![]() Of these patients, only seven confirmed cases of NSF occurred after 2008 ( 22). ( 21) demonstrated no new cases of NSF among 52,954 contrast-enhanced magnetic resonance examinations, including 6490 patients with an eGFR 0.1 mmol/kg). However, they remain absolutely contraindicated in patients with AKI or stage 4 or 5 CKD (eGFR <30 ml/min per 1.73 m 2).ĪCR, American College of Radiology CAR, Canadian Association of Radiologists.Īfter becoming aware of NSF in patients with severe renal disease and its association with GBCAs, many institutions adopted restrictive policies regarding the use of GBCAs and several studies demonstrated a significant decline in incidence of NSF ( 18–20). Several studies have shown that use of these lower-stability GBCAs in patients with normal kidney function or mild-to-moderate CKD (stage 3 eGFR 30–59 ml/min per 1.73 m 2) is without clinically significant risk of NSF ( 8). These three GBCAs are now classified as “group 1” agents by the American College of Radiology (ACR) and “high-risk” agents by the Canadian Association of Radiology (CAR) ( Table 1). This theory was proposed in part because of the strong association of NSF with lower-stability linear nonionic GBCAs gadoversetamide and gadodiamide, and an ionic linear agent gadopentetate dimeglumine ( 17). The most prevalent belief is that delayed clearance of GBCAs allows gadolinium to dissociate from the chelating agent and deposit in tissue ( 17), resulting in fibrous connective tissue and plaque formation. Based on clinical reports, the most important factor appears to be severely reduced renal function. Multiple factors may contribute, most notably patient-specific risk factors and the stability of the GBCA, which is a result of its molecular structure. It is unclear if this could at least partially relate to interspecies differences. Conversely, patients with only one administration of a GBCA have developed NSF ( 15, 16). A confounding issue is that many people with severe kidney disease received multiple exposures to GBCAs and did not develop NSF. Several mouse models of NSF have been developed to investigate the underlying pathophysiology however, they tend to use doses which are higher than those approved by the FDA and older linear agents ( 12–14). A conclusive mechanism of causation for NSF has not been determined. NSF results in fibrosis of the skin and internal organs and can be fatal. The safety of GBCAs in patients with kidney disease came into question in 2006 when a strong association was found between the use of GBCAs in patients with severe kidney disease and the development of nephrogenic systemic fibrosis (NSF) ( 9–11). Although some case reports have linked AKI to GBCA administration, most cases involve patients with advanced renal disease or diabetes and with doses that exceed US Food and Drug Administration (FDA) recommendations ( 8). Initially, it was thought that GBCAs would be safer than iodinated contrast media for patients with kidney disease because they are less nephrotoxic at clinically administered doses ( 8). Numerous studies have demonstrated the benefit of GBCAs for a variety of diagnostic indications including improving sensitivity and specificity for malignancy, demyelination, central nervous system malignancy, and infection ( 3–7). Gadolinium-based contrast agents (GBCAs) have been used for contrast-enhanced magnetic resonance imaging (MRI) since 1988 with >450 million intravenous GBCA doses administered worldwide and overall have had an excellent safety record ( 1, 2).
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