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Increasing numbers of patients in the developed world are exposed to contrast medium during cardiac catheterisation procedures, and the pressure to increase cardiac laboratory throughput of patients with suspected coronary disease is unrelenting. For this reason, the problem of radiocontrast induced nephropathy (RCIN) assumes greater and greater importance. How is the fallout from contrast exposure to be minimised?
Scale of the problem
Radiocontrast use in all branches of medicine is reported to be the third most common cause of new onset renal failure in hospital patients.1 Although varying definitions of nephropathy have been employed in the literature, including a 25% rise, a 50% rise or a doubling of serum creatinine concentration, it is clear that this is a common complication of cardiac catheterisation. In the recent epidemiological report by McCullough and colleagues, 1826 unselected patients undergoing coronary intervention were found to have a 14.5% incidence of acute contrast induced renal failure as defined by a 25% rise in serum creatinine.2 This may seem a relatively small decline in renal function but it has important consequences in terms of prolonged in-patient stay and cost.3 More severe derangements in renal function increase morbidity, mortality, and the risk of developing end stage renal failure.3 ,4 Of the McCullough group, 7.7 per 1000 required renal replacement therapy, an outcome that was associated with a 36% in-hospital mortality and a two year survival of less than 20%. The incidence of RCIN is likely to be higher following interventional procedures than after angiography alone but is certainly not confined to the former.
Patients at highest risk
The pathogenesis of RCIN is likely complex.5Currently, it is widely accepted that ischaemic damage to the renal medulla and a direct toxic effect of contrast medium upon renal tubular cells is of importance. Patients most …