More contrast, no more brightness

Although the mechanism of contrast-induced nephropathy (CIN) is not known [1], experimental data suggest that it is secondary to arteriolar vasoconstriction mediated by endothelin 1 in response to the delivery of a large hyperosmotic contrast material to the juxtaglomerular apparatus [2]. Although a transient rise in serum creatinine greater than 1 mg/dL occurs in at least 5% of patients undergoing angiography [3], worsening in renal function can occur in up to 40% of patients when risk factors are present, such as prior renal impairment, diabetes (especially in combination), decreased cardiac output sates, volume depletion, hyperuricemia, anemia, hypertension, proteinuria, multiple myeloma, the administration of certain drugs such as gentamycin, angiotensin-converting enzyme inhibitors and nonsteroidal anti-inflammatory agents, and an amount of total contrast volume over 3 mL/Kg [4–8]. Clinically, CIN presents as an increase in serum creatinine, occurring 24 to 48 hr after angiography, peaking over 3–5 days, with complete slow resolution over 7–10 days in 75% of the cases [9]. However, renal function may not return to its baseline level, with some patients (10%) requiring even permanent dialysis [9,10], all of which carries an increased risk of death [11]. It must be differentiated from the renal failure due to cholesterol embolization, which appears weeks or months following cardiac catheterization [8]. On the other hand, although there is a growing concern about the appearance and prevention of CIN, mainly high-risk patients have been analyzed [12,13] and there has been little emphasis about its occurrence in those patients with normal renal function prior to the administration of contrast media. In this issue, Lindsay et al. report the retrospective single-center analysis of 5,967 consecutive patients who underwent successful PCI with no major in-hospital complications and normal pre-PCI renal function, followed-up for 1 year. A serum creatinine rise (SCr) 50% of baseline was found in 208 patients (3.5%), and of these only 3 (1.4%) required temporary dialysis. These patients with SCr more often reported hypertension and diabetes mellitus; a greater number of stenoses were treated, a significantly larger amount of contrast agent was used, and more extracoronary vascular disease was present. Other independent predictors of SCr were hemodynamic instability (pulmonary edema) in the periprocedural period and complications of the PCI including a neurological episode or entry site complication requiring surgical repair. The most important contribution of this study is that as previously reported in patients with decreased renal function [14], those patients with normal pre-PCI renal function who developed an SCr 50% of baseline had an increased late (1 year) mortality, as well as a higher incidence of myocardial infarction and need for target vessel revascularization. A possible mechanism to account for this finding is that a normal baseline creatinine does not rule out an occult renal dysfunction, which has been associated with increased late adverse events, even when the renal insufficiency is mild [15]. Of interest is that the need for dialysis was temporary, only in 0.05% of the total group and in 1.4% of those with an SCr. Other factor to be considered in the development of CIN in patients undergoing angiography is the osmolarity of the contrast medium used. Ninety-five percent of patients in the study by Lindsay et al. received lowosmolar contrast medium. Recently, the use of a specific iso-osmolar contrast medium, Iodixanol, in patients with diabetes and elevated baseline creatinine undergoing coronary or aortofemoral angiography, produced a much lower SCr when compared with other low-osmolar contrast media [16]. Although other prophylactic measures have been advocated to reduce the incidence of CIN such as the periprocedural administration of N-acetylcysteine [17] or fenoldopam [12,18], these agents offered no additional benefit than hydration with saline alone in high-risk patients [13]. Isotonic hydration reduces CIN more than half-isotonic hydration in patients undergoing PCI [19]. In conclusion, according to the results of this unique study, a normal baseline serum creatinine does not rule out the development of CIN in patients undergoing PCI, mainly in high-risk patients and in those who develop periprocedural complications, although its incidence is only 3.5% and the need for dialysis was not permanent.