Nephrogenic Fibrosing Dermopathy and High-Dose Erythropoietin Therapy

Swaminathan, Sundararaman; Ahmed, Iftikhar; McCarthy, James T.; Albright, Robert C.; Pittelkow, Mark R.; Caplice, Noel M.; Griffin, Matthew; Leung, Nelson

doi:10.7326/0003-4819-145-3-200608010-00021

Cited by 115 publications

(87 citation statements)

References 5 publications

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“…To date, it has only been reported in patients with severely impaired renal function (SIRF), endstage renal disease (ESRD), and those in acute renal failure (ARF) (2)(3)(4)(5). The many other risk factors thought to be associated with NSF include: edema (6), metabolic acidosis, thrombotic events, high-dose erythropoietin (EPO) (7,8), systemic inflammation (9), recent surgery, kidney disease (10), and gadolinium (Gd 3þ )-based contrast agent (GBCA) exposure (11,12), especially when used at relatively high dose GBCA (5,13). NSF, which was first recognized by Cowper et al (1) and linked to GBCA in 2006 (11), is characterized by induration, thickening, and tightening of the skin.…”

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confidence: 99%

Mechanism of NSF: New evidence challenging the prevailing theory

Newton¹,

Jimenez

2009

Magnetic Resonance Imaging

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Nephrogenic systemic fibrosis (NSF) has been associated with the administration of gadolinium‐based contrast agents in patients with severely impaired renal function (SIRF), endstage renal disease (ESRD), or acute renal failure (ARF). Since the vast majority of these patients do not get NSF, it is highly likely that patient factors play a role in its development. Although “free” or dechelated gadolinium is thought by some to be the only trigger of NSF, recent evidence suggests that chelated gadolinium may be important. Chelated gadolinium such as Omniscan (gadodiamide) and Magnevist (gadopentetate) can directly stimulate macrophages and monocytes in vitro to release profibrotic cytokines and growth factors capable of initiating and supporting the tissue fibrosis that is characteristic of NSF. In addition, an effect of chelated gadolinium on fibroblasts has also been demonstrated. Chelated gadolinium in the form of Omniscan, Magnevist, MultiHance, and ProHance increased proliferation of human dermal fibroblasts. Indeed, increased numbers of macrophages, together with activated fibroblasts and fibrocytes, are essential cells in the fibrotic process and are present in NSF skin. Accordingly, it is important that chelated gadolinium, in combination with patient cofactors, is considered in the etiology of NSF associated with enhanced scans. J. Magn. Reson. Imaging 2009;30:1277–1283. © 2009 Wiley‐Liss, Inc.

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confidence: 99%

Mechanism of NSF: New evidence challenging the prevailing theory

Newton¹,

Jimenez

2009

Magnetic Resonance Imaging

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“…4,30 In a small cohort, others (W. A. H.) identified an inverse relationship between Gd levels in tissue and relative doses of ESA. These investigators speculated that this might be a result of a ''threshold phenomenon'' for NSF that, potentially, might be reached in a variety of ways (a greater amount of Gd accumulation, or a lesser amount of Gd accumulation with other profibrotic events, eg, high ESA dosing).…”

Section: Discussionmentioning

confidence: 99%

Revisiting nephrogenic systemic fibrosis in 6 kidney transplant recipients: A single-center experience

Lemy

Marmol

Kolivras

et al. 2010

Journal of the American Academy of Dermatology

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“…Related host cofactors have not been identified, though elevated serum calcium and phosphate concentrations, exposure to high dose erythropoietin, and iron overload have been considered. 10,11 The diagnosis of NSF requires compatible clinical findings along with consistent histopathology. Suspicious clinical findings in a patient with underlying kidney disease (AKI, CKD stages 4 and 5) who has been exposed to a GBC agent, should prompt skin biopsy.…”

Section: What Is Nephrogenic Systemic Fibrosis?mentioning

confidence: 99%

Nephrogenic systemic fibrosis: What the hospitalist needs to know

Fine

Perazella

2010

Journal of Hospital Medicine

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Nephrogenic systemic fibrosis (NSF) has now been linked to gadolinium‐based contrast (GBC) exposure in those with compromised kidney function, particularly those with end‐stage renal disease (ESRD). When ESRD is present, symptoms can be quite devastating for the patient including severe pain and immobility and even death. For those at risk, avoidance of GBC exposure, whenever possible, is absolutely essential to prevent this potentially devastating complication. Identifying those at risk depends in some circumstances on appropriate recognition of renal dysfunction and understanding appropriate use of glomerular filtration rate (GFR) estimation formulas. Although hemodialysis (but not peritoneal dialysis) removes gadolinium, the availability of dialysis should never be used as a justification for GBC use in this high‐risk population. Unfortunately there is a lack of a universally effective therapy. Resolution of acute kidney injury (AKI) appears to attenuate disease in most cases, while kidney transplantation has been associated with variable success. Journal of Hospital Medicine 2010;5:46–50. © 2010 Society of Hospital Medicine.

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Nephrogenic Fibrosing Dermopathy and High-Dose Erythropoietin Therapy

Cited by 115 publications

References 5 publications

Mechanism of NSF: New evidence challenging the prevailing theory

Mechanism of NSF: New evidence challenging the prevailing theory

Revisiting nephrogenic systemic fibrosis in 6 kidney transplant recipients: A single-center experience

Nephrogenic systemic fibrosis: What the hospitalist needs to know

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