Akut koroner sendromda perkütan koroner girişim yapılan hastalarda kontrast nefropati prevalansı

Muhammed Karadeniz; Hüseyin Kandemir; Taner Sarak; Çağlar Alp

doi:10.32322/jhsm.410522

Research Article

The prevalence of contrast nephropathy in patients undergoing percutaneous coronary intervention in acute coronary syndrome

Year 2018, Volume: 1 Issue: 2, 34 - 39, 30.06.2018

Muhammed Karadeniz Hüseyin Kandemir Taner Sarak Çağlar Alp

https://doi.org/10.32322/jhsm.410522

Cited By: 2

Abstract

Objective: Contrast nephropathy (KMN) is
defined as an acute renal injury due to intravenous contrast agents applied in
diagnostic or therapeutic interventions and is an important cause of
hospitalization due to acute renal failure. In this study, the frequency of
coronary intervention and contrast agent nephropathy was investigated in acute
coronary syndrome.

Material and Method: According
to the European Urogenital Radiology Society Guide, "An increase of 25 or
0.5 mg/dl in serum creatinine within 3 days after administration of contrast
medium without any other etiological cause". After approval of the Ethics
Committee, 336 patients who met the inclusion criteria were included in the
study. Patients younger than 18 years of age with chronic renal insufficiency,
heart failure, coronary by-pass history, serum creatinine control after the
procedure and patients without percutaneous coronary intervention were excluded
from the study.

Results: BMD was detected in 11.9% of the 336
patients included in the study. The mean age of 40 patients who developed CMN
was 73.9±10.2 / year, and the mean age of 296 patients who did not have CMN was
59.4±12.3 /year. The mean age was significantly higher in the DM group (p
<0.001). The mean body mass index (BMI) was 28.2 ± 4.7kg / m² in the
non-developing group, while the BMI average was 26.5 ± 3.3kg / m². The mean VKI
was lower in the DM group (p = 0.044). The mean SYNTAX score was 16.6 ± 8.3 in
the non-developing group, whereas the mean in the group with the improved KMN
was 22.5 ± 10.3. The SYNTAX score was higher in the KMN-developing group than
in the non-KMN group (p=0.001). There was no difference between two groups in
terms of AKS type, DM, HT and sex (p=0.713, p=0.317, p=0.055, p=0.589).

Conclusion: Strategies should be implemented to
prevent other CMD developments, provided that hydration is absolute before and
after the procedure in groups at risk for which contrast media should be given.

Keywords

Contrast nephropathy, acute coronary syndrome, percutaneous coronary intervention

References

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Akut koroner sendromda perkütan koroner girişim yapılan hastalarda kontrast nefropati prevalansı

Year 2018, Volume: 1 Issue: 2, 34 - 39, 30.06.2018

Muhammed Karadeniz Hüseyin Kandemir Taner Sarak Çağlar Alp

https://doi.org/10.32322/jhsm.410522

Cited By: 2

Abstract

Amaç: Kontrast madde
nefropatisi (KMN), tanı veya tedavi
amaçlı yapılan girişimlerde uygulanan intravenöz kontrast ajanlara bağlı olarak
gelişen akut böbrek hasarı olarak tanımlanmıştır ve akut böbrek yetersizliğine
bağlı olarak hastaneye yatışlarda önemli bir nedendir. Bu çalışmada akut
koroner sendromda koroner girişim ve kontrast madde nefropatisi sıklığı
araştırılmıştır.

Gereç ve Yöntem: Avrupa Ürogenital Radyoloji Cemiyeti Kılavuzu’na göre KMN tanımı; “başka
bir etiyolojik sebep olmaksızın, kontrast madde verilmesinden sonraki 3 gün
içinde serum kreatinin düzeyinde başl25 veya 0.5 mg/dl artış olması” olarak
kabul edilmiştir. Etik Kurul onayı sonrası dahil edilme
kriterlerine uyan 336 hasta çalışmaya alındı. 18 yaşından küçük, kronik böbrek
yetersizliği olan, kalp yetmezliği olan, koroner by-pass öyküsü olan, işlem
sonrası serum kreatinini kontrol edilemeyen hastalar ve perkütan koroner
girişim yapılmayan hastalar çalışma dışı bırakıldı.

Sonuçlar: Çalışmaya dahil edilen 336 hastanın %11,9’unda
KMN saptandı. KMN gelişen 40 hastanın yaş ortalaması 73,9±10,2/yıl, KMN
gelişmeyen 296 hastanın yaş ortalaması 59,4±12,3/yıl idi. KMN gelişen grupta
yaş ortalaması istatistiksel olarak anlamlı derecede yüksek bulundu
(p<0.001). KMN gelişmeyen hasta grubunda vücut kitle indeksi (VKİ)
ortalaması 28,2±4,7kg/m² iken, KMN gelişen grupta VKİ ortalaması 26,5±3.3kg/m²
idi. KMN gelişen grupta VKİ ortalaması daha düşük bulundu (p=0.044). KMN gelişmeyen
hasta grubunda SYNTAX skoru ortalama 16,6±8,3 iken, KMN gelişen hasta grubunda
ortalama 22,5±10,3 idi. KMN gelişen grupta SYNTAX skoru KMN gelişmeyen gruba
göre daha yüksek bulundu (p=0.001). AKS tipi, DM, HT ve cinsiyet açısından iki
grup arasında fark bulunmadı (p=0.713, p=0.317,p=0.055, p=0.589).

