Effect of Radiologic Contrast Media on Cell Volume Regulation in Rabbit Proximal Renal Tubules

Galtung, Hilde Kanli; Løken, Mona; Sakariassen, Kjell S.

doi:10.1016/s1076-6332(03)80547-0

Cited by 8 publications

(5 citation statements)

References 19 publications

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“…Decreased tubular metabolism was also found in slices of rat renal tissue treated with CM, along with other indicators of cellular damage (increased levels of N ‐acetyl‐β‐ d ‐glucosaminidase, lactate dehydrogenase and δ‐glutamyltransferase) 96 . Other tubular functional impairments caused by CM include impairment of the cell volume regulatory response to changes in osmolarity 97 …”

Section: Toxicity Of Contrast Media and Tubulesmentioning

confidence: 85%

“…96 Other tubular functional impairments caused by CM include impairment of the cell volume regulatory response to changes in osmolarity. 97 Zager et al 33 studied cell membrane damage induced by CM in rat isolated proximal tubules and found a loss of membrane linked proteins including Na + ⁄ K + -ATPase and caveolin. Osmolarity was not associated with such damage and a comparison of the effects of pro-and anti-oxidants in cultured tubular cells showed that oxidative stress did not seem to be caused directly by CM.…”

Section: Toxicity Of Contrast Media and Tubulesmentioning

confidence: 99%

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Pathophysiology of renal tissue damage by iodinated contrast media

Sendeski

2011

Clin Exp Pharma Physio

147

119

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1. The present review focuses on the cytotoxic effects of iodinated contrast media (CM) that are shared by all types of CM. 2. Although the clinical nephrotoxicity of CM has been progressively improved, all currently available CM still possess a level of cytotoxicity, which is probably caused by iodine. 3. The toxicity caused by specific CM properties, such as osmolarity, viscosity and ionic strength, can be differentiated from the cytotoxicity common to all CM in studies using cell culture, isolated blood vessels and isolated tubules. 4. The cytotoxicity induced by CM leads to apoptosis and cell death of endothelial and tubular cells and may be initiated by cell membrane damage, together with oxidative stress. 5. Cell damage may be aggravated by factors such as tissue hypoperfusion and hypoxia, properties of individual CM, such as ionic strength, high osmolarity and/or viscosity, and clinically unfavourable conditions. 6. Clinically detectable renal failure may result from the summation of all these factors.

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Section: Toxicity Of Contrast Media and Tubulesmentioning

confidence: 85%

Section: Toxicity Of Contrast Media and Tubulesmentioning

confidence: 99%

Pathophysiology of renal tissue damage by iodinated contrast media

Sendeski

2011

Clin Exp Pharma Physio

147

119

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“…The osmolar effects of contrast media may result in osmotic water movement out of cells, thereby decreasing sodium level by endogenous dilution, producing a so-called translational hyponatremia (Adrogue and Madias 2000;Sirken et al 2004). Some experimental studies showed that contrast media can induce prolonged shrinkage of renal tubular cells and red blood cells and decrease these cells' ability to regulate cellular volume (Galtung et al 2000(Galtung et al , 2001(Galtung et al , 2002, which may be an early precursor to apoptosis (Maeno et al 2000). Therefore, transient contrast-induced translocational hyponatremia may be a main mechanism of increased plasma osmolar gap at hour 6 in the CIAKI group of our study.…”

Section: Discussionmentioning

confidence: 99%

Increased Plasma Osmolar Gap Is Predictive of Contrast-Induced Acute Kidney Injury

Kim

Sung

Kang

et al. 2012

Tohoku J. Exp. Med.

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Contrast-induced acute kidney injury (CIAKI) is a common complication after percutaneous coronary artery intervention (PCI). It is urgent to find a novel, easily measurable and accurate predictor for the early detection of CIAKI. Hyperosmolarity and large amounts of contrast media are risk factors for CIAKI. However, there is no study on plasma osmolar gap as a predictor of CIAKI. We enrolled 89 patients undergoing elective PCI and tested changes of serum sodium, osmolar gap, and renal function at 0, 6, 12 and 24 hours. Plasma osmolar gap was calculated using the following formula: measured plasma osmolarity -[2(Na) + serum urea nitrogen/2.8 + glucose/18]. CIAKI was defined as follows: increase in serum creatinine of ≥ 50%, increase in serum creatinine of ≥ 0.3 mg/dL, or decrease in estimated glomerular filtration rate of ≥ 25% within 24 hours after PCI. The incidence of CIAKI was 13.5% (12/89 patients). The CIAKI group had higher plasma osmolar gaps 6 hours after PCI. The adjusted hazard ratio of the plasma osmolar gap from hour 6 (1-mOsm/L increments) to the development of CIAKI was 1.12 (95% confidence interval [CI], 1.01-1.26; P = 0.041). Sensitivity and specificity of 7 mOsm/L or higher plasma osmolar gap at hour 6 were 70.0% and 76.6%, respectively (area under the ROC curve = 0.77 [95% CI, 0.65-0.89]). Increased plasma osmolar gap may precede the development of CIAKI in patients undergoing PCI. In conclusion, plasma osmolar gap may be a useful predictor for the development of CIAKI.

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“…21 CIN is due to vasoconstriction-mediated renal medullary ischemia and direct toxic damage to the renal tubular epithelial cells. [22][23][24][25] In addition, in the setting of kidney transplantation, cold ischemia induces an ischemia/reperfusion stress that is responsible for tubular damage, which may decrease graft survival. 16 Some experimental studies have suggested that this ischemic effect can be worsened by ICMI.…”

mentioning

confidence: 99%

The use of contrast media in deceased kidney donors does not affect initial graft function or graft survival

Vigneau

Fulgencio

Godier

et al. 2006

Kidney International

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Patients receiving cadaveric kidney transplants often experience delayed graft function. As iodinated contrast media injection (ICMI), necessary for cerebral angiography, which is often used to diagnose brain death, can be nephrotoxic, we compared renal function recovery (RFR) and 1-year and long-term graft survival according to the method used to diagnose brain death. Data from 9921 cadaveric kidneys, transplanted between 1 January 1998 and 31 December 2003, were retrieved from the French National Registry for organ donation. We defined RFR as the number of days for the recipient to reach a plasma creatinine less than 250 mumol/l, and/or a 24-h urine output greater than 1000 ml. RFR and 1-year and long-term graft survival were compared between four different donor groups (according to ICMI and diabetes mellitus). A total of 41.5% of deceased donors received ICMI before organ procurement and 1.95% of them were diabetic. History of ICMI or diabetes in the donor did not influence RFR or 1-year graft survival. Long-term graft survival was decreased in the group of patients transplanted with a diabetic graft as compared to patients transplanted with a non-diabetic graft (P=0.001). History of ICMI in the donor did not affect long-term graft survival in the non-diabetic donor group (P=0.2); however, in the diabetic group, ICMI tended to decrease long-term graft survival (P=0.056). ICMI did not affect RFR or graft survival in non-diabetic deceased donors. However, its use in diabetic deceased donors requires further study.

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Effect of Radiologic Contrast Media on Cell Volume Regulation in Rabbit Proximal Renal Tubules

Cited by 8 publications

References 19 publications

Pathophysiology of renal tissue damage by iodinated contrast media

Pathophysiology of renal tissue damage by iodinated contrast media

Increased Plasma Osmolar Gap Is Predictive of Contrast-Induced Acute Kidney Injury

The use of contrast media in deceased kidney donors does not affect initial graft function or graft survival

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