Elektif koroner anjiyografi yapılan hastalarda hipomagnezemi ve kontrast ilişkili nefropati riski ilişkisi
Amaç: Bu çalışma, hipomagnezeminin (hipoMg) elektif koroner anjiyografi sonrası kontrast kaynaklı nefropati (KKN) geliştirme riski üzerindeki etkisini değerlendirmeyi amaçlamaktadır.
Yöntem: Bu çalışma, üçüncü basamak bir eğitim ve araştırma hastanesinde yürütülen tek merkezli ileriye dönük, gözlemsel bir çalışmadır. 31 Aralık 2018 ve 28 Şubat 2022 tarihleri arasında koroner anjiyografi işlemi geçirmiş ve işlem öncesi başlangıç Mg seviyeleri olan 223 tane hasta bu çalışmaya dahil edilmiştir. CIN, uygulamadan sonra 48-72 saat içinde başlangıca göre serum kreatinin konsantrasyonunda >0.5 mg/dl veya > %25 artış olarak tanımlanmıştır. HipoMg, Mg< 1.60 mg/dL olarak tanımlanmıştır.
Bulgular: Kaydedilen 223 hastanın 28'inde (%12.6) KKN meydana geldi. KKN, hipoMg'si olan hastaların %36.4'ünde ve hipoMg'si olmayanların %11,3'ünde meydana gelmiştir. (P=0,02). Çok değişkenli lojistik regresyon analizi, başlangıç Mg düzeylerinin KKN' nin bağımsız öngörücüleri olduğunu bulunmuştur.
Sonuç: HipoMg, artan KKN riski ile ilişkilendirilmiştir. Bu sonuçlar, hipoMG’de magnezyum replasmanı yapılmasının, kontrast madde kullanılan tanısal/girişimsel işlemlerden önce fayda sağlayabileceğini düşündürmektedir.
Hypomagnesemia and the risk of contrast-induced nephropathy in patients undergoing elective coronary angiography
Objective: The present study aimed to assess the influence of hypomagnesemia (hypoMg) on the risk of developing contrast-induced nephropathy (CIN) after coronary angiography.
Methods: This is a single-center prospective, observational study conducted at a tertiary referral hospital. Between December 31, 2016, and February 28, 2021, 223 patients who had undergone coronary angiography procedures and had preprocedural baseline Mg levels were enrolled in this study. CIN was defined as an increase of >0.5 mg/dl or >25 % in serum creatinine concentration over baseline within 48-72 h after administration. HypoMg was defined as Mg< 1.60 mg/dL.
Results: Of 223 patients enrolled, CIN occurred in 28 patients (12.6%). CIN occurred in 36.4 % of the patients with hypoMg and 11.3 % of those with non-hypoMg (P=0.02). Multivariate logistic regression analysis found that baseline Mg levels were independent predictors of CIN.
Conclusion: HypoMg was associated with an increased risk for CIN. These results suggest magnesium replacement in hypomagnesemia may be beneficially indicated before diagnostic/interventional studies using contrast media.
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- 1. McCullough PA. Contrast-induced acute kidney injury. J Am Coll Cardiol. 2008;51(15):1419-28. DOI: 10.1016/j.jacc.2007.12.035
- 2. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis. 2002;39(5):930-6. DOI: 10.1053/ajkd.2002.32766
- 3. Martin H, Richert L, Berthelot A. Magnesium deficiency induces apoptosis in primary cultures of rat hepatocytes. J Nutr. 2003;133(8):2505-11. DOI: 10.1093/jn/133.8.2505
- 4. Feng H, Guo L, Gao H, Li XA. The deficiency of calcium and magnesium induces apoptosis via scavenger receptor BI. Life Sci. 2011;88(13-14):606-12. DOI: 10.1016/j.lfs.2011.01.020
- 5. Muñoz-Castañeda JR, Pendón-Ruiz de Mier MV, Rodríguez M, Rodríguez-Ortiz ME. Magnesium Replacement to Protect Cardiovascular and Kidney Damage? Lack of Prospective Clinical Trials. Int J Mol Sci. 2018;19(3). DOI: 10.3390/ijms19030664
- 6. Pere AK, Lindgren L, Tuomainen P, Krogerus L, Rauhala P, Laakso J, et al. Dietary potassium and magnesium supplementation in cyclosporine-induced hypertension and nephrotoxicity. Kidney Int. 2000;58(6):2462-72. DOI: 10.1046/j.1523-1755.2000.00429.x
- 7. Kumar G, Solanki MH, Xue X, Mintz R, Madankumar S, Chatterjee PK, et al. Magnesium improves cisplatin-mediated tumor killing while protecting against cisplatin-induced nephrotoxicity. Am J Physiol Renal Physiol. 2017;313(2):F339-f50. DOI: 10.1152/ajprenal.00688.2016
- 8. Andreucci M, Faga T, Serra R, De Sarro G, Michael A. Update on the renal toxicity of iodinated contrast drugs used in clinical medicine. Drug Healthc Patient Saf. 2017;9:25-37. DOI: 10.2147/DHPS.S122207
- 9. Katholi RE, Woods WT, Jr., Taylor GJ, Deitrick CL, Womack KA, Katholi CR, et al. Oxygen free radicals and contrast nephropathy. Am J Kidney Dis. 1998;32(1):64-71. DOI: 10.1053/ajkd.1998.v32.pm9669426
- 10. Firouzi A, Maadani M, Kiani R, Shakerian F, Sanati HR, Zahedmehr A, et al. Intravenous magnesium sulfate: new method in prevention of contrast-induced nephropathy in primary percutaneous coronary intervention. Int Urol Nephrol. 2015;47(3):521-5. DOI: 10.1007/s11255-014-0890-z
- 11. Rihal CS, Textor SC, Grill DE, Berger PB, Ting HH, Best PJ, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation. 2002;105(19):2259-64. DOI: 10.1161/01.cir.0000016043.87291.33
- 12. Li WH, Li DY, Han F, Xu TD, Zhang YB, Zhu H. Impact of anemia on contrast-induced nephropathy (CIN) in patients undergoing percutaneous coronary interventions. Int Urol Nephrol. 2013;45(4):1065-70. DOI: 10.1007/s11255-012-0340-8
- 13. Altura BM, Altura BT. Vascular smooth muscle and prostaglandins. Fed Proc. 1976;35(12):2360-6. DOI:***
- 14. Altura BM, Altura BT. New perspectives on the role of magnesium in the pathophysiology of the cardiovascular system. II. Experimental aspects. Magnesium. 1985;4(5-6):245-71. DOI:***
- 15. Shechter M, Sharir M, Labrador MJ, Forrester J, Silver B, Bairey Merz CN. Oral magnesium therapy improves endothelial function in patients with coronary artery disease. Circulation. 2000;102(19):2353-8. DOI: 10.1161/01.cir.102.19.2353
- 16. Agus ZS. Hypomagnesemia. J Am Soc Nephrol. 1999;10(7):1616-22. DOI: 10.1681/ASN.V1071616