Radiographic contrast media induced nephropathy: experimental observations and the protective effect of calcium channel blockers

Yx, Wang; Yf, Jia; Km, Chen; Sk, Morcos

doi:10.1259/bjr.74.888.741103

Cited by 45 publications

(28 citation statements)

References 21 publications

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“…A large number of drugs have been used to protect renal function after PCI, such as aminophylline (Shammas et al 2001;Rohani 2010), theophylline (Wang et al 2001), atrial natriuretic peptide (Chen 2009;Morikawa et al 2009), B-type natriuretic peptide (Zhang et al 2010), mannitol (Kelly et al 2008), prostaglandins (McCullough andTumlin 2009), N-acetylcysteine (Thiele et al 2010), sodium bicarbonate (Masuda 2008) and statins (Xinwei et al 2009); however, few of them (Kowalczyk et al 2007;Zoungas et al 2009) have shown exact protective effects.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Anisodamine on Renal Function in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Wang

et al. 2011

Tohoku J. Exp. Med.

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ST-segment elevation myocardial infarction (STEMI) is the most severe type of heart attack, and primary percutaneous coronary intervention (PCI) is the first line treatment for STEMI. However, these patients are at higher risk of contrast-induced nephropathy (CIN), which increases the length of hospital stay and mortality rate. Anisodamine, an alkaloid extracted from a Chinese herb, has been shown to exert protective effects on the renal function. The aim of this study was to investigate the protective effect of anisodamine on CIN in STEMI patients undergoing primary PCI. A total of 126 consecutive STEMI patients were randomly assigned to receive anisodamine (n = 60) or placebo (control, n = 66) from admission to 24 hours after PCI. The serum creatinine (SCr) concentrations, estimated glomerular filtration rate (eGFR) and incidence of CIN were measured on admission, and 24, 48 and 72 hours after PCI between the two groups. We found that the renal function of all patients after PCI underwent a course from injury to recovery. The incidence of CIN was 5.0%, 8.3%, and 6.7% at 24, 48 and 72 hours, respectively, after primary PCI in anisodamine group, while in control group it was 16.7%, 22.7%, and 19.7%, respectively. The incidence of CIN in anisodamine group was lower than that in control group during 72 hours after PCI (all P < 0.05). In conclusion, intravenous infusion of anisodamine before and after primary PCI may reduce the occurrence of CIN in STEMI patients undergoing primary PCI, without serious side effects.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Anisodamine on Renal Function in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Wang

et al. 2011

Tohoku J. Exp. Med.

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“…Combined acute inhibition of the synthesis of NO with L-nitroarginine methyl ester (L-NAME) and of prostacyclin synthesis with indomethacin predisposes rats to severe renal injury from radiographic contrast media (23). The marked impairment of relaxation of renal vessels contracted with norepinephrine observed in the present study suggests a pivotal role of the cyclic AMP system in addition to the cyclic GMP-mediated signaling mechanisms.…”

Section: Discussionmentioning

confidence: 58%

Ionic radiocontrast inhibits endothelium-dependent vasodilation of the canine renal artery in vitro: possible mechanism of renal failure following contrast medium infusion

Discigil¹,

Évora

Pearson

et al. 2004

Braz J Med Biol Res

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To determine if radiocontrast impairs vascular relaxation of the renal artery, segments (4-5 mm in length) of canine renal artery were suspended in vitro in organ chambers to measure isometric force (95% O 2 /5% CO 2 , at 37ºC). Arterial segments with and without endothelium were placed at the optimal point of their length-tension relation and incubated with 10 µM indomethacin to prevent synthesis of endogenous prostanoids. The presence of nonionic radiocontrast (iohexol, Omnipaque 350, 1 ml in 25 ml control solution, 4% (v/v)) did not alter endothelium-dependent relaxation to acetylcholine in rings precontracted with both norepinephrine and prostaglandin F 2α (N = 6). When the rings were precontracted with prostaglandin F 2α , the presence of ionic contrast did not inhibit the relaxation of the arteries. However, in canine renal arteries contracted with norepinephrine, the presence of ionic radiocontrast (diatrizoate meglumine and diatrizoate sodium, MD-76, 1 ml in 25 ml control solution, 4% (v/v)) inhibited relaxation in response to acetylcholine, sodium nitroprusside (N = 6 in each group), and isoproterenol (N = 5; P < 0.05). Rings were relaxed less than 50% of norepinephrine contraction. Following removal of the contrast, vascular relaxation in response to the agonists returned to normal. These results indicate that ionic radiocontrast nonspecifically inhibits vasodilation (both cAMP-mediated and cGMP-mediated) of canine renal arteries contracted with norepinephrine. This reversible impairment of vasodilation could inhibit normal renal perfusion and act as a mechanism of renal failure following radiocontrast infusion. In the adopted experimental protocol the isoproterenol-induced relaxation of renal arteries precontracted with norepinephrine was more affected, suggesting a pivotal role of the cAMP system.

