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Original Research |
1 Department of Radiology, Loma Linda University Medical Center, 11234 Anderson
St., MC Room 2605, Loma Linda, CA 92354.
2 Department of Surgery, Transplant Division, Loma Linda University Medical
Center, Loma Linda, CA.
3 Department of Medicine, Nephrology Division, Loma Linda University Medical
Center, Loma Linda, CA.
Received August 16, 2006;
accepted after revision November 21, 2006.
Address correspondence to D. R. Broome.
Abstract
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MATERIALS AND METHODS. A retrospective chart review was performed for all 12 patients diagnosed with NSF at our institution between 2000 and 2006 to identify the clinical manifestations, timing, and dose of gadodiamide administration; dialysis records; concurrent medications; comorbid conditions and surgeries; laboratory findings; imaging findings; and clinical outcome. A review of the dialysis and MR records between 2000 and 2006 showed 559 MRI examinations on 168 dialysis patients (including 301 contrast-enhanced examinations).
RESULTS. NSF was diagnosed by clinical findings and tissue diagnosis. All 12 patients had renal insufficiency—eight with dialysis-dependent chronic renal insufficiency and four with acute hepatorenal syndrome. All 12 patients developed skin fibrosis within 2-11 weeks after gadodiamide administration. The odds ratio for development of NSF after gadodiamide exposure was 22.3. No other common event or exposure could be found. Four patients had abnormal scintigraphic bone scans with skin and muscle uptake and lower-extremity MRI finding of edema in the muscles, intermuscular fascia, and skin. Despite the fact that 10 patients were dialyzed within 2 days of gadodiamide administration, this did not prevent the development of NSF.
CONCLUSION. Development of NSF was strongly associated with gadodiamide administration in the setting of either acute hepatorenal syndrome or dialysis-dependent chronic renal insufficiency.
Keywords: dialysis • MR contrast agents • MR imaging • nephrogenic systemic fibrosis • nuclear medicine • renal disease
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In this article, we present a retrospective chart review of 12 patients with NSF at our institution, all of whom received IV double-dose gadodiamide 2-11 weeks before the development of skin fibrosis.
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The names of all patients receiving inpatient and outpatient dialysis at our medical center from January 2000-August 2006 were entered into our PACS system to determine how many had undergone MRI examinations either with or without contrast enhancement. During this time, only one gadolinium-based contrast medium, gadodiamide, was administered to patients at our institution. The contrast dose (0.1 or 0.2 mmol/kg) and body part imaged were recorded. Nearly all the abdominal and pelvic MRI examinations included an MR angiogram and were dosed at 0.2 mmol/kg. Nearly all the remaining MRI examinations were dosed at 0.1 mmol/kg during this time period. The prevalence, likelihood ratio, and odds ratio for developing NSF after gadodiamide exposure compared with unenhanced MRI examinations were calculated using a 2 x 2 contingency table. The likelihood ratio and odds ratio for developing NSF after double-dose (0.2 mmol/kg) gadodiamide administration compared with single dose (0.1 mmol/kg) administration also was calculated using a 2 x 2 contingency table.
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Six patients had a vascular surgery performed within a 17-day period after gadodiamide injection, including liver transplantation (four patients), arteriovenous graft revision (one patient), and thrombectomy of renal transplant and right external iliac vein thrombus (one patient). A left thigh fasciotomy was performed on one patient for suspected necrotizing fasciitis 4 weeks after gadodiamide injection. Two patients had acute venous thrombosis including the patient who required arteriovenous graft revision and the patient who required renal transplant venous thrombectomy. Two other patients had systemic lupus erythematosus with antiphospholipid syndrome and history of recurrent deep venous thrombosis, but no episode of acute deep venous thrombosis in the interval between IV gadodiamide injection and development of NSF symptoms. Evaluation of the patient medications taken at time of gadodiamide injection and during the interval before the development of disease symptoms showed no common medications among the patients. However, six patients were taking prednisone during this time interval, and six patients were on erythropoietin. Two patients had previously received gadodiamide for MRI examinations before they were on dialysis and did not subsequently develop NSF with those exposures. Five patients received a second IV injection of gadodiamide 1-2 months after the primary exposure but after the onset of clinical symptoms of NSF. None of the NSF patients received any other gadolinium-based contrast material at our facility or any other MRI facility in the 3 months before their development of skin fibrosis.
