Prevention, Incidence, and Outcomes of Contrast-Induced Acute Kidney Injury

Weisbord, Steven D.; Mor, Maria K.; Resnick, Abby L.; Hartwig, Kathryn C.; Sonel, Ali F.; Fine, Michael J.; Palevsky, Paul M.

doi:10.1001/archinte.168.12.1325

Cited by 113 publications

(75 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As part of a larger, prospective, observational study investigating the prevention of CIAKI in patients undergoing coronary or noncoronary angiography or computed tomography at an academically affiliated VA Healthcare System between February 1, 2005 and July 31, 2006, we conducted this substudy of patients who underwent computed tomography (19). We prospectively identified all subjects scheduled to undergo computed tomography with IV iodinated contrast in either the inpatient or outpatient setting and recorded the most recent serum creatinine (Scr) within the 60 d before the procedure.…”

Section: Patient Populationmentioning

confidence: 99%

Incidence and Outcomes of Contrast-Induced AKI Following Computed Tomography

Weisbord

Mor

Resnick

et al. 2008

Clinical Journal of the American Society of Nephrology

Self Cite

180

127

View full text Add to dashboard Cite

Background and objectives: Most studies of contrast-induced acute kidney injury (CIAKI) have focused on patients undergoing angiographic procedures. The incidence and outcomes of CIAKI in patients undergoing nonemergent, contrastenhanced computed tomography in the inpatient and outpatient setting were assessed.Design, setting, participants, & measurements: Patients with estimated glomerular filtration rates (GFRs) <60 ml/min per 1.73 m 2 undergoing nonemergent computed tomography with intravenous iodinated radiocontrast at an academic VA Medical Center were prospectively identified. Serum creatinine was assessed 48 to 96 h postprocedure to quantify the incidence of CIAKI, and the need for postprocedure dialysis, hospital admission, and 30-d mortality was tracked to examine the associations of CIAKI with these medical outcomes.Results: A total of 421 patients with a median estimated GFR of 53 ml/min per 1.73 m 2 were enrolled. Overall, 6.5% of patients developed an increase in serum creatinine >25%, and 3.5% demonstrated a rise in serum creatinine >0.5 mg/dl. Although only 6% of outpatients received preprocedure and postprocedure intravenous fluid, <1% of outpatients with estimated GFRs >45 ml/min per 1.73 m 2 manifested an increase in serum creatinine >0.5 mg/dl. None of the study participants required postprocedure dialysis. Forty-six patients (10.9%) were hospitalized and 10 (2.4%) died by 30-d follow-up; however, CIAKI was not associated with these outcomes.Conclusions: Clinically significant CIAKI following nonemergent computed tomography is uncommon among outpatients with mild baseline kidney disease. These findings have important implications for providers ordering and performing computed tomography and for future clinical trials of CIAKI.

show abstract

Section: Patient Populationmentioning

confidence: 99%

Incidence and Outcomes of Contrast-Induced AKI Following Computed Tomography

Weisbord

Mor

Resnick

et al. 2008

Clinical Journal of the American Society of Nephrology

Self Cite

180

127

View full text Add to dashboard Cite

show abstract

“…There are many strategies available to clinicians to mitigate the risk of contrastinduced nephropathy. However, studies have shown that these techniques (pre-hydration with intravenous fluids and administration of N-acetylcysteine) are inconsistently used in practice [4]. A systematic review and meta-analysis of contrast induced acute kidney injury showed no difference between patients who did and did not receive contrast, regardless of previous renal insufficiency, making the withholding of contrasted imaging unnecessary [5].…”