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“…Although the physiological and pathophysiological mechanisms of Ca 2+ overload in ischemic kidney and RCN have not been fully elucidated, there is evidence indicating that increased cytosolic Ca 2+ may be an important mediator of epithelial cell apoptosis and necrosis [21]. In addition, Ca 2+ channel blockers have been reported to have a protective effect against RCN and ischemic ARF [22,23]. In the present study, ioversol exposure induced a significant increase in [Ca 2+ ] i in NRK-52E cells.…”

Section: Discussionmentioning

confidence: 99%

Selective Inhibition of the Reverse Mode of Na<sup>+</sup>/Ca<sup>2+</sup> Exchanger Attenuates Contrast-Induced Cell Injury

Yang

Jia

et al. 2013

Am J Nephrol

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Background: The precise mechanisms underlying radiocontrast nephropathy (RCN) are not well understood. Intracellular Ca²⁺ overload is considered to be a key factor in RCN. The Na⁺/Ca²⁺ exchanger (NCX) system is one of the main pathways of intracellular Ca²⁺ overload. We investigated whether intracellular Ca²⁺ overload via the NCX system was involved in contrast-induced renal tubular cytotoxicity. Methods: NRK-52E cells were exposed to ioversol (100 mg iodine/ml) for 4 h. KB-R7943 (inhibitor of reverse mode of NCX, 4 × 10^-5, 4 × 10^-6M) was added 1 h before incubation with ioversol. Cell viability and permeability were determined by 3-(4,5-dimethyldiazol-2-yl)-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase assay. Apoptosis was determined by flow cytometry. Intracellular Ca²⁺ concentration ([Ca²⁺]_i) and reactive oxygen species (ROS) were detected by confocal microscopy. The expression of NCX1 mRNA and caspase-3 protein was evaluated by reverse transcription-polymerase chain reaction and Western blot, respectively. Results: Ioversol exposure induced significantly increased lactate dehydrogenase release and decreased 3-(4,5-dimethyldiazol-2-yl)-2,5-diphenyl tetrazolium bromide conversion in NRK-52E cells. Significantly increased apoptosis and caspase-3 protein expression were observed in the NRK-52E cells exposed to ioversol for 4 h. Ioversol treatment induced a significant increase in [Ca²⁺]_i and intracellular ROS. KB-R7943 dose-dependently and significantly suppressed the increase in [Ca²⁺]_i, intracellular ROS and caspase-3 overexpression induced by ioversol and attenuated the contrast-induced NRK-52E cell apoptosis. No significant changes in NCX1 mRNA expression were observed following contrast exposure. Conclusion: Intracellular Ca²⁺ overload via the reverse mode of NCX, followed by ROS overproduction and caspase-3 overexpression played an important role in the contrast-induced renal tubular cytotoxicity. The reverse mode of the NCX inhibitor KB-R7943 attenuated contrast-induced renal tubular cytotoxicity.

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Radiographic contrast media induced nephropathy: experimental observations and the protective effect of calcium channel blockers

Cited by 45 publications

References 21 publications

Protective Effects of Anisodamine on Renal Function in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Protective Effects of Anisodamine on Renal Function in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Ionic radiocontrast inhibits endothelium-dependent vasodilation of the canine renal artery in vitro: possible mechanism of renal failure following contrast medium infusion

Selective Inhibition of the Reverse Mode of Na<sup>+</sup>/Ca<sup>2+</sup> Exchanger Attenuates Contrast-Induced Cell Injury

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