Kontrast madde nefropatisinde bir risk faktörü olarak metabolik sendrom

Year 2025, Volume: 8 Issue: 3, 476 - 482, 30.05.2025

Belma Özlem Tural Balsak , Şehmus Özmen , Davut Akın , Mehmet Emin Yılmaz

https://doi.org/10.32322/jhsm.1654419

https://izlik.org/JA68LK72TW

Abstract

AMAÇ: Kontrast maddenin artan miktarda kullanımı, kontrast madde nefropatisini Akut Böbrek Yetmezliğinin giderek sık rastlanan bir nedeni haline getirmiştir. Kontrast madde nefropatisi için, önceden var olan böbrek yetmezliği, diyabet, hipovolemi, ileri yaş, kalp yetmezliği, fazla kontrast madde kullanımı, nefrotoksik ilaçlar risk faktörlerini oluşturmaktadır. Metabolik Sendromun kontrast madde nefropatisi için risk faktörü olup olmadığı ile ilgili literatürde az sayıda çalışma yapılmış ve risk faktörü olduğu belirlenmiştir. Çalışmamızda, metabolik sendrom ve insülin direnci ile kontrast madde nefropatisi arasındaki ilişki incelenmiştir.
MATERYAL VE METOD: Bu çalışmaya Dicle Üniversitesi Tıp Fakültesi dahili bilimler kliniklerinde yatan ve herhangi bir nedenle kontrastlı bilgisayarlı tomografi çekilen 94 hasta dahil edildi. Çalışmaya kreatinin seviyesi 1.0 ve üzerindeki hastalar alındı. Hastaların tomografi öncesi ve tomografiden 48 saat sonraki kreatinin değerlerine bakılarak kontrast madde nefropatisi gelişen hastalar tespit edildi. Tüm hastalar metabolik sendrom yönünden IDF kriterleri kullanılarak değerlendirildi. HOMA-IR değerleri hesaplandı.
BULGULAR: Çalışmaya 73 erkek, 21 kadın hasta alındı. Toplam 94 hastanın 10’unda kontrast madde nefropatisi gelişti. Kontrast madde nefropatisi gelişen grubun %60’ ında, gelişmeyen grubun %38,1’inde metabolik sendrom saptandı. İnsülin direnci kontrast madde nefropatisi gelişen grupta %30, gelişmeyen grupta %17,9 oranında görüldü. Hasta sayısının azlığından dolayı aradaki bu fark istatistiksel anlamlılığa ulaşmadı.
Hastaların değerlendirilen albümin, üre, kreatinin, ürik asit, CRP, hemoglobin değerleri arasında kontrast madde nefropatisi gelişen ve gelişmeyen gruplar arasında anlamlı fark saptandı. İki grup arasında bazal kreatinin klirensleri ve kreatinin ≥1.3 olanlarda belirgin fark saptandı. Renal fonksiyon bozukluğunun kontrast madde nefropatisiyle ilişkili olduğu görüldü.
SONUÇ: Kontrast madde nefropatisi görüntüleme tekniklerinin gelişmesiyle birlikte daha sık görülmeye başlandı. Son yıllarda metabolik sendrom da kontrast madde nefropatisi risk faktörü olarak suçlanmaktadır. Sonuç olarak, bu çalışmada kontrast madde nefropatisi gelişen grupta daha yüksek oranda metabolik sendromlu hasta saptanmasına rağmen bu fark istatistiki anlamlılığa ulaşmamıştır. Ancak yine de oranın yüksek olması nedeniyle metabolik sendromlu hastalara kontrast madde verilirken dikkatli olunmalıdır.

