Contrast Medium Induced Nephropathy: Animal Experiments

Thomsen, Henrik S.; Golman, Klaes; Hemmingsen, Lars; Larsen, Svend; Skaarup, P.; Svendsen, Ove

doi:10.1007/978-3-642-77369-3_5

Cited by 22 publications

(7 citation statements)

References 43 publications

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“…Reverse movement from the extracellular space into the intravascular compartment occurs, and a state of equilibrium is generally reached within 2 h. Continuous elimination through the glomeruli also occurs. Less than 1 % is excreted extrarenally in patients with normal renal function (Thomsen et al 1993). Following intravascular administration in patients with normal renal function, the elimination half-life of contrast media is about 2 h, and 75 % of the administered dose is excreted in the urine within 4 h (Katzberg 1997).…”

Section: Renal Handling Of Contrast Mediamentioning

confidence: 99%

Contrast Medium-Induced Nephropathy

Thomsen¹,

Stacul²,

Webb³

2014

Medical Radiology

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Section: Renal Handling Of Contrast Mediamentioning

confidence: 99%

Contrast Medium-Induced Nephropathy

Thomsen¹,

Stacul²,

Webb³

2014

Medical Radiology

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“…It is mainly excreted through the kidneys with less than 1% eliminated via extrarenal routes in patients with normal kidney function. [ 48 ] The half-life of CM is about 2 h with 75% excreted within 4 h and 98% within 24 h.[ 49 50 ]…”

Section: Nonpharmacological Approachmentioning

confidence: 99%

Contrast-induced nephropathy

et al. 2013

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Contrast-induced nephropathy (CIN) is a serious complication of angiographic procedures resulting from the administration of contrast media (CM). It is the third most common cause of hospital acquired acute renal injury and represents about 12% of the cases. CIN is defined as an elevation of serum creatinine (Scr) of more than 25% or ≥0.5 mg/dl (44 μmol/l) from baseline within 48 h. More sensitive markers of renal injury are desired, therefore, several biomarkers of tubular injury are under evaluation. Multiple risk factors may contribute to the development of CIN; these factors are divided into patient- and procedure-related factors. Treatment of CIN is mainly supportive, consisting mainly of careful fluid and electrolyte management, although dialysis may be required in some cases. The available treatment option makes prevention the corner stone of management. This article will review the recent evidence concerning CIN incidence, diagnosis, and prevention strategies as well as its treatment and prognostic implications.

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“…This is not surprising since CM administration does not normally induce CIN and morbidity justifying renal biopsy. Thus, most of the morphological description of these changes is based on experimental in vitro and in vivo animal studies (6,7,9,12,30,34,35,37,50,51,(53)(54)(55). Furthermore, there is only scant literature describing histomorphological renal changes after administration of Gd-CM (2,22,50,53).…”

mentioning

confidence: 99%

Histomorphological changes after renal X-ray arteriography using iodine and gadolinium contrast media in an ischemic porcine model

Elmståhl

Leander²,

Grant³

et al. 2007

Acta Radiol

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In ischemic porcine kidneys, the histomorphological changes caused by Gd-CM are similar to those caused by I-CM. Vacuolation appears to be independent of the osmolality and viscosity of the CM, and does not seem to be an indicator of renal impairment. "High-osmolal" Gd-CM are more nephrotoxic than "low- and iso-osmolal" I-CM when compared in equal volumes of concentrations, resulting in equal X-ray attenuation.

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Contrast Medium Induced Nephropathy: Animal Experiments

Cited by 22 publications

References 43 publications

Contrast Medium-Induced Nephropathy

Contrast Medium-Induced Nephropathy

Contrast-induced nephropathy

Histomorphological changes after renal X-ray arteriography using iodine and gadolinium contrast media in an ischemic porcine model

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