Signs and symptoms of NSF were divided into early (< 2 weeks after the gadodiamide injection) and late (2-11 weeks after the gadodiamide injection). Most signs and symptoms described were bilateral and symmetric, usually starting in the peripheral extremities and spreading proximally. Lower extremity involvement was noted in all 12 patients, and upper extremity involvement was seen in eight patients. Three patients had abdominal wall involvement, but none had face or neck involvement. Early signs or symptoms were seen in all patients, most frequently consisting of extremity edema or swelling (eight patients), arthralgia or myalgia (four patients), and extremity weakness (three patients). These nonspecific signs and symptoms were difficult to prospectively attribute to the gadodiamide because they may be seen with renal failure and other coexisting medical conditions. Late signs and symptoms consisted of persistent skin fibrosis changes in the extremities described as woody induration, skin tightness, or skin thickening. These findings developed in 11 patients between 2 and 8 weeks after gadodiamide injection and in one patient 11 weeks after gadodiamide injection. The skin findings showed slightly raised and erythematous or brawny nodular plaques, linear striations, or confluent regions of fibrosis (Fig. 1A). Seven patients developed contractures or symptoms described as stiffness in both lower and/or upper extremities (Fig. 1B). An additional four patients developed extremity myopathy/weakness during this latent period.
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Abnormal imaging findings on bone scintigraphy and extremity MRI would suggest that NSF is a systemic disorder of connective tissue involving skeletal muscle, skin, and tendons. Four patients underwent whole-body bone scans using 99mTc HDP (hydroxymethylene diphosphonate) performed 6-8 weeks after gadodiamide administration. The scans, obtained at 2-3 hours, showed symmetric increased uptake in the muscles, tendons, and skin (Figs. 2A, 3A, and 3B). Peripheral upper-extremity uptake was noted in three patients. There was also abdominal wall uptake in one patient and chest wall uptake in another patient. These same four patients also had MRI examinations of the lower extremities that showed skin thickening and an edematous pattern of low T1 signal and high T2 signal throughout the skeletal muscle, inter-muscular fascia, and skin (Figs. 2B and 2C). The MRI findings were thought to represent a polymyositis process, although myonecrosis was found on four patients who underwent muscle biopsy. One patient developed such severe myositis and asymmetric swelling in the left thigh that a fasciotomy was performed for suspected necrotizing fasciitis. However, bacterial cultures of this region revealed no organism, and a muscle biopsy revealed severe myonecrosis. One day later the patient developed similar symptoms in the right thigh. Because of the bilateral involvement, negative cultures, and slow disease progression, this was felt to represent NSF with the subsequent development of persistent skin fibrosis/thickening (Fig. 2A, 2B, 2C).
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A total of 559 MRI examinations were performed on 168 dialysis patients at our institution between January 2000 and August 2006. This included 301 gadodiamide-enhanced and 258 unenhanced MRI examinations. From a 2 x 2 contingency table (12 NSF cases among 301 gadodiamide-exposed cases, zero NSF cases among the 258 gadodiamide-unexposed patients), the odds ratio (Haldane's estimator) was 22.3 (95% confidence interval, 1.3-378.9) and the likelihood ratio was 1.89 (95% confidence interval, 1.75-2.05). The prevalence of NSF among the gadodiamide-exposed dialysis patients was 4.0%. Of the 301 patients who underwent gadodiamide-enhanced MR examinations, 207 of the examinations were performed with 0.2 mmol/kg of gadodiamide (of which 12 patients later developed NSF), and 94 were performed with 0.1 mmol/kg (of which none developed NSF). Using a 2 x 2 contingency table (with all 12 NSF cases with double dosing and 195 double-dosed cases and 94 single-dosed cases without NSF) the odds ratio and likelihood ratio for development of NSF with double-dose compared with single-dose gadodiamide administration were 12.1 (95% confidence interval, 0.7-206.2) and 1.48 (95% confidence interval, 1.36-1.61) patients, respectively.
