Injection of low and iso-osmolar contrast medium decreases oxygen tension in the renal medulla

Liss, Per; Nygren, Anders; Erikson, Uno; Ulfendahl, H. R.

doi:10.1046/j.1523-1755.1998.00811.x

Cited by 139 publications

(108 citation statements)

References 29 publications

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“…In the already hypoxic outer medulla, Po 2 fell from 26 mmHg at baseline to mean levels as low as 9 mmHg. Liss et al (10) reported a comparable decline of medullary Po 2 from approximately 30 to 15 mmHg with the administration of ionic and nonionic lowosmolar radiocontrast agents, as well as iso-osmolar dyes. The intensification of medullary hypoxia by contrast agents has also been documented noninvasively in rats (11) and humans (12), using blood oxygen-level-dependent magnetic resonance imaging (MRI), detecting increased unsaturated hemoglobin concentration within the renal medulla over extended periods of time.…”

Section: Physiologic Medullary Hypoxia Aggravated By Radiocontrast Amentioning

confidence: 90%

“…All measurements represent parenchymal Po 2 determined in the outer medulla. For iothalamate, cortical measurements are shown as well (7,10). may represent reduced regional microcirculatory blood flow, as well as enhanced oxygen consumption, that may not be fully compensated even during increased regional oxygen delivery.…”

Section: Radiocontrast-induced Decrease In Renal Oxygen Supplymentioning

confidence: 99%

See 1 more Smart Citation

Renal Parenchymal Hypoxia, Hypoxia Adaptation, and the Pathogenesis of Radiocontrast Nephropathy

Heyman¹,

Rosen²,

Rosenberger³

2008

Clinical Journal of the American Society of Nephrology

202

164

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Background and objectives: Renal parenchymal PO 2 declines after the administration of iodinated radiocontrast agents, reaching critically low levels of approximately 10 mmHg in medullary structures.Design, setting, participants, & measurements: In this review, the causes of renal parenchymal hypoxia and its potential role in the pathogenesis of contrast nephropathy are appraised.Results: Commonly associated predisposing factors are associated with a propensity to enhance renal hypoxia. Indeed, animal models of radiocontrast nephropathy require the induction of such predisposing factors, mimicking clinical scenarios that lead to contrast nephropathy in high-risk individuals. In these models, in association with medullary hypoxic damage, a transient local cellular hypoxia response is noted, initiated at least in part by hypoxia-inducible factors. Some predisposing conditions that are distinguished by chronically aggravated medullary hypoxia, such as tubulointerstitial disease and diabetes, are characterized by a priori upregulation of hypoxia-inducible factors, which seems to confer tolerance against radiocontrastrelated hypoxic tubular damage. Renal dysfunction under such circumstances likely reflects to some extent altered intrarenal hemodynamics, rather than acute tubular injury.Conclusions: Real-time, noninvasive novel methods may help to differentiate between evolving tubular damage and altered hemodynamics and in the design of appropriate preventive interventions.

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Section: Physiologic Medullary Hypoxia Aggravated By Radiocontrast Amentioning

confidence: 90%

Section: Radiocontrast-induced Decrease In Renal Oxygen Supplymentioning

confidence: 99%

Renal Parenchymal Hypoxia, Hypoxia Adaptation, and the Pathogenesis of Radiocontrast Nephropathy

Heyman¹,

Rosen²,

Rosenberger³

2008

Clinical Journal of the American Society of Nephrology

202

164

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“…These include sepsis that induces renal vasoconstriction through the release of endothelin and the use of radiocontrast imaging dyes that increase oxygen consumption for solute reabsorption and reduce regional inner medullary blood flow. [54][55][56][57][58][59][60][61] More generalized reductions in blood flow represent another major cause of AKI. These can result from hemorrhage, decompensated liver cirrhosis, treatment with non-steroidal anti-inflammatory drugs, congestive heart failure, and renal artery occlusion or stenosis.…”

Section: Repeated Episodes Of Acute Kidney Injurymentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

120

111

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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“…Iopromide was previously shown actually to increase RMBF in control rats, although it reduces RMBF in diabetic rats 23 ; however, a reduction in PO 2 by iopromide has also been reported. 24 Taken together, the experimental setting seems to be crucial for determining the ultimate effect of CM on RMBF and PO 2 . In this study, iopromide did not reduce PO 2 or RMBF, which may in part rely on our particular dehydration protocol: Our rats were not given water for 12 h before the experiment.…”

Section: Renal Circulation and Oxygenationmentioning

confidence: 99%

Viscosity of Contrast Media Perturbs Renal Hemodynamics

Seeliger¹,

Flemming²,

Wronski³

et al. 2007

Journal of the American Society of Nephrology

145

132

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Contrast-induced nephropathy is a common cause of acute renal failure, and the mechanisms underlying this injury are not completely understood. We sought to determine how physicochemical properties of contrast media may contribute to kidney damage in rats. We administered contrast media of equivalent iodine concentrations but differing physiocochemical properties: the high-osmolality iopromide was compared to the high-viscosity iodixanol. In addition, the non-iodinated substances mannitol (equivalent osmolality to iopromide) and dextran (equivalent viscosity to iodixanol) were also studied. Both types of contrast media transiently increased renal and hindquarter blood flow. The high-osmolality agents iopromide and mannitol markedly increased urine production whereas iodixanol, which caused less diuresis, significantly enhanced urine viscosity. Only the high-viscosity agents iodixanol and dextran decreased renal medullary blood flux, erythrocyte concentration, and pO 2 . Moreover, iodixanol prolonged the tubuloglomerular feedback response and increased plasma creatinine levels to a greater extent than iopromide or dextran. Therefore, the viscosity of contrast media may play a significant role in contrast-induced nephropathy.

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Injection of low and iso-osmolar contrast medium decreases oxygen tension in the renal medulla

Cited by 139 publications

References 29 publications

Renal Parenchymal Hypoxia, Hypoxia Adaptation, and the Pathogenesis of Radiocontrast Nephropathy

Renal Parenchymal Hypoxia, Hypoxia Adaptation, and the Pathogenesis of Radiocontrast Nephropathy

Hypoxia: The Force that Drives Chronic Kidney Disease

Viscosity of Contrast Media Perturbs Renal Hemodynamics

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