Comparison of Iodinated Contrast Media-Induced Renal Vasoconstriction in Human, Rabbit, Dog, and Pig Arteries

Rauch, Dieter; Drescher, Peter; Pereira, Francesca J.; Knes, Jane M.; Will, James A.; Madsen, Paul O.

doi:10.1097/00004424-199706000-00001

Cited by 33 publications

(14 citation statements)

References 17 publications

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“…An important study conducted by Tumlin et al [50 ]showed a reduced renal blood flow in 50% of the patients in the first 4 h after cardiac catheterization. A dose-related vasoconstriction of in vitro kidney arteries has been observed during exposure to CM in humans and in animal models [51]. The in vivo injection of CM in animals determined a biphasic hemodynamic response.…”

Section: Pathophysiology Of Contrast-induced Nephropathymentioning

confidence: 99%

Contrast-Induced Nephropathy in Percutaneous Coronary Interventions: Pathogenesis, Risk Factors, Outcome, Prevention and Treatment

Aurelio¹,

Durante²

2014

Cardiology

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Contrast-induced nephropathy (CIN) is a well-known adverse event of therapeutic and diagnostic procedures requiring the adminstration of contrast medium (CM). The lack of a universal CIN definition and glomerular filtration rate markers that vary have resulted in a variety of reported incidences. The development of CIN is associated with an increase in the length of hospital stay and the risk of death. Preexisting renal dysfunction, age, diabetes, congestive heart failure and the volume of CM administered are all associated with a risk for developing CIN. The literature suggests the use of low-osmolarity CM and supports volume supplementation before administration. Moreover, other strategies to avoid CIN, including treatment with N-acetylcisteine and sodium bicarbonate have variable levels of evidence. This review examines the main components of the pathogenesis and risk factors of CIN and possible preventive measures and therapies.

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Section: Pathophysiology Of Contrast-induced Nephropathymentioning

confidence: 99%

Contrast-Induced Nephropathy in Percutaneous Coronary Interventions: Pathogenesis, Risk Factors, Outcome, Prevention and Treatment

Aurelio¹,

Durante²

2014

Cardiology

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“…over 1 h) renal hemodynamic disturbances that may in part explain CM-related renal injury (21,22). over 1 h) renal hemodynamic disturbances that may in part explain CM-related renal injury (21,22).…”

Section: Hemodynamic Effects Of Iodinated CMmentioning

confidence: 99%

The serial effect of iodinated contrast media on renal hemodynamics and oxygenation as evaluated by ASL and BOLD MRI

Zhang

Wang

Yang

et al. 2012

Contrast Media & Molecular

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Contrast-induced nephropathy is a prevalent cause of renal failure, and the mechanisms underlying this injury are not fully understood. We utilized noninvasive functional MRI in order to determine the serial effect of a single administration of iodinated contrast media (CM) on renal hemodynamics and oxygenation. Fifteen rabbits were randomized to receive an intravenous injection of CM (i.e. iopamidol-370; 6 ml kg(-1) body weight) or an equivalent amount of 0.9% saline. Both arterial spin-labeling and blood oxygen level-dependent imaging sequences were performed at 24 h before and at intervals of 1, 24, 48 and 72 h after injection to obtain serial renal blood flow (RBF) and relative spin-spin relaxation rate (R(2)*). Results showed that, in the iopamidol group, the mean cortical RBF decreased at 1 h (p = 0.04 vs baseline), reached its minimum at 24 h (p = 0.01) and gradually returned to baseline by 48 h (p = nonsignificant, NS). The outer medullary RBF decreased to its minimum by 24 h (p = 0.00) and remained less than baseline until 72 h. R(2)* in inner stripes was dramatically increased at 1 h (p = 0.00), remained elevated at 24 h (p = 0.05), but returned to baseline by 48 h (p = NS). R(2)* values within the cortex and outer stripes and inner medulla were slightly increased, but the changes did not reach a statistical significance (p = NS). Saline did not produce positive change in either RBF or R(2)* within different compartments of the kidney. We conclude that iopamidol is associated with a relatively longer-term hypoperfusion in whole kidney and decreased oxygen level in the inner stripes of the outer medulla.

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“…Changes consistent with osmotic nephrosis were observed in 22.3% of patients undergoing renal biopsy within 10 days of contrast exposure [10]. After injection of contrast media, a transient increase is followed by a more prolonged decrease in renal blood flow in animals and humans [11]. Endothelin-1 has been implicated as the most likely causative agent in a number of studies [12,13].…”

Section: Pathogenesis Of Cinmentioning

confidence: 99%

Contrast‐induced nephropathy

Pučelíková

Dangas

Mehran

2007

Cathet Cardio Intervent

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Contrast induced nephropathy (CIN) is an iatrogenic disorder, resulting from exposure to contrast media. Contrast-induced hemodynamic and direct cytotoxic effects on renal structures are highly evident in its pathogenesis, whereas other mechanisms are still poorly understood. CIN is typically defined as an increase in serum creatinine by either 0.5 mg/dl or by 25% from baseline within the first 2-3 days after contrast administration. Although rare in the general population, CIN has a high incidence in patients with an underlying renal disorder, in diabetics, and the elderly. The risk factors are synergistic in their ability to produce CIN. The best way to prevent CIN is to identify the patients at risk and to provide adequate peri-procedural hydration. The role of various drugs in prevention of CIN is still controversial and warrants future studies. Despite remaining uncertainty regarding the degree of nephrotoxicity produced by various contrast agents, in current practice non-ionic low-osmolar contrast media are preferred over the high-osmolar contrast media in patients with renal impairment.

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Comparison of Iodinated Contrast Media-Induced Renal Vasoconstriction in Human, Rabbit, Dog, and Pig Arteries

Abstract: Responses in rabbit and dog renal arteries were similar to those in human renal arteries and could serve as models for investigating CM-induced renal vasoconstriction.

Cited by 33 publications

References 17 publications

Contrast-Induced Nephropathy in Percutaneous Coronary Interventions: Pathogenesis, Risk Factors, Outcome, Prevention and Treatment

Contrast-Induced Nephropathy in Percutaneous Coronary Interventions: Pathogenesis, Risk Factors, Outcome, Prevention and Treatment

The serial effect of iodinated contrast media on renal hemodynamics and oxygenation as evaluated by ASL and BOLD MRI

Contrast‐induced nephropathy

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