The clinical outcome of the 12 NSF patients included three patients with severe long-term inability to ambulate due to contractures and myopathy—two wheelchair-bound and the third bedridden. The latter patient developed progressive severe skin ulcerations and died from liver failure from severe recurrent hepatitis C five months after the onset of NSF. One patient had worsening of a severe disability from limited to full-time wheelchair requirement. Four patients had mild disability and required a cane to ambulate for a short period of time. The remaining patients had no disability, although skin changes have persisted to variable degrees depending on therapy.
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One intriguing model for the pathogenesis of NSF has been proposed by Cowper et al. [12] and states that a combination of events leads to the development of NSF beginning with renal disease, followed by allergen deposition leading to circulating fibrocyte deposition, a dominant cell found in the histopathologic examination of skin in patients with NSF and considered to be a main actor in wound healing and fibrosis. The suggestion that endothelial damage and elevated levels of cytokines may lead to development of the disease is supported by the fact that eight of our 12 patients had either undergone vascular surgery, experienced deep venous thrombosis, or had coagulopathies within the interval between gadodiamide injection and development of skin fibrosis. The imaging findings of skin, muscle, and tendon uptake of bone scintigraphy agents in this study are likely due to the deposition and activity of fibrocytes within these tissues. The MRI findings of low T1 and T2 signal skin thickening are consistent with the dermal fibrosis noted on skin histology. Although the extremity MRI muscle findings of low T1 and high T2 signal may represent a myositis response, more likely they represent myonecrosis based on the few muscle biopsy results in this study. Although the bone scan and extremity MRI findings are nonspecific and were noted after the onset of skin fibrosis, they may be useful studies to confirm the development of NSF. However, the definitive method of diagnosis of NSF is clinical assessment and a deep skin biopsy sufficient to sample the dermis, subcutaneous fat, and fascia. Most of the dermal spindle cells will stain positive for CD34 and procollagen I. This profile is identical to the immunohistochemical profile of the circulating fibrocyte [13].
Five different gadolinium chelates have received U.S. Food and Drug Administration (FDA) approval as paramagnetic MR contrast agents for central nervous system and (in some cases) body imaging indications, but none specifically for MR angiography indications. IV gadolinium at standard doses of 0.1 mmol/kg has been shown to be a safe contrast agent with relatively few adverse reactions in healthy and renally impaired patients—with minor reactions in approximately 3-4% of patients and severe reactions (< 1% of patients) according to the package inserts. Double and even triple dosing of gadodiamide has been reported to be safe with a similar incidence of adverse reactions as the standard dose (0.1 mmol/kg) [14]. Gadoteridol (FDA approved in 1992) and gadodiamide (FDA approved in 1993) have subsequently received FDA approval for double and triple dosing, which has become increasingly popular for abdominal MRI and many MR angiography examinations. It is interesting to note that the onset of first reported cases of NSF in 1997 coincides closely with the rapid rise in the use of high-dose gadolinium injection for MRI and MR angiography in the last decade. The first Medline-indexed article describing the use of gadolinium-enhanced MR angiography in renal patients was also published in 1997 [15]. To date, the only gadolinium-based contrast agent reported to be associated with NSF is gadodiamide. However, the reporting of this association is still quite immature and other gadolinium agents may be found to have a similar association.