Keywords

Kontrast Madde Nefropatisi , Metabolik Sendrom , İnsülin Direnci

Metabolic syndrome as a risk factor in contrast-induced nephropathy

https://izlik.org/JA68LK72TW

Abstract

Aims: The expanding use of contrast media has made contrast-induced acute kidney injury (CI-AKI) a cause of acute renal failure. This study investigated the relationship between metabolic syndrome (MS), insulin resistance, and contrast-induced acute kidney injury.
Methods: This study encompassed 94 hospitalized patients (73 male) with creatinine levels of 1.0 and above who underwent contrast-enhanced computed tomography for various reasons in the internal medicine clinics of Dicle University Faculty of Medicine. Patients whose creatinine levels were routinely measured before and 48 hours after tomography and whose anamnesis information was sufficient for the International Diabetes Federation metabolic syndrome criteria were retrospectively included in the study. HOMA-IR values ​​were calculated.
Results: CI-AKI developed in 10 (10.6%) patients out of 94. MS was identified in 60% of the group that developed CI-AKI and 38.1% that did not. Insulin resistance was observed in 30% of the group that developed CI-AKI and 17.9% that did not. Despite the observed difference, it did not achieve statistical significance. Considerable differences were found between the two groups regarding albumin, urea, creatinine, uric acid, C-reactive protein, and hemoglobin levels. CI-AKI was significantly more common in individuals with low creatinine clearance and in those with creatinine ≥1.3 mg/dl.
Conclusion: Our study showed that a higher rate of patients with MS was detected in the group with CI-AKI. MS has been accused of being a risk factor for CI-AKI. Therefore, caution should be exercised when administering contrast to patients with MS.