Sonuç: Kontrast madde verilmesi gereken risk altındaki
gruplarda işlem öncesinde ve sonrasında hidrasyon mutlak olması şartıyla diğer
KMN gelişmesini önleyici stratejiler uygulanmalıdır.

Keywords

Kontrast nefropati, akut koroner sendrom, perkütan koroner girişim

References

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4. Detrenis, S. Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art. Nephrol Dial Transplant 2005; 20(8): 1542-50.
5. Morcos SK, Thomsen HS, Webb JA. Conrast-media-induced nephrotoxicity: a consensus report. Contrast Media Safety Committee, European Society of Urogenital Radiology (ESUR) Eur Radiol 1999;9:1602-13.
6. Spinler SA, Goldfarb S. Nephrotoxicity of contrast media after cardiac angiography:Pathogenesis, clinical course, and preventive measures, including the role of lowosmolalitycontrast media. Ann Pharmacother 1992;26:56-64.
7. Lepor NE, Mathur VS. Radiocontrast Nephropathy. Curr Interv Cardiol Rep 2000;2:335-341.
8. Asif A, Epstein M. Prevention of radiocontrast-induced nephropathy. Am JKidney Dis 2004; 44: 12-24.
9. Merten GJ, Burgess WP, Gray LV, Holleman JH. Prevention of contrastinducednephropathy with sodium bicarbonate: a randomized controlled trial.JAMA 2004; 291: 2328-34.
10. Jorgensen AL. Contrast-induced nephropathy: pathophysiology and preventive strategies. Crit Care Nurse 2013;33:37–46.
11. Brendan J, Barrett M, Patrick SP. Contrast-induced Nephropathy in Emergency Department Patients Receiving Abdominal Contrast-Enhanced Computed Tomography. Ann Emerg Med 2008;52:136.
12. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis 2002;39:930–6.
13. Detrenis, S. Lights and shadows on the pathogenesis of contrast-inducednephropathy: state of the art. Nephrol Dial Transplant 2005; 20(8): 1542-50.
14. Heyman SN, Rosenberger C, Rosen S. Regional alterations in renalhaemodynamics and oxygenation: a role in contrast medium-inducednephropathy. Nephrol Dial Transplant 2005; 20 Suppl 1: i6.
15. Pflueger A. Role of adenosine in contrast media-induced acute renal failurein diabetes mellitus. Mayo Clin Proc 2000; 75(12): 1275-83.
16. Porter GA. Contrast-associated nephropathy. Am J Cardiol 1989; 64(9): 22E.2E.
17. Heyman SN, Reichman J, Brezis M. Pathophysiology of radiocontrast nephropathy: a role for medullary hypoxia. Invest Radiol 1999; 34(11): 685-91.
18. Deray G, Martinez F, Cacoub P, Baumelou B, Baumelou A, Jacobs C. A role of adenosine, calcium and ischemia in radiocontrast media induced intrarenal vasoconstriction. Am J Nephrol 1990; 10(4): 316-22.
19. Heyman SN, Clark BA, Kaiser N, Spokes K, Rosen S, Brezis M. Radiocontrast induced endothelin release in vivo and in vitro. J Am Soc Nephrol 1992; 3(1): 58-65.
20. Agmon Y, Dinour D, Brezis M. Disparate effects of adenosine A-1 and A-2 receptor agonists on intrarenal blood flow. Am J Physiol 1993; 265(6): F802-6.
21. Arend LJ, Bakris GL, Burnett JC Jr. Role of intrarenal adenosine in the renal hemodynamic response to contrast media. J Lab Clin Med 1987; 110(4): 406-11.
22. Bakris GL, Burnett JC Jr. A role of calcium in radiocontrast-induced reduction in renal hemodynamics. Kidney Int 1985; 27(2): 465-8.
23. Smith MW, Ambudkar IS, Phelps PC, Rogec AL, Trump BF. MgCl2-induced changes in cytosolic Ca2+ of cultured rabbit renal tubular cells. Biochim Biophys Acta 1987; 931(2):13042.
24. Brezis M, Heyman SN, Dinour D, Epstein FH, Rosen S. Role of nitric oxide in renal medullary oxygenation: studies in isolated and intact rat kidney. J Clin Invest 1991; 88(2): 390-5.
25. Agmon Y, Peleg H, Greenfeld Z, Rosen S, Brezis M. Nitric oxide and prostanoids protect the renal outer medulla from radiocontrast toxicity in the rat. J Clin Invest 1994; 94(3): 1069-75.
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Details

Primary Language	Turkish
Subjects	Health Care Administration
Journal Section	Original Article
Authors	Muhammed Karadeniz Hüseyin Kandemir Taner Sarak Çağlar Alp
Publication Date	June 30, 2018
Published in Issue	Year 2018 Volume: 1 Issue: 2

Cite

AMA	Karadeniz M, Kandemir H, Sarak T, Alp Ç. Akut koroner sendromda perkütan koroner girişim yapılan hastalarda kontrast nefropati prevalansı. J Health Sci Med / JHSM. June 2018;1(2):34-39. doi:10.32322/jhsm.410522

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