Marckmann et al. [11] have postulated that NSF may result from a toxic reaction from free gadolinium (Gd3+), liberated from the chelate but not adequately excreted due to impaired renal function. Transmetallation, the release of free gadolinium from the chelate and subsequent binding to endogenous ions, is dependent on the molecular conditional thermodynamic stability. Gadolinium contrast media with lower conditional stability constant values would be more likely to undergo transmetallation. The conditional stability constants (at a pH of 7.4) of the FDA-approved major contrast agents are: gadodiamide, 1014.9; gadoversetamide, 1015.0; gadoteridol, 1017.1; gadopentetate dimeglumine, 1018.1; and gadobenate dimeglumine, 1018.4 [16, 17]. If this postulate is true, contrast media such as gadodiamide and gadoversetamide, which have 1,000-fold lower conditional stability constants than the more stable gadolinium chelates, would be more likely to release free gadolinium and result in NSF. To minimize the risk of release of free gadolinium, contrast manufacturers have added additional chelate to bind the free gadolinium. The excess chelate content (according to the latest U.S. package inserts) of FDA-approved gadolinium contrast agents are as follows: gadodiamide (12 mg/mL), gadoversetamide (28.4 mg/mL), gadoteridol (0.23 mg/mL), gadopentetate (0.4 mg/mL), and gadobenate (0 mg/mL). Although some have theorized that the excess chelate with gadodiamide may contribute to the higher incidence of NSF [11], more likely the excess chelate has a protective effect in binding the free gadolinium.
MRI and MR angiography examinations are commonly requested for patients with endstage liver and renal disease to evaluate for transplant eligibility, visualization of vascular anatomy, and posttransplant complications. Gadolinium-enhanced MRI traditionally has been preferred over contrast-enhanced CT because many of these patients have impaired renal function. Gadolinium-based contrast media (at doses of 0.1-0.2 mmol/kg) are considered less nephrotoxic than iodinated contrast agents [18], although there is considerable controversy in the literature regarding the safety of gadolinium-based contrast media administered to patients with renal failure [19]. Despite numerous studies on the safety of gadolinium-based contrast agents in renal insufficiency and dialysis patients, none has reported NSF as a complication before Grobner's study [10]. Our study also confirmed that dialysis patients are at significant risk for the development of NSF when gadodiamide is administered: The prevalence rate is 4% and the odds ratio is 22.3. The risk was significantly higher when a 0.2 mmol/kg dose of gadodiamide was administered. Also, our study showed that NSF can develop when gadodiamide is administered in the setting of acute renal failure. All of our acute renal failure NSF patients had hepatorenal syndrome and subsequently underwent liver transplantation within a 17-day interval after gadodiamide administration. Several publications have confirmed that liver transplant patients are particularly prone to the development of NSF [5, 20]. For this reason, caution should be exercised in performing gadodiamide-enhanced MRI examinations in patients with acute hepatorenal syndrome in the immediate pre- or post-liver transplant period.
NSF is a disfiguring and potentially debilitating disease without a consistently effective treatment or prevention regimen. In the Danish study, seven of 13 patients were severely disabled and one died [11]. In our study, four of the 12 patients developed severe ambulatory disability and four patients developed short-term ambulatory disability. Plasmapheresis has been used with some success at our institution to treat NSF [5]. Other treatment options such as extracorporeal photopheresis, physical therapy, oral corticosteroids, oral pentoxifylline, and ultraviolet therapy have been tried with anecdotal success [2]. In the recent Public Health Advisory, the FDA stated that it may be prudent to institute prompt dialysis to prevent NSF in patients with advanced kidney dysfunction who receive gadolinium contrast [9]. Several reports have shown that 68% of gadolinium is eliminated after a 3-hour dialysis session and approximately 98% after three consecutive dialysis sessions [21]. In our study, three patients had received daily dialysis for three consecutive days starting on the day of gadodiamide administration. Theoretically the dialysis should have removed up to 98% of the injected gadodiamide in these patients, but dialysis did not prevent their developing NSF. It is probable that the gadodiamide-triggered event occurs quite rapidly in patients with renal insufficiency and is not reversed by hemodialysis. It is somewhat impractical to schedule patients for immediate dialysis after injection of gadodiamide to attempt to prevent this disorder. Further studies will need to be performed to study the efficacy of immediate dialysis in preventing NSF.
