Contrast-induced nephropathy

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Contrast-induced nephropathy
SpecialtyNephrology, radiology

Contrast-induced nephropathy (CIN) is a purported form of

medical imaging contrast
material without another clear cause for the acute kidney injury.

Despite extensive speculation, the actual occurrence of contrast-induced nephropathy has not been demonstrated in the literature.

kidney function.[2]

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

old age.[4]

Decreased kidney function

European guidelines classify a pre-existing decreased

kidney function to be a risk factor of contrast-induced nephropathy in the following cases:[5]

To calculate

muscle mass, liver failure, or cirrhosis.[5]

Mehran score

The Mehran score is a

diabetes mellitus, contrast media volume, decreased kidney function (serum creatinine level >1.5 g/dL or decreased estimated glomerular filtration rate).[6][7]

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]

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

statins with N-acetylcysteine and intravenous saline is also supported.[9]

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

contrast medium exposure one of the following occurs:[18]

  1. Absolute serum creatinine increase of ≥0.3 mg/dl (>26.4 µmol/L)[18]
  2. Relative serum creatinine increase of ≥50 % (≥1.5-fold above baseline)[18]
  3. 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

External links