Contrast-induced nephropathy
Contrast-induced nephropathy | |
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Specialty | Nephrology, radiology |
Contrast-induced nephropathy (CIN) is a purported form of
Despite extensive speculation, the actual occurrence of contrast-induced nephropathy has not been demonstrated in the literature.
Terminology
Given the increasing doubts about the contribution of radiocontrast to acute kidney injury, the American College of Radiology has proposed the name contrast-associated acute kidney injury (CA-AKI) (formerly referred to as post-contrast acute kidney injury; PC-AKI) because it does not imply a causal role, with the name contrast-induced acute kidney injury (CI-AKI) (formerly referred to as contrast-induced nephropathy; CIN) reserved for the rare cases where radiocontrast is likely to be causally related.[3]
Risk factors
There are multiple risk factors of contrast-induced nephropathy, whereof a 2016 review emphasized
Decreased kidney function
European guidelines classify a pre-existing decreased
- Estimated glomerular filtration rate (eGFR) < 45 ml/min/1.73 m2 of body surface area before intra-arterial administration with first-pass renal exposure (not passing lungs or peripheral circulation before kidneys), or in the intensive care unit
- eGFR < 30 ml/min/1.73 m2 before intravenousadministration or intra-arterial administration with second-pass renal exposure
- Known or suspected acute kidney injury
To calculate
Mehran score
The Mehran score is a
Other factors
European guidelines include the following procedure-related risk factors:[5]
- Large doses of contrast given intra-arterially with first-pass renal exposure
- Use of contrast agents with high osmolality (limited use today)
- Multiple contrast injections within 48–72 h. Swedish guidelines also include gadolinium MRI contrast agents in this aspect.
Swedish guidelines list the following additional risk factors:[5]
- Hypoxia
- Cirrhosis
- NSAIDor nephrotoxic medication
- Individuals on dialysis with residual renal function of at least 400 ml urine/24h
- Individuals having undergone kidney transplantation
Prevention
The main alternatives in people with a risk of contrast-induced nephropathy are:[citation needed]
- Adjustment of the radiocontrast dose
- Treating or mitigating risk factors
- Using no intravenous contrast for the investigation.
- Switching to another modality such as MRI.
Dose adjustment
According to European guidelines, the ratio of the contrast dose (in grams of iodine) divided by the absolute estimated glomerular filtration rate (GFR) should be less than 1.1 g/(ml/min) for intra-arterial contrast medium administration with first-pass renal exposure (not passing lungs or peripheral tissue before reaching the kidneys).[5] Swedish guidelines are more restrictive, recommending a ratio of less than 0.5 g/(ml/min) in patients with risk factors and irrespective of route of administration, and even more caution in first-pass renal exposure.[5]
Treating or mitigating risk factors
Hydration by
- Oral hydration may be as effective as the intravenous route for volume expansion to prevent contrast-induced nephropathy, according to a review in 2013.[8]
- methylxanthines theophylline and aminophylline, may help[10] although studies have conflicting results.[11]
- N-acetylcysteine (NAC) by mouth twice a day, on the day before and of the procedure if creatinine clearance is estimated to be less than 60 mL/min [1.00 mL/s]) may reduce risk.[medical citation needed] Some authors believe the benefit is not overwhelming.[12] A systematic review concluded that NAC is "likely to be beneficial" but did not recommend a specific dose.[13][needs update]
- Ascorbic acid may be protective against CIN, according to a systematic review of randomized controlled trials.[14]
- Matched hydration, meaning infusion of a volume of normal saline equal to the urine output, has been found to reduce kidney injury, dialysis, adverse events and mortality compared to standard therapy.[15][16]
Diagnosis
CIN is classically defined as a serum creatinine increase of at least 25% and/or an absolute increase in serum creatinine of 0.5 mg/dL[17] after using iodine contrast agent without another clear cause for acute kidney injury,[4] but other definitions have also been used.[2]
The
- Absolute serum creatinine increase of ≥0.3 mg/dl (>26.4 µmol/L)[18]
- Relative serum creatinine increase of ≥50 % (≥1.5-fold above baseline)[18]
- Urine output reduced to ≤0.5 mL/kg/hour for at least 6 hours[18]
Mechanism
The mechanism of contrast-induced nephropathy is not entirely understood, but is thought to include direct damage from reactive oxygen species, contrast-induced increase in urine output, increased oxygen consumption, changes in dilation and narrowing of the blood vessels to the kidneys, and changes in urine viscosity.[citation needed]
Prognosis
It is unclear if CIN causes persisting decline in renal function since few studies has followed patients for more than 72 hours.[18] In one meta-analysis the decline in renal function was shown to persist in 1.1 % of the patients with CIN.[19]
Clinical relevance
Doubts regarding the significance of the phenomenon appeared in the scientific literature. Several studies have shown that intravenous contrast material administration was not associated with excess risk of acute kidney injury, dialysis, or death, even among patients with comorbidities reported to predispose them to nephrotoxicity.[1] Moreover, hydration, the most established prevention measure to prevent contrast-induced nephropathy was shown to be ineffective in the POSEIDON trial,[20] raising further doubts regarding the significance of this disease state.[21] A meta-analysis of 28 studies of AKI after CT with radiocontrast showed no causal relationship between the use of radiocontrast and AKI.[2]
References
- ^ PMID 25203000.
- ^ S2CID 27167779.
- ISBN 978-1-55903-012-0. Retrieved 2022-08-02.
- ^ PMID 26830221.
- ^ S2CID 52057355.
- PMID 15464318.
- ^ PMID 23555863.
- ^ PMID 26830221.
- PMID 17512638.
- PMID 15911721.
- PMID 15547209.
- PMID 16973048.
- PMID 23994417.
- PMID 28231903.
- S2CID 27646564.
- PMID 16436769.
- ^ ISBN 978-1-55903-012-0. Retrieved 20 November 2020.
- S2CID 6307799.
- S2CID 7882106.
- ^ John Mandrola (2017-03-07). "Contrast-Induced Nephropathy: Signal or Noise?". Medscape. Retrieved 2017-09-28.