In June 2006, the FDA issued a public health advisory concerning the use of high-dose gadolinium-containing contrast agents in patients with advanced renal failure [9]. Because of the association of NSF with the use of IV gadodiamide, our institution has adopted a policy regarding the use of gadodiamide in renal insufficiency patients until more medical research becomes available: We are no longer administering IV gadodiamide to dialysis patients or end-stage renal disease patients with a creatinine clearance of < 15 mL/min. We also are avoiding double- or triple-dose injections of gadodiamide, and we are exercising caution in administering gadodiamide to patients with acute renal failure, particularly with hepatorenal syndrome. Our department has begun screening patients scheduled for contrast-enhanced MRI examinations by obtaining a recent serum creatinine level and calculated creatinine clearance if they have a history of kidney disease or diabetes mellitus. Inpatients older than 60 years also will have their serum creatinine and calculated creatinine clearance checked before gadodiamide administration.
Given the limited reporting of the association of NSF with gadolinium-based contrast, a cause-and-effect linkage has not yet been proven. There will be a tremendous pressure among researchers to associate all cases of NSF with gadolinium-based contrast. This could inaccurately link specific MR contrast agents to NSF. Future reporting of this association should adhere to certain reasonable research criteria, as we have done. The diagnosis of NSF should be confirmed by skin biopsy and should not be based solely on clinical manifestations. The specific MR contrast agent should be documented in the contrast administration records and should not simply be inferred. The temporal relationship of contrast administration and development of NSF should be documented and should likely conform to the time period of 2 weeks to 3 months reported in this and other series. The possibility that patients may have been exposed to multiple MR contrast agents during the 3-month period should be verified, including those administered at other facilities.
In conclusion, NSF is a disfiguring and potentially disabling or fatal disorder that appears to be strongly associated with or triggered by IV injection of double-dose gadodiamide for MRI and MR angiography examinations in patients with acute or chronic renal insufficiency who are usually, but not always, on dialysis. NSF can show abnormal soft uptake of bone scintigraphy agents and abnormal MR signal in the muscles and skin of the extremities and less commonly the torso. Dialysis following the administration of gadodiamide did not appear to prevent the development of NSF in our patients.
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L. P. Golding and J. M. Provenzale Nephrogenic Systemic Fibrosis: Possible Association with a Predisposing Infection Am. J. Roentgenol., April 1, 2008; 190(4): 1069 - 1075. [Abstract] [Full Text] [PDF]
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G. Soulez, M. Pasowicz, G. Benea, L. Grazioli, J. P. Niedmann, M. Konopka, P. C. Douek, G. Morana, F. K. W. Schaefer, A. Vanzulli, et al. Renal Artery Stenosis Evaluation: Diagnostic Performance of Gadobenate Dimeglumine-enhanced MR Angiography--Comparison with DSA Radiology, April 1, 2008; 247(1): 273 - 285. [Abstract] [Full Text] [PDF]
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W. M. Shabana, R. H. Cohan, J. H. Ellis, H. K. Hussain, I. R. Francis, L. D. Su, S. K. Mukherji, and R. D. Swartz Nephrogenic Systemic Fibrosis: A Report of 29 Cases Am. J. Roentgenol., March 1, 2008; 190(3): 736 - 741. [Abstract] [Full Text] [PDF]
