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Contrast-induced nephropathy (CIN) nephrotoxicity usually occurs within the first 48 hours after dye administration.
Over 80 million doses given in 2003. The problem is decreasing due to prevention and attenuation.
Incidence depends on population, definition, and prevention used.
Gadolinium, which is used with MRI, can rarely cause CIN. However, nephrogenic systemic fibrosis is another outcome. Symmetrical, bilateral papules, plaques, and subcutaneous nodules. It is often preceded by edema. Associated with extreme pain. Affects heart, lung, diaphragm, striated muscle, and great vessels. Only seen in renal disease.
a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.
Risk factors for CIN include:
There are risk stratifiers that allow prediction of damage.
Vasoconstriction follows adenosine activity ,endothelin release, and calcium influx.
Lasts 3-5 hours, leading to acute tubular necrosis.
Release of ROS.
80% of patients with CIN have a rise in 24hours, peaks in 3-5 days, and returns to baseline in 1-3 weeks.
Selection of patients for contrast, and discuss with radiology whether contrast is helpful.
Hydration is the most important prophylaxis. Oral intake is helpful, though should include some salt to prevent free water distribution. IV fluids are preferable with normal saline or isotonic sodium bicarbonate. Ideal is 12hours pre-and post, but 1hr 3ml/kg pre.
Avoid NPO unless crucial.
Mucomyst N-acetyl cysteine has unclear benefits, though is relatively cheap and well-tolerated.
Dieuretics, mannitol, and endothelin antagonists may cause harm.
NASIDs MUST be stopped prior to dye. Dieuretics should be held, according to some. It is unclear what to do with ACE and ARB, though some hold it if hypertension will not be substantial.
Dye dosing is one of the most important risk factors. Controlled dosing.
AKI aggrevaes vascular pathology, leading to high-morbidity and poor outcome in many.
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