PURPOSE: To retrospectively analyze nephrogenic systemic fibrosis (NSF) cases at our center, to determine prior gadolinium based contrast agent (GBCA) administration and to evaluate possible common risk factors for the development of NSF by reviewing laboratory data and concurrent medications. MATERIALS AND METHODS: A total of four data bases (pathology, MRI, dialysis, and medical records) were cross-referenced for identification and evaluation of NSF patients. Medical history of NSF patients was assessed as for previous deep venous thrombosis (DVT), surgery, or infections. Laboratory data (creatinine, anion gap, calcium, phosphorus, and albumin) as well as concurrent medication were evaluated. Findings were compared to those of a control group of non-NSF dialysis patients. RESULTS: Between October 2003 and February 2007 a total of nine NSF cases were identified. All patients had undergone contrast-enhanced MRI prior to the diagnosis of NSF. Only one gadolinium chelate had been used at our MRI center (Omniscan, gadodiamide; GE Healthcare). Of nine patients, eight were receiving dialysis at the time of the MRI scan. During the same time 312 dialysis patients received gadodiamide. Thus, the prevalence of NSF within dialysis patients exposed to gadodiamide was 2.6%. NSF patients presented with a higher creatinine and anion gap than the control patients. Other laboratory values as well as medication did not show a significant difference. There were no patterns regarding previous history of DVT, surgery, or infection in the NSF group. CONCLUSION: Our findings are consistent with the previously reported association between gadodiamide exposure and NSF. All NSF patients had severe renal insufficiency with glomerular filtration rate (GFR) < 30 (highest GFR = 25 mL/minute) at the time of last gadodiamide administration, and on average had received 71 mL of gadodiamide over an average of 2.9 administrations.
PURPOSE: To retrospectively analyze nephrogenic systemic fibrosis (NSF) cases at our center, to determine prior gadolinium based contrast agent (GBCA) administration and to evaluate possible common risk factors for the development of NSF by reviewing laboratory data and concurrent medications. MATERIALS AND METHODS: A total of four data bases (pathology, MRI, dialysis, and medical records) were cross-referenced for identification and evaluation of NSF patients. Medical history of NSF patients was assessed as for previous deep venous thrombosis (DVT), surgery, or infections. Laboratory data (creatinine, anion gap, calcium, phosphorus, and albumin) as well as concurrent medication were evaluated. Findings were compared to those of a control group of non-NSF dialysis patients. RESULTS: Between October 2003 and February 2007 a total of nine NSF cases were identified. All patients had undergone contrast-enhanced MRI prior to the diagnosis of NSF. Only one gadolinium chelate had been used at our MRI center (Omniscan, gadodiamide; GE Healthcare). Of nine patients, eight were receiving dialysis at the time of the MRI scan. During the same time 312 dialysis patients received gadodiamide. Thus, the prevalence of NSF within dialysis patients exposed to gadodiamide was 2.6%. NSF patients presented with a higher creatinine and anion gap than the control patients. Other laboratory values as well as medication did not show a significant difference. There were no patterns regarding previous history of DVT, surgery, or infection in the NSF group. CONCLUSION: Our findings are consistent with the previously reported association between gadodiamide exposure and NSF. All NSF patients had severe renal insufficiency with glomerular filtration rate (GFR) < 30 (highest GFR = 25 mL/minute) at the time of last gadodiamide administration, and on average had received 71 mL of gadodiamide over an average of 2.9 administrations.
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