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 N. ISSA, E. D. POGGIO, R. A. FATICA, R. PATEL, P. M. RUGGIERI, and R. J. HEYKA Nephrogenic systemic fibrosis and its association with gadolinium exposure during MRI Cleveland Clinic Journal of Medicine, February 1, 2008; 75(2): 95 - 111. [Abstract] [Full Text] [PDF]
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M. Horger, G. Fierlbeck, J. Kuemmerle-Deschner, N. Tzaribachev, M. Wehrmann, C. D. Claussen, and J. Fritz MRI Findings in Deep and Generalized Morphea (Localized Scleroderma) Am. J. Roentgenol., January 1, 2008; 190(1): 32 - 39. [Abstract] [Full Text] [PDF]
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C. U. Herborn, V. M. Runge, D. M. Watkins, J. M. Gendron, and L. G. Naul MR Angiography of the Renal Arteries: Intraindividual Comparison of Double-Dose Contrast Enhancement at 1.5 T with Standard Dose at 3 T Am. J. Roentgenol., January 1, 2008; 190(1): 173 - 177. [Abstract] [Full Text] [PDF]
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J. R. Leyendecker, C. E. Barnes, and R. J. Zagoria MR Urography: Techniques and Clinical Applications RadioGraphics, January 1, 2008; 28(1): 23 - 46. [Abstract] [Full Text] [PDF]
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J. R. Dillman, J. H. Ellis, R. H. Cohan, P. J. Strouse, and S. C. Jan Frequency and Severity of Acute Allergic-Like Reactions to Gadolinium-Containing IV Contrast Media in Children and Adults Am. J. Roentgenol., December 1, 2007; 189(6): 1533 - 1538. [Abstract] [Full Text] [PDF]
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 A. Kahana, M. J. Lucarelli, A. M. Grayev, J. J. Van Buren, C. N. Burkat, and L. R. Gentry Noninvasive Dynamic Magnetic Resonance Angiography With Time-Resolved Imaging of Contrast KineticS (TRICKS) in the Evaluation of Orbital Vascular Lesions Arch Ophthalmol, December 1, 2007; 125(12): 1635 - 1642. [Abstract] [Full Text] [PDF]
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 L A Ratnam, S R Nelson, and A M Belli Investigating progressive unexplained renal impairment and hypertension BMJ, November 24, 2007; 335(7629): 1094 - 1096. [Full Text] [PDF]
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J. L. Nortier and V. del Marmol Nephrogenic systemic fibrosis the need for a multidisciplinary approach Nephrol. Dial. Transplant., November 1, 2007; 22(11): 3097 - 3101. [Full Text] [PDF]
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D. G. Lohan, F. Barkhordarian, R. Saleh, M. Krishnam, N. Salamon, S. G. Ruehm, and J. P. Finn MR Angiography at 3 T for Assessment of the External Carotid Artery System Am. J. Roentgenol., November 1, 2007; 189(5): 1088 - 1094. [Abstract] [Full Text] [PDF]
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S. Thurnher, S. Miller, G. Schneider, C. Ballarati, G. Bongartz, C. U. Herborn, S. Schoenberg, M. A. Cova, G. Morana, K. Niazi, et al. Diagnostic Performance of Gadobenate Dimeglumine Enhanced MR Angiography of the Iliofemoral and Calf Arteries: A Large-Scale Multicenter Trial Am. J. Roentgenol., November 1, 2007; 189(5): 1223 - 1237. [Abstract] [Full Text] [PDF]
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M. Shiehmorteza, R. F. Hanna, and M. S. Middleton Can Gadopentetate Dimeglumine Be Safely Administered More Rapidly Than the FDA-Approved Injection Rate for Liver Imaging? Am. J. Roentgenol., October 1, 2007; 189(4): W231 - W231. [Full Text] [PDF]
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D. R. Broome, A. C. Cottrell, and E. Kanal Response to "Will Dialysis Prevent the Development of Nephrogenic Systemic Fibrosis After Gadolinium-Based Contrast Administration?" Am. J. Roentgenol., October 1, 2007; 189(4): W234 - W235. [Full Text] [PDF]
