephropathy the Culprit?

Remote Ischemic Preconditioning and Renoprotection

The effect of radiological contrast media on renal function and inflammatory markers in people with diabetes – a clinical study and review

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