ST Elevasyonlu Miyokart İnfarktüsü Hastalarında Serum Ozmolaritesinin Kontrast Nefropatisi Üzerine Etkisi

Abstract

Giriş: Kontrast ilişkili nefropati (KİN) ST elevasyonlu miyokart infarktüsü (STEMİ) hastalarında artmış mortalitenin en önemli nedenlerinden birisidir. Çalışmamızda perkütan koroner girişim uygulanan STEMİ hastalarında serum ozmolaritesinin KİN üzerine etkisini incelemeyi amaçladık. Hastalar ve Yöntem: STEMİ olan 163 ardışık hasta çalışmaya dahil edildi. Ardından hastalar KİN gelişmeyen grup 1 ve gelişen grup 2 olarak ikiye ayrıldı. Bazal klinik, serum ozmolaritesini içeren laboratuvar ve demografik özellikler her iki grupta karşılaştırıldı. Bulgular: Yüz kırk dört KİN olmayan hasta grup 1, yirmi iki KİN olan hasta grup 2 olarak alındı. Serum ozmolaritesi KİN gelişen hastalarda daha yüskek saptandı [289.06 (284.75-292.39), 291.71 (289.69-295.72); p= 0.004]. Ayrıca yaş (OR: 1.097, CI: 1.033-1.164; p= 0.002) ve serum ozmolaritesi (OR: 1.117, CI: 1.008- 1.238; p= 0.035) KİN’in bağımsız öngördürücüleri olarak saptandı. Sonuç: Artmış serum ozmolaritesi perkütan koroner girişim uygulanan STEMİ hastalarında KİN ile ilişkilidir. Bu ilişki koroner arter hastalığı tedavi edilse bile artmış kötü klinik sonlanımlardan sorumlu olabilir.

The Impact of Serum Osmolarity on Contrast-Induced Nephropathy in Patients with ST-Segment Elevation Myocardial Infarction

Abstract

Introduction: Contrast-induced nephropathy (CIN) is one of the most important causes for increased mortality rates in ST-segment elevation myocardial infarction (STEMI) patients. In our study, we aimed to investigate the impact of serum osmolarity on CIN in patients with STMEI who were undergoing percutaneous coronary intervention. Patients and Methods: A total of 163 consecutive patients with STEMI were enrolled in this study. The patients were divided into two groups; patients without CIN were assigned to group 1 and patients with CIN were assigned to group 2. The baseline clinical, laboratory and demographic features, including the serum osmolarity, were compared for both groups. Results: A total of 144 patients without CIN comprised group 1, while 22 patients with CIN comprised group 2. The serum osmolarity level [289.06 (284.75-292.39), 291.71 (289.69-295.72); p= 0.004] was higher in patients with CIN. Additionally, age (OR: 1.097, CI: 1.033-1.164; p= 0.002) and serum osmolarity (OR:1.117, CI: 1.008-1.238; p= 0.035) were found to be independent predictors of CIN. Conclusion: Higher serum osmolarity is related with CIN in STEMI patients who are undergoing percutaneous coronary intervention. This could cause increased adverse clinical outcomes, even if the underlying coronary artery disease is treated successfully.

Keywords

• Contrast-induced nephropathy,serum osmolarity,STEMI

References

1. 1. Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, Blaha MJ, et al. Executive summary: heart disease and stroke statistics-2014 update: a report from the American Heart Association. Circulation 2014;129:399-410.
2. 2. Narula A, Mehran R, Weisz G, Dangas GD, Yu J, Généreux P, et al. Contrast-induced acute kidney injury after primary percutaneous coronary intervention: results from the HORIZONS-AMI substudy. Eur Heart J 2014;35:1533-40.
3. 3. Mehran R, Aymong ED, Nikolsky E, Lasic Z, Iakovou I, Fahy M, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 2004;44:1393-9.
4. 4. Deardorff DL. Osmotic strength, osmolality, and osmolarity. Am J Hosp Pharm 1980;37:504-9.
5. 5. Arevalo-Lorido JC, Gomez JC, Formiga F, Conde-Martel A, Carrera-Izquierdo M, Muela-Molinero A, et al. High serum osmolarity at admission determines a worse outcome in patients with heart failure: is a new target emerging? Int J Cardiol 2016;221:238-42.
6. 6. Briongos Figuero S, Jimenez-Mena M, Ortega Marcos J, Camine Lopez A, Fernandez Santos S, de la Cal Segura T, et al. Dehydration and serum hyperosmolarity as new predictors of mortality after acute coronary syndrome. Int J Cardiol 2014;172:e472-4.
7. 7. Mehran R, Nikolsky E. Contrast-induced nephropathy: definition, epidemiology, and patients at risk. Kidney Int Suppl 2006;100:11-5.
8. 8. Bhagat CI, Garcia-Webb P, Fletcher E, Beilby JP. Calculated vs. measured plasma osmolalities revisited. Clin Chem 1984;30:1703-5.

9. 9. James MT, Samuel SM, Manning MA, Tonelli M, Ghali WA, Faris P, et al. Contrast-induced acute kidney injury and risk of adverse clinical outcomes after coronary angiography: a systematic review and meta-analysis. Circ Cardiovasc Interv 2013;6:37-43.
10. 10. Guitterez NV, Diaz A, Timmis GC, O’Neill WW, Stevens MA, Sandberg KR, et al. Determinants of serum creatinine trajectory in acute contrast nephropathy. J Interv Cardiol 2002;15:349-54.
11. 11. Seeliger E, Lenhard DC, Persson PB. Contrast media viscosity versus osmolality in kidney injury: lessons from animal studies. Biomed Res Int 2014;2014:358136.
12. 12. Reinhardt HW, Seeliger E. Toward an integrative concept of control of total body sodium. News Physiol Sci 2000;15:319-25.
13. 13. Seeliger E, Lunenburg T, Ladwig M, Reinhardt HW. Role of the renin-angiotensin-aldosterone system for control of arterial blood pressure following moderate deficit in total body sodium: balance studies in freely moving dogs. Clin Exp Pharmacol Physiol 2010;37:e43-51.
14. 14. Schwartz L, Guais A, Pooya M, Abolhassani M. Is inflammation a consequence of extracellular hyperosmolarity? J Inflamm (Lond) 2009;6:21.
15. 15. Abolhassani M, Wertz X, Pooya M, Chaumet-Riffaud P, Guais A, Schwartz L. Hyperosmolarity causes inflammation through the methylation of protein phosphatase 2A. Inflamm Res 2008;57:419-29.
16. 16. Hubert A, Cauliez B, Chedeville A, Husson A, Lavoinne A. Osmotic stress, a proinflammatory signal in Caco-2 cells. Biochimie 2004;86:533-41.
17. 17. Nemeth ZH, Deitch EA, Szabo C, Hasko G. Hyperosmotic stress induces nuclear factor-kappaB activation and interleukin-8 production in human intestinal epithelial cells. Am J Pathol 2002;161:987-96.
18. 18. Roncal Jimenez CA, Ishimoto T, Lanaspa MA, Rivard CJ, Nakagawa T, Ejaz AA, et al. Fructokinase activity mediates dehydration-induced renal injury. Kidney Int 2014; 86:294-302.
19. 19. Kuwabara M, Hisatome I, Roncal-Jimenez CA, Niwa K, Andres-Hernando A, Jensen T, et al. Increased serum sodium and serum osmolarity are independent risk factors for developing chronic kidney disease; 5 year cohort study. PLoS One 2017;12:e0169137.