In their comprehensive meta-analysis which included data from all available studies on Contrast-induced Nephropathy (CIN) involving 3563 patients , the authors affirm that CIN is the development of acute renal failure after administration of radiocontrast in the absence of other identifiable causes (1) . However, as some studies evaluated patients having either cardiac catheterization or computed tomography or other arteriography, their systematic examination of potential sources of heterogeneity will be extended to differentiate between patients in whom contrast agents are introduced into the venous or arterial bed, and between patients in whom cardiac catheterization was accessed via the radial or the femoral approach . In fact, it could be a crucial difference among potential risk factors for acute kidney injury when contrast medium is introduced by intra-arterial administration, due to the possible cholesterol crystal embolization occurring after intravascular trauma with angiographic catheters during invasive vascular procedures. In this case , the role of contrast medium in pathophysiology of renal damage might be marginal, if any, due to a possibly undiagnosed atheroembolic renal disease (AERD) masked under a supposed CIN, and a further difference in the degree of AERD might depend on the site of approach ( if radial or femoral). While AERD and CIN share as common setting the need for the use of intravascular contrast medium for diagnostic procedures, pathophysiology of renal damage is completely different: for CIN it is dealing with alteration in renal hemodynamics , rheological properties , and paracrine factors (adenosine, endothelin, reactive oxygen species) or direct cytotoxic effects on renal tubular cells(2,3) , while in the case of AERD the renal parenchyma is mechanically damaged by cholesterol crystals able to trigger inflammatory responses(4,5). Unfortunately, differential diagnosis may be difficult on clinical basis , when local and systemic signs of cholesterol embolism in other organs (gut, skin, upper and lower extremities) such as livedo reticularis , purple toes syndrome, eosinophilia and serum complement consumption are lacking. Many difficulties have been reported in diagnosing AERD, that is labelled as the great masquerader, with an incidence in autopsy studies from 4% in elderly subjects over 65 yr with minimal atherosclerosis to 77% in older patients with severe atherosclerosis, and up to >12% of cases following coronary angioplasty in clinical studies,. Therefore, assessing for heterogeneity in the vascular access will help in differentiating homogeneous clinical entities similar in pathogenesis and , therefore, prevention and treatment.
References
1) Zoungas S, Ninomiya T, Huxley R, Cass A, Jardine M, Gallagher M, Patel A, Vasheghani-Farahani A, Sadigh G, Perkovic V Systematic review: sodium bicarbonate treatment regimens for the prevention of contrast- induced nephropathy. Ann Intern Med. 2009 ; 151(9):631-8.
2) Solomon R, Dumouchel W. Contrast media and nephropathy: findings from systematic analysis and Food and Drug Administration reports of adverse effects. Invest Radiol. 2006; 41(8):651-60.
3) Brar SS, Hiremath S, Dangas G, Mehran R, Brar SK, Leon MB. Sodium bicarbonate for the prevention of contrast induced-acute kidney injury: a systematic review and meta-analysis. Clin J Am Soc Nephrol. 2009 ;4(10):1584-92.
4) Baykal C, Buyukbabani N, Aysuna N, Ark E. Clinical outcomes of renal cholesterol crystal embolization. J Nephrol. 1999 ;12:266-9.
5) Khan AM, Jacobs S. Trash feet after coronary angiography. Heart. 2003 ;89: 17.
None declared