Contrast-induced nephropathy: Difference between revisions
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{{Infobox medical condition | |||
| name = Contrast-induced nephropathy | |||
| synonyms = Contrast-induced acute kidney injury | |||
| field = [[Nephrology]] | |||
| symptoms = [[Nausea]], [[vomiting]], [[shortness of breath]], [[edema]] | |||
| complications = [[Acute kidney injury]], [[chronic kidney disease]] | |||
| onset = Within 48-72 hours after contrast exposure | |||
| duration = Usually resolves within 1-2 weeks | |||
| causes = [[Iodinated contrast media]] | |||
| risks = [[Chronic kidney disease]], [[diabetes mellitus]], [[dehydration]], [[heart failure]] | |||
| diagnosis = [[Serum creatinine]] increase, [[urinalysis]] | |||
| prevention = [[Hydration]], use of low-osmolar or iso-osmolar contrast agents | |||
| treatment = Supportive care, [[dialysis]] if severe | |||
| frequency = 1-2% in general population, up to 50% in high-risk patients | |||
}} | |||
'''Contrast-induced nephropathy''' ('''CIN''') is a form of [[kidney damage]] in which there has been recent exposure to medical imaging contrast material without another clear cause for the acute kidney injury. CIN is associated with a significant increase in morbidity and mortality, length of hospital stay and in healthcare costs. | '''Contrast-induced nephropathy''' ('''CIN''') is a form of [[kidney damage]] in which there has been recent exposure to medical imaging contrast material without another clear cause for the acute kidney injury. CIN is associated with a significant increase in morbidity and mortality, length of hospital stay and in healthcare costs. | ||
==Definition== | ==Definition== | ||
Contrast-induced nephropathy is traditionally defined as a serum creatinine increase of 25% or more from baseline or an absolute increase of 0.5 mg/dL within 48-72 hours of intravascular iodinated contrast material exposure, in the absence of an alternative etiology. | Contrast-induced nephropathy is traditionally defined as a serum creatinine increase of 25% or more from baseline or an absolute increase of 0.5 mg/dL within 48-72 hours of intravascular iodinated contrast material exposure, in the absence of an alternative etiology. | ||
==Epidemiology== | ==Epidemiology== | ||
The incidence of CIN varies widely, depending on the definition used, the population studied, and the prophylactic measures taken. In the general population, the incidence of CIN has been reported to be less than 2%. However, in patients with pre-existing [[renal insufficiency]], diabetes mellitus, or both, the incidence of CIN can exceed 25%. | The incidence of CIN varies widely, depending on the definition used, the population studied, and the prophylactic measures taken. In the general population, the incidence of CIN has been reported to be less than 2%. However, in patients with pre-existing [[renal insufficiency]], diabetes mellitus, or both, the incidence of CIN can exceed 25%. | ||
==Pathophysiology== | ==Pathophysiology== | ||
The pathophysiology of CIN is complex and not completely understood. It is believed to involve direct toxicity to renal tubular epithelial cells and renal medullary hypoxia due to alterations in renal blood flow. | The pathophysiology of CIN is complex and not completely understood. It is believed to involve direct toxicity to renal tubular epithelial cells and renal medullary hypoxia due to alterations in renal blood flow. | ||
==Prevention and Treatment== | ==Prevention and Treatment== | ||
Prevention of CIN includes identification of high-risk patients, appropriate choice and dosing of contrast material, and prophylactic hydration. Treatment of established CIN is supportive, as there is currently no specific therapy available. | Prevention of CIN includes identification of high-risk patients, appropriate choice and dosing of contrast material, and prophylactic hydration. Treatment of established CIN is supportive, as there is currently no specific therapy available. | ||
==See Also== | ==See Also== | ||
* [[Acute kidney injury]] | * [[Acute kidney injury]] | ||
* [[Renal insufficiency]] | * [[Renal insufficiency]] | ||
* [[Diabetes mellitus]] | * [[Diabetes mellitus]] | ||
[[Category:Kidney diseases]] | [[Category:Kidney diseases]] | ||
[[Category:Radiology]] | [[Category:Radiology]] | ||
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{{Kidney-disease-stub}} | {{Kidney-disease-stub}} | ||
{{Medicine-stub}} | {{Medicine-stub}} | ||
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Latest revision as of 05:17, 4 April 2025
| Contrast-induced nephropathy | |
|---|---|
| Synonyms | Contrast-induced acute kidney injury |
| Pronounce | N/A |
| Specialty | N/A |
| Symptoms | Nausea, vomiting, shortness of breath, edema |
| Complications | Acute kidney injury, chronic kidney disease |
| Onset | Within 48-72 hours after contrast exposure |
| Duration | Usually resolves within 1-2 weeks |
| Types | N/A |
| Causes | Iodinated contrast media |
| Risks | Chronic kidney disease, diabetes mellitus, dehydration, heart failure |
| Diagnosis | Serum creatinine increase, urinalysis |
| Differential diagnosis | N/A |
| Prevention | Hydration, use of low-osmolar or iso-osmolar contrast agents |
| Treatment | Supportive care, dialysis if severe |
| Medication | N/A |
| Prognosis | N/A |
| Frequency | 1-2% in general population, up to 50% in high-risk patients |
| Deaths | N/A |
Contrast-induced nephropathy (CIN) is a form of kidney damage in which there has been recent exposure to medical imaging contrast material without another clear cause for the acute kidney injury. CIN is associated with a significant increase in morbidity and mortality, length of hospital stay and in healthcare costs.
Definition[edit]
Contrast-induced nephropathy is traditionally defined as a serum creatinine increase of 25% or more from baseline or an absolute increase of 0.5 mg/dL within 48-72 hours of intravascular iodinated contrast material exposure, in the absence of an alternative etiology.
Epidemiology[edit]
The incidence of CIN varies widely, depending on the definition used, the population studied, and the prophylactic measures taken. In the general population, the incidence of CIN has been reported to be less than 2%. However, in patients with pre-existing renal insufficiency, diabetes mellitus, or both, the incidence of CIN can exceed 25%.
Pathophysiology[edit]
The pathophysiology of CIN is complex and not completely understood. It is believed to involve direct toxicity to renal tubular epithelial cells and renal medullary hypoxia due to alterations in renal blood flow.
Prevention and Treatment[edit]
Prevention of CIN includes identification of high-risk patients, appropriate choice and dosing of contrast material, and prophylactic hydration. Treatment of established CIN is supportive, as there is currently no specific therapy available.
See Also[edit]
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