Keywords

Contrast-induced acute kidney injury , insulin resistance , metabolic syndrome

References

• Detrenis S, Meschi M, Musini S, Savazzi G. Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art. Nephrol Dial Transplant. 2005;20(8):1542-1550.
• Davenport MS, Cohan RH, Khalatbari S, Ellis JH. The challenges in assessing contrast-induced nephropathy: where are we now? AJR Am J Roentgenol. 2014;202:784-789. doi:10.2214/AJR.13.11369
• Davenport MS, Perazella MA, Yee J, et al. Use of intravenous iodinated contrast media in patients with kidney disease: consensus statements from the American College of Radiology and the National Kidney Foundation. Radiology. 2020;294:660-668. doi: 10.1148/radiol.201919 2094
• Khwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract. 2012;120(4):c179-c184. doi:10.1159/000339789
• van der Molen AJ, Reimer P, Dekkers IA, et al. Post-contrast acute kidney injury-part 1: Definition, clinical features, incidence, role of contrast medium and risk factors: recommendations for updated ESUR Contrast Medium Safety Committee guidelines. Eur Radiol. 2018;28(7):2845-2855. doi:10.1007/s00330-017-5246-5
• Moos SI, van Vemde DN, Stoker J, Bipat S. Contrast induced nephropathy in patients undergoing intravenous (IV) contrast enhanced computed tomography (CECT) and the relationship with risk factors: a meta-analysis. Eur J Radiol. 2013;82(9):e387-e399. doi:10.1016/j.ejrad.2013.04. 029
• Toprak O, Cirit M, Yesil M, et al. Metabolic syndrome as a risk factor for contrast-induced nephropathy in non-diabetic elderly patients with renal impairment. Kidney Blood Press Res. 2006;29(1):2-9. doi:10.1159/ 000092481
• Lebovitz HE. Insulin resistance: definition and consequences. Exp Clin Endocrinol Diabetes. 2001;109(Suppl 2):S135-S148. doi:10.1055/ s-2001-18576
• Lebovitz HE. Oral therapies for diabetic hyperglycemia. Endocrinol Metab Clin North Am. 2001;30(4):909-933. doi:10.1016/s0889-8529(05) 70221-8
• Li Y, Wang J. Contrast-induced acute kidney injury: a review of definition, pathogenesis, risk factors, prevention and treatment. BMC Nephrol. 2024;25(1):140. doi:10.1186/s12882-024-03570-6
• Gussenhoven MJ, Ravensbergen J, van Bockel JH, Feuth JD, Aarts JC. Renal dysfunction after angiography; a risk factor analysis in patients with peripheral vascular disease. J Cardiovasc Surg (Torino). 1991;32(1): 81-86.
• Kidney Disease Outcome Quality Initiative. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis. 2002;39:17-31.
• Maddox TG. Adverse reactions to contrast material: recognition, prevention, and treatment. Am Fam Physician. 2002;66(7):1229-1234.
• Scharnweber T, Alhilali L, Fakhran S. Contrast-induced acute kidney injury: pathophysiology, manifestations, prevention, and management. Magn Reson Imaging Clin N Am. 2017;25(4):743-753. doi:10.1016/j.mric. 2017.06.012
• Kusirisin P, Chattipakorn SC, Chattipakorn N. Contrast-induced nephropathy and oxidative stress: mechanistic insights for better interventional approaches. J Transl Med. 2020;18(1):400. doi:10.1186/s12967-020-02574-8
• Hansel B, Giral P, Nobecourt E, et al. Metabolic syndrome is associated with elevated oxidative stress and dysfunctional dense high-density lipoprotein particles displaying impaired antioxidative activity. J Clin Endocrinol Metab. 2004;89(10):4963-4971. doi:10.1210/jc.2004-0305 
• Gleeson TG, Bulugahapitiya S. Contrast-induced nephropathy. AJR Am J Roentgenol. 2004;183(6):1673-1689. doi:10.2214/ajr.183.6.01831673 
• Itoh Y, Yano T, Sendo T, Oishi R. Clinical and experimental evidence for prevention of acute renal failure induced by radiographic contrast media. J Pharmacol Sci. 2005;97(4):473-488. doi:10.1254/jphs.crj05002x 
• Toprak O, Cirit M. Risk factors and therapy strategies for contrast-induced nephropathy. Ren Fail. 2006;28(5):365-381. doi:10.1080/0886022 0600683524
• Davidson CJ, Laskey WK, Hermiller JB, et al. Randomized trial of contrast media utilization in high-risk PTCA: the COURT trial. Circulation. 2000;101(18):2172-2177. doi:10.1161/01.cir.101.18.2172
• Gruberg L, Mintz GS, Mehran R, et al. The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency. J Am Coll Cardiol. 2000;36(5):1542-1548. doi:10.1016/s0735-1097(00)00917-7
• Taliercio CP, Vlietstra RE, Ilstrup DM, et al. A randomized comparison of the nephrotoxicity of iopamidol and diatrizoate in high risk patients undergoing cardiac angiography. J Am Coll Cardiol. 1991;17(2):384-390. doi:10.1016/s0735-1097(10)80103-2
• Lautin EM, Freeman NJ, Schoenfeld AH, et al. Radiocontrast-associated renal dysfunction: incidence and risk factors. AJR Am J Roentgenol. 1991;157(1):49-58. doi:10.2214/ajr.157.1.2048539
• McCullough PA, Soman SS. Contrast-induced nephropathy. Crit Care Clin. 2005;21(2):261-280. doi:10.1016/j.ccc.2004.12.003
• Andrade L, Campos SB, Seguro AC. Hypercholesterolemia aggravates radiocontrast nephrotoxicity: protective role of L-arginine. Kidney Int. 1998;53(6):1736-1742. doi:10.1046/j.1523-1755.1998.00906.x
• Yang DW, Jia RH, Yang DP, Ding GH, Huang CX. Dietary hypercholesterolemia aggravates contrast media-induced nephropathy. Chin Med J (Engl). 2004;117(4):542-546.
• Manske CL, Sprafka JM, Strony JT, Wang Y. Contrast nephropathy in azotemic diabetic patients undergoing coronary angiography. Am J Med. 1990;89(5):615-620. doi:10.1016/0002-9343(90)90180-l
• Schillinger M, Haumer M, Mlekusch W, Schlerka G, Ahmadi R, Minar E. Predicting renal failure after balloon angioplasty in high-risk patients. J Endovasc Ther. 2001;8(6):609-614. doi:10.1177/152660280100800614
• Gruberg L, Mintz GS, Mehran R, et al. The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency. J Am Coll Cardiol. 2000;36(5):1542-1548. doi:10.1016/s0735-1097(00)00917-7 
• Mudge GH. Uricosuric action of cholecystographic agents. A possible factor in nephrotoxicity. N Engl J Med. 1971;284(17):929-933. doi:10. 1056/NEJM197104292841701
• Ishizaka N, Ishizaka Y, Toda E, Nagai R, Yamakado M. Association between serum uric acid, metabolic syndrome, and carotid atherosclerosis in Japanese individuals. Arterioscler Thromb Vasc Biol. 2005;25(5):1038-1044. doi:10.1161/01.ATV.0000161274.87407.26 
• Perlstein TS, Gumieniak O, Hopkins PN, et al. Uric acid and the state of the intrarenal renin-angiotensin system in humans. Kidney Int. 2004; 66(4):1465-1470. doi:10.1111/j.1523-1755.2004.00909.x 
• Wu MJ, Tsai SF, Lee CT, Wu CY. The predictive value of hyperuricemia on renal outcome after contrast-enhanced computerized tomography. J Clin Med. 2019;8(7):1003. doi:10.3390/jcm8071003
• Kodzwa R. ACR manual on contrast media: 2018 updates. Radiol Technol. 2019;91(1):97-100.