Contrast-induced nephropathy: Difference between revisions
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==Background== | ==Background== | ||
* Vasoconstriction leading to ischemia in the deeper portion of the outer medulla | *;Often defined as creatinine rise of more than 0.5 mg/dL or ≥25% above baseline<ref>Goldfarb, S. et al. Contrast-Induced Acute Kidney Injury: Specialty-Specific Protocols for Interventional Radiology, Diagnostic Computed Tomography Radiology, and Interventional Cardiology. Mayo Clin Proc. Feb 2009; 84(2): 170–179 [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664588/ Text]</ref> | ||
* Toxic to kidney tubular cells, inducing vacuolization, change in mitochondrial function, and apoptosis | *Vasoconstriction leading to ischemia in the deeper portion of the outer medulla | ||
*Toxic to kidney tubular cells, inducing vacuolization, change in mitochondrial function, and apoptosis | |||
*Less likely to occur with low and iso-osmolar contrast agents | |||
===Healthy Patients=== | |||
*CIN not likely to occur in patients with a Cr<1.5 or a GFR >60ml/min<ref>Davenport MS. et al. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology. 2013 Apr;267(1):94-105</ref><ref>Sinert R, Brandler E, et al. Acad Emerg Med2012;19(11):1261</ref> | |||
===Impaired Renal Function=== | |||
*Administration should follow your local hospital protocols | |||
*Less likely to occur in iso-osmolar contrast agents (iodixanol/Visipaque) and possibly not even an occurrence if the serum creatinine is greater than 2.0 mg/dL. <ref>McDonald RJ, McDonald JS, et al. Radiology. 2013;267(1):106</ref> | |||
==Clinical Features== | ==Clinical Features== | ||
* 0.5mg/dl absolute or >25% relative increase in serum creatinine 48-72hrs after contrast exposure | * 0.5mg/dl absolute or >25% relative increase in serum creatinine 48-72hrs after contrast exposure | ||
Revision as of 00:37, 13 June 2014
Background
- Often defined as creatinine rise of more than 0.5 mg/dL or ≥25% above baseline[1]
- Vasoconstriction leading to ischemia in the deeper portion of the outer medulla
- Toxic to kidney tubular cells, inducing vacuolization, change in mitochondrial function, and apoptosis
- Less likely to occur with low and iso-osmolar contrast agents
Healthy Patients
Impaired Renal Function
- Administration should follow your local hospital protocols
- Less likely to occur in iso-osmolar contrast agents (iodixanol/Visipaque) and possibly not even an occurrence if the serum creatinine is greater than 2.0 mg/dL. [4]
Clinical Features
- 0.5mg/dl absolute or >25% relative increase in serum creatinine 48-72hrs after contrast exposure
Differential Diagnosis
- Poor renal perfusion
- Nephrotoxic medications
Workup
- Same for AKI
Management
- Hydration
- N-acetylcysteine
See Also
Sources
- Golshahi, J, Hasri H, Gharipour M. Contrast-induced nephropathy; A literature review. J Nephropathol. 2014;3(2):51-56.
- Persson PB, Hansell P, Liss P. Pathophysiology of contrast medium induced nephropathy. Kidney Int. 2005;68:14–22
- ↑ Goldfarb, S. et al. Contrast-Induced Acute Kidney Injury: Specialty-Specific Protocols for Interventional Radiology, Diagnostic Computed Tomography Radiology, and Interventional Cardiology. Mayo Clin Proc. Feb 2009; 84(2): 170–179 Text
- ↑ Davenport MS. et al. Contrast material-induced nephrotoxicity and intravenous low-osmolality iodinated contrast material. Radiology. 2013 Apr;267(1):94-105
- ↑ Sinert R, Brandler E, et al. Acad Emerg Med2012;19(11):1261
- ↑ McDonald RJ, McDonald JS, et al. Radiology. 2013;267(1):106