Abstract
Gadolinium-based contrast media (GBCM) toxicity in patients with kidney disease is a concern for the possible development of systemic nephrogenic fibrosis and possible renal complications. This review focuses on the pathological mechanisms underlying the potential kidney toxicity of gadolinium. Gadolinium, as a free compound (Gd3+), is highly toxic in humans because it competes with divalent calcium (Ca2+) and magnesium (Mg2+) ions, interfering in some relevant biologic processes. Its toxicity is blunted by the complexing of Gd3+ with a carrier, allowing its use in magnetic resonance imaging. The binding reaction between gadolinium and a carrier is thermodynamically reversible. Consequently, under some conditions, gadolinium can be released in the interstitial space as a free Gd3+ compound with the possibility of toxicity. Other metals such as iron, copper, and calcium can interfere with the binding between gadolinium and its carrier because they compete for the same binding site. This process is known as transmetallation. In patients with kidney impairment, conditions such as low clearance of the Gd-carrier complex, acid-base derangements, and high serum phosphorous can increase the presence of free Gd3+, leading to a higher risk for toxicity.
Highlights
Gadolinium is used as a contrast media agent in magnetic resonance imagining (MRI).Until recently, gadolinium-based contrast media (GBCM) was considered to have a low risk of nephrotoxicity or other side effects
This concern for toxicity was largely related to the association of nephrogenic systemic fibrosis (NSF) in patients with kidney impairment [2] and with its potential nephrotoxicity [3,4,5]
This review explores the pathological aspects of GBCM toxicity and analyses reports showing how new biomarkers of kidney damage could reveal gadolinium-induced nephrotoxicity
Summary
Gadolinium is used as a contrast media agent in magnetic resonance imagining (MRI). Until recently, gadolinium-based contrast media (GBCM) was considered to have a low risk of nephrotoxicity or other side effects. Some reports have demonstrated the potential toxicity of GBCM, especially in patients with kidney impairment [1]. In some conditions such as kidney impairment, a subclinical kidney injury may occur where there is a lack of serum creatinine rise. This injury may decrease kidney reserve and, over time, may manifest as clinically evident chronic kidney disease (CKD). This review explores the pathological aspects of GBCM toxicity and analyses reports showing how new biomarkers of kidney damage could reveal gadolinium-induced nephrotoxicity
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