CIN 같은 것은 없을지도 뉴질랜드 사람들이 잘 정리

Journal of the New Zealand Medical Association, 24-July-2009, Vol 122 No 1299

Contrast-induced nephropathy: does it really exist?

Tim M Buckenham

In contemporary hospital practice there is increasing reliance on sophisticated diagnostic imaging—its efficacy is significantly reduced without the administration of intravascular iodinated contrast media.

In this issue of the Journal, Dr Tarek Darwish summarises the evidence for the existence of contrast-induced nephropathy (CIN) and the strategies commonly used to minimise the nephrotoxicity of iodinated contrast.1 His article poses an important question as to the existence of CIN as an entity and refers to recent evidence suggesting iodinated contrast medial (ICM) administration may not be necessary to induce nephropathy in hospitalised patients undergoing enhanced imaging.

The possibility of CIN being over-estimated has important ramifications. Most radiology departments have developed protocols aimed at identifying those at risk of CIN prior to imaging, usually by measuring serum creatinine and/or glomerular filtration rate (GFR). Patients at risk, e.g., those with pre-existing renal failure and/or diabetes, may either be offered alternative imaging that does not use ICM or be pre-hydrated.

The problem with these protocols is they create other risks for the patient, in particular the alternative imaging strategy may be less efficacious leading to under-diagnosis, and if that modality is gadolinium-enhanced magnetic resonance imaging (MRI), we are selecting the subgroup at highest risk of developing nephrogenic systemic fibrosis and exposing them to paramagnetic contrast media.

What is the evidence that CIN has been over-estimated and is it sufficient to relax the stringent protocols that are currently in place?

The general consensus that intravascular administration of iodinated contrast media is a significant cause of iatrogenic nephropathy has recently been challenged.

Newhouse and colleagues, in a recent article entitled Frequency of serum creatinine changes in the absence of iodinated contrast material: implications for studies of contrast nephrotoxicity, suggest that the creatinine rise that occurs in many hospitalised patients has not been taken into account (“background noise”) and may have led to the over-estimation of creatinine rises secondary to iodinated contrast media.2

Other investigators have produced similar findings, with Bruce and Pozniak reviewing 15,357 patient observations, with 6533 patients receiving intravenous iodinated contrast and 8824 unmatched controls receiving no contrast.3,4 There was no difference in the rate of renal dysfunction between the two groups (as defined as an increase in creatinine of 25% over baseline).

In the subgroup with pre-existing renal dysfunction (creatinine of 1.0–2.5 mg/dL), 22% of those who had iodinated contrast media developed CIN, compared with 11% in the non-contrast group.

This paper raises the multifactorial aetiology of CIN and suggests the concept of hospital-induced nephropathy (HIN) reflects the multifactorial aetiology of renal dysfunction in hospitalised patients undergoing enhanced imaging.

Where does this new research leave us?

Newhouse and colleagues have alerted us to the complexity of assessing the role of ICM in causing renal dysfunction in patients undergoing enhanced imaging. However, due to the absence of matched patients, it is not possible to reduce or dismantle the current protocols surrounding the intravascular administration of contrast media, particularly as these protocols are often set up to allow the responsibility for contrast administration to be devolved to trained nursing staff who rely on robust guidelines as they are often not in a position to make individual clinical-based decisions which require the advice of a radiologist.

Will the question of CIN’s existence ever be resolved?

This is unlikely, unless new studies randomise patient groups between contrast and no contrast, or select an appropriate matched patient group. Both these options are impractical and are unlikely to occur.

In the meantime, we need to give thought to how we manage those patients perceived to be at risk of CIN and, in the light of Newhouse’s study, have an enhanced consciousness of the risk/benefit ratio of offering patients alternative imaging that may be less effective at making the diagnosis or puts them at risk of other conditions such as nephrogenic systemic fibrosis.4

Competing interests: None known.

Author information: Tim M Buckenham, Clinical Professor of Radiology and Consultant Vascular Radiologist (and a Sub-Editor of the NZMJ), Christchurch Hospital, Christchurch

Correspondence: Professor Tim Buckenham, Radiology Department, Christchurch Public Hospital, Private Bag 4710, Christchurch, New Zealand. Fax: +64 (0)3 3540620; email: TimB2@cdhb.govt.nz

References:

1. Darwish T. An evidence-based approach to minimise contrast-induced nephropathy. N Z Med J. 2009;122(1299). http://www.nzma.org.nz/journal/122-1299/3711
2. Newhouse JH, Kho D, Rao QA, Starren J. Frequency of serum creatinine changes in the absence of iodinated contrast material: implications for studies of contrast nephrotoxicity. AJR Am J Roentgenol. 2008;191(2):376–82.
3. Baumgarten DA, Ellis JH. Contrast-induced nephropathy: contrast material not required? AJR Am J Roentgenol. 2008;191(2):383–6.
4. Bruce R, Pozniak M. Comparing eGFR changes between intravenous contrast recipients and normal controls. Society of Uroradiology 2008 Annual Meeting Abstract Book. Houston, TX: Society of Uroradiology; 2008:2.