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T. A. Collidge, P. C. Thomson, P. B. Mark, J. P. Traynor, A. G. Jardine, S. T. W. Morris, K. Simpson, and G. H. Roditi Gadolinium-enhanced MR Imaging and Nephrogenic Systemic Fibrosis: Retrospective Study of a Renal Replacement Therapy Cohort Radiology, October 1, 2007; 245(1): 168 - 175. [Abstract] [Full Text] [PDF]
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 S. Swaminathan and S. V. Shah New Insights into Nephrogenic Systemic Fibrosis J. Am. Soc. Nephrol., October 1, 2007; 18(10): 2636 - 2643. [Abstract] [Full Text] [PDF]
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R. J. Gibbons, P. A. Araoz, and E. E. Williamson The Year in Cardiac Imaging J. Am. Coll. Cardiol., September 4, 2007; 50(10): 988 - 1003. [Full Text] [PDF]
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T. C. Lauenstein, K. Salman, R. Morreira, T. Heffron, J. R. Spivey, E. Martinez, P. Sharma, and D. R. Martin Gadolinium-Enhanced MRI for Tumor Surveillance Before Liver Transplantation: Center-Based Experience Am. J. Roentgenol., September 1, 2007; 189(3): 663 - 670. [Abstract] [Full Text] [PDF]
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G. Saab, A. Abu-Alfa, E. A. Sadowski, and A. Djamali Are Patients with Moderate Renal Failure at Risk for Developing Nephrogenic Systemic Fibrosis? Radiology, September 1, 2007; 244(3): 930 - 932. [Full Text] [PDF]
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G. Saab and A. Abu-Alfa Will Dialysis Prevent the Development of Nephrogenic Systemic Fibrosis After Gadolinium-Based Contrast Administration? Am. J. Roentgenol., September 1, 2007; 189(3): W169 - W169. [Full Text] [PDF]
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P. C Thomson, T. A Collidge, P. B Mark, and J. P Traynor Gadolinium contrast may be risky in kidney disease BMJ, June 30, 2007; 334(7608): 1335 - 1336. [Full Text] [PDF]
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R. J. Stanley Our Practice of Radiology: Reflections on its Growth and Stature Am. J. Roentgenol., June 1, 2007; 188(6): 1439 - 1439. [Full Text] [PDF]
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E. Kanal, A. J. Barkovich, C. Bell, J. P. Borgstede, W. G. Bradley Jr., J. W. Froelich, T. Gilk, J. R. Gimbel, J. Gosbee, E. Kuhni-Kaminski, et al. ACR Guidance Document for Safe MR Practices: 2007 Am. J. Roentgenol., June 1, 2007; 188(6): 1447 - 1474. [Full Text] [PDF]
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H. S. Thomsen and S. K. Morcos Nephrogenic Systemic Fibrosis and Nonionic Linear Chelates Am. J. Roentgenol., June 1, 2007; 188(6): W580 - W580. [Full Text] [PDF]
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D. R. Broome and M. S. Girguis Reply Am. J. Roentgenol., June 1, 2007; 188(6): W581 - W581. [Full Text] [PDF]
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Y.-Y. Ng, R.-C. Lee, S.-H. Shen, and G. Kirk Gadolinium-Associated Nephrogenic Systemic Fibrosis: Double Dose, Not Single Dose Am. J. Roentgenol., June 1, 2007; 188(6): W582 - W582. [Full Text] [PDF]
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D. R. Broome and M. S. Girguis Reply Am. J. Roentgenol., June 1, 2007; 188(6): W583 - W583. [Full Text] [PDF]
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S. J. Karlik Gadodiamide-Associated Nephrogenic Systemic Fibrosis Am. J. Roentgenol., June 1, 2007; 188(6): W584 - W584. [Full Text] [PDF]
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H. P. Forman Back to the Beginning Am. J. Roentgenol., February 1, 2007; 188(2): 295 - 296. [Full Text] [PDF]
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