Section: Discussion and Teachable Momentmentioning

confidence: 99%

A case of abdominal pain and fear of intravenous contrast

M¹,

Pandit²,

Fritz³

2017

Int Med Care

View full text Add to dashboard Cite

A 66-year-old male with a past medical history of 50-pack-year tobacco smoking and atrial fibrillation presented to an outside facility with abdominal pain and hematochezia. Of note, he was not taking his home medications of Metoprolol and Coumadin for a few weeks due to lack of insurance. He was found to have lactic acidosis, acute kidney injury, and significant leukocytosis. The patient was transferred to our facility for further evaluation and management.On presentation to our ED, the patient was in atrial fibrillation with a rate of 104. He reaffirmed his story and provided additional history, including chronic symptoms suggestive of claudication. A nonenhanced CT of the abdomen and pelvis was obtained in the ED and revealed mural thickening of a jejunal loop.After evaluation by the vascular surgery service, further contrasted imaging was deferred due to acute renal failure. An ultrasound of the abdominal vessels was performed. The preliminary interpretation was deemed to be inconclusive, and the patient was followed clinically on the medicine service.Over the following 24 hours, the patient developed acute neurovascular changes in the bilateral lower extremities, with total paralysis and sensory changes. Emergent CT angiogram ( Figure 1) showed complete abrupt occlusion of the aorta just above the level of the diaphragmatic crus with non opacification of the abdominal aorta and its branches extending to the iliac arteries and evidence of renal and bowel ischemia. The patient was then taken emergently to the OR for aortic thrombectomy. The extent of his vascular insult was significant, and the patient ultimately passed away. It was only after the events of the surgery that a formal read on the ultrasound revealed that the patient had no blood flow within the aorta and branch vessels. Discussion and teachable momentAcute mesenteric ischemia has persisted as a source of mortality across several decades [1]. The etiology of mesenteric ischemia is commonly associated with cardio-embolic events and native vascular disease. However the cause of ischemia in this case was a massive occlusion of the abdominal aorta, which is unusual [2]. Occlusion of the aorta can be seen in large abdominal aortic aneurysms, and rarely from embolic events.Despite absent aortic flow on ultrasound, our patient did not exhibit symptoms of aortic occlusion for several hours, resulting in a delay of surgical intervention. It was not until CT angiography was performed that assurance of the patient's diagnosis was made and surgical intervention was enacted. We believe our patient suffered a thromboembolic event from a cardiogenic source, given his history of atrial fibrillation without anti-coagulation. However, acute thrombosis is possible, given identified atherosclerosis on imaging, smoking history, and description of chronic symptoms. While a cardiac thrombus would typically go to the brain, a large thrombus, as presumed in this case, could bypass the brachiocephalic arteries and progress through the aorta.Our case highlights several im...

show abstract

“…Practical inclusion criteria for a prevention trial would be CKD based on a GFR of 15-59 ml/min per 1.73 m 2 and the presence of at least one other risk factor such as heart failure, diabetes, or proteinuria among patients with an eGFR of 45-59 ml/min per 1.73 m 2 . Event rates for AKI and AKI requiring dialysis are expected to be 10%-15% and 1.0%, respectively, in patients with CKD (20). For phase 2 studies, an appropriate primary study outcome might be an increase in SCr of $0.5 mg/dl or $25% with multiple SCr assessments over a minimum of 96 hours.…”

Section: Discussionmentioning

confidence: 99%

Design of Clinical Trials in Acute Kidney Injury

Okusa¹,

Molitoris²,

Palevsky³

et al. 2012

Clinical Journal of the American Society of Nephrology

Self Cite

View full text Add to dashboard Cite

SummaryAKI is an important clinical problem that has become increasingly more common. Mortality rates associated with AKI remain high despite advances in supportive care. Patients surviving AKI have increased long-term mortality and appear to be at increased risk of developing CKD and progressing to ESRD. No proven effective pharmacologic therapies are currently available for the prevention or treatment of AKI. Advances in addressing this unmet need will require the development of novel therapeutic agents based on precise understanding of key pathophysiological events and the implementation of well designed clinical trials. To address this need, the National Institute of Diabetes and Digestive and Kidney Diseases sponsored the "Clinical Trials in Acute Kidney Injury: Current Opportunities and Barriers" workshop in December 2010. The event brought together representatives from academia, industry, the National Institutes of Health, and the US Food and Drug Administration. We report the discussions of workgroups that developed outlines of clinical trials for the prevention of AKI in two patient populations: patients undergoing elective surgery who are at risk for or who develop AKI, and patients who are at risk for contrast-induced AKI. In both of these populations, primary prevention or secondary therapy can be delivered at an optimal time relative to kidney injury. The workgroups detailed primary and secondary endpoints for studies in these groups, and explored the use of adaptive clinical trial designs for trials of novel preventive strategies to improve outcomes of patients with AKI.

show abstract

Prevention, Incidence, and Outcomes of Contrast-Induced Acute Kidney Injury

Cited by 113 publications

References 24 publications

Incidence and Outcomes of Contrast-Induced AKI Following Computed Tomography

Incidence and Outcomes of Contrast-Induced AKI Following Computed Tomography

A case of abdominal pain and fear of intravenous contrast

Design of Clinical Trials in Acute Kidney Injury

Contact Info

Product

Resources

About