Contrast Medium-Induced Acute Kidney Injury

Sadat, Umar; Usman, Ammara; Boyle, Jonathan R.; Hayes, Paul D.; Solomon, Richard

doi:10.1159/000430770

Cited by 837 publications

(18 citation statements)

References 53 publications

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“…8,9 We found a high sensitivity at the lower cutoff of 0. 28,29 Comparing hospital length of stay, we found a significant difference between AKI stage 2-3 and those with no AKI or stage 1 AKI.…”

Section: Discussionmentioning

confidence: 85%

Urinary [TIMP‐2] × [IGFBP7] for risk prediction of acute kidney injury in decompensated heart failure

Schanz

Shi

Wasser

et al. 2017

Clinical Cardiology

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Background In acute decompensated heart failure (ADHF) the risk of acute kidney injury (AKI) is high. Early detection of patients at risk for AKI is important. We tested urinary [TIMP‐2] × [IGFBP7], a new US Food and Drug Administration–cleared test to assess AKI risk, in a cohort of hospitalized ADHF patients. Hypothesis In patients with ADHF, urinary [TIMP‐2] × [IGFBP7] is associated with moderate to severe AKI and related to increased mortality. Methods We enrolled 400 patients in the emergency department at Robert‐Bosch Hospital, Stuttgart, Germany. We examined the predictive ability of urinary [TIMP‐2] × [IGFBP7] (units: [ng/mL]2/1000) for development of AKI stage 2 or 3 within 24 hours of sample collection in patients with ADHF. Operating characteristics were determined for the validated cutoffs of 0.3 and 2.0. Results Forty patients had ADHF upon presentation and sufficient data for AKI staging. 27.5% developed AKI stage 2–3 within 7 days. Urinary [TIMP‐2] × [IGFBP7] discriminated for AKI stage 2–3 over the first day with an area under the ROC curve of 0.84 (95% confidence interval: 0.72‐0.93) and over 7 days with an AUC of 0.77 (95% confidence interval: 0.65‐0.88). For the first day, sensitivity was 86% at the 0.3 cutoff and specificity was 95% at the 2.0 cutoff for prediction of AKI stage 2–3. There was a trend (P = 0.08) for higher mortality in patients with urinary [TIMP‐2] × [IGFBP7] >2.0 and AKI 2–3. Conclusions Urinary [TIMP‐2] × [IGFBP7] is a promising marker for AKI risk assessment in patients with ADHF.

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Section: Discussionmentioning

confidence: 85%

Urinary [TIMP‐2] × [IGFBP7] for risk prediction of acute kidney injury in decompensated heart failure

Schanz

Shi

Wasser

et al. 2017

Clinical Cardiology

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“…The most common and accepted definition of CIAKI is a rise in serum creatinine of at least 0.5 mg/dL or a 25% increase from the baseline value assessed 48 hours after contrast media administration . Contrast‐induced acute kidney injury is associated with multiple adverse events, including progressive loss of kidney function, major cardiac complications, and prolonged hospitalization …”

Section: Discussionmentioning

confidence: 99%

“…Comprehensive specialty‐specific protocols have been proposed to prevent CIAKI in risk‐stratified patient groups . These measures should include halting nephrotoxic medications, minimizing contrast media volumes, and using low‐ or iso‐osmolality contrast media . Hydration before and after contrast media administration decreases the rates of CIAKI because it reduces the contrast media concentration in the kidneys.…”

Section: Discussionmentioning

confidence: 99%

The Perils of Contrast Media

2018

AORN Journal

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“…There are an increasing number of both diagnostic investigations and therapeutic procedures performed using radio-contrast. Furthermore an ageing population, with a higher incidence of underlying renal impairment, make it imperative that greater attention is focused on the aetiology of CIN in order to formulate effective prophylactic and therapeutic strategies to reduce its incidence and associated morbidity and mortality [19]. Contemporary evidence has highlighted significantly higher mortality rates in patients who suffer acute kidney injury after emergency aneurysm surgery at both 30-days and 12-months [20].…”

Section: Discussionmentioning

confidence: 99%

“…With this in mind urine collection was performed at baseline, 48 and 96 h followed by sacrifice of the mouse, in order to maximise the observed level of renal damage following contrast administration. Serum creatinine however, is relatively insensitive only rising out of the normal range when 50% of the functioning renal mass is lost [19]. Furthermore even modest changes in serum creatinine have a strong association with in-hospital mortality [21].…”

Section: Discussionmentioning

confidence: 99%

Ascorbic acid ameliorates renal injury in a murine model of contrast-induced nephropathy

et al. 2017

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BackgroundContrast induced nephropathy (CIN) is the commonest cause of iatrogenic renal injury and its incidence has increased with the advent of complex endovascular procedures. Evidence suggests that ascorbic acid (AA) has a nephroprotective effect in percutaneous coronary interventions when contrast media are used. A variety of biomarkers (NGAL, NGAL:creatinine, mononuclear cell infiltration, apoptosis and RBP-4) in both the urine and kidney were assayed using a mouse model of CIN in order to determine whether AA can reduce the incidence and/or severity of renal injury.MethodsTwenty-four BALB/c mice were divided into 4 groups. Three groups were exposed to high doses of contrast media (omnipaque) in a well-established model of CIN, and then treated with low or high dose AA or placebo (saline). CIN severity was determined by measurement of urinary neutrophil gelatinase-associated lipocalin (NGAL):creatinine at specific time intervals. Histological analysis was performed to determine the level of mononuclear inflammatory infiltration as well as immunohistochemistry to determine apoptosis in the glomeruli by staining for activated caspase-3 and DNA nicking (TUNEL assays). Reverse transcriptase PCR (rtPCR) of mRNA transcripts prepared from mRNA extracted from mouse kidneys was also performed for both lipocalin-2 (Lcn2) encoding NGAL and retinol binding protein-6 (RBP4) genes. NGAL protein expression was also confirmed by ELISA analysis of kidney lysates.ResultsUrinary NGAL:creatinine ratio was significantly lower at 48 h with a 44% and 62% (204.3μg/mmol versus 533.6μg/mmol, p = 0.049) reduction in the low and high dose AA groups, respectively. The reduced urinary NGAL:creatinine ratio remained low throughout the time period assessed (up to 96 h) in the high dose AA group. In support of the urinary analysis ELISA analysis of NGAL in kidney lysates also showed a 57% reduction (12,576 ng/ml versus 29,393 ng/ml) reduction in the low dose AA group. Immunohistochemistry for apoptosis demonstrated decreased TUNEL and caspase-3 expression in both low and high dose AA groups.ConclusionsAscorbic acid reduced the frequency and severity of renal injury in this murine model of CIN. Further work is required to establish whether AA can reduce the incidence of CIN in humans undergoing endovascular procedures.

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Contrast Medium-Induced Acute Kidney Injury

Cited by 837 publications

References 53 publications

Urinary [TIMP‐2] × [IGFBP7] for risk prediction of acute kidney injury in decompensated heart failure

Urinary [TIMP‐2] × [IGFBP7] for risk prediction of acute kidney injury in decompensated heart failure

The Perils of Contrast Media

Ascorbic acid ameliorates renal injury in a murine model of contrast-induced nephropathy

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