Contrast-induced nephropathy: pathogenesis and prevention

Cronin, Robert E.

doi:10.1007/s00467-009-1204-z

Cited by 55 publications

(52 citation statements)

References 139 publications

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“…1 Accounting for 10% of acute renal failure in hospitalized patients, 2 it is a serious clinical problem associated with increased morbidity and mortality, extended length of hospital stay, and increased health care costs. 3 The present studies and guidelines show that older age is a risk factor for the development of CIN, 1,[4][5][6][7] but the exact pathogenesis of CIN in the elderly is not clearly understood. Recently, studies have shown that renal ischemia, direct toxicity to renal tubular epithelium cells, oxidative stress, and tubular obstruction are considerably linked to the pathogenesis of CIN.…”

Section: Introductionmentioning

confidence: 99%

Aged Rats Are Susceptible to Nephrotoxicity Induced by Iodinated Contrast Media

et al. 2012

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Objective: The objective of this study is to evaluate the effect and mechanism of aging on iodinated-contrast-mediainduced nephropathy in male rats. Methods: Twenty-four healthy male rats were initially divided into 12-month-old and 24-month-old age groups (adult and older age groups, respectively; n ¼ 12/group); subsequently, each age group was randomly divided into saline control (NS) and contrast media (CM) groups (n ¼ 6/group). CM (76% diatrizoate, 10 mL/kg b.w.) was given through the caudal vein. Urinary creatinine (Ucr) and serum creatinine (Scr) were detected by an automatic biochemical analyzer. The activities of renal malondialdehyde (MDA), superoxide dismutase (SOD), angiotensinconverting enzyme (ACE), angiotensin II (Ang II), and reduced form of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) were determined by spectrophotometric assays with commercially available kits according to the manufacturers' protocols. Renal histological changes were observed by hematoxylin and eosin staining and scored semiquantitatively. Results: In diatrizoate-injected aged rats, Scr, the activities of ACE, Ang II, MDA, and NADPH oxidase in renal tissues were significantly increased (p < 0.01). The histologic scores were higher in the aged animals with CM treatment than those of control or adult rats (p < 0.01). There was an increasing trend but no significant statistical difference in renal ACE, Ang II, MDA, and NADPH oxidase or histologic scores in adult CM-injected rats compared with control animals (p > 0.05). Conclusions: Older age is an aggravating factor of iodinated-contrast-media-induced nephropathy in male rats. Oxidative stress and the renin-angiotensin system (RAS) may play an important role in nephrotoxicity induced by iodinated contrast media, especially in aged male rats.

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Section: Introductionmentioning

confidence: 99%

Aged Rats Are Susceptible to Nephrotoxicity Induced by Iodinated Contrast Media

et al. 2012

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“…CIN is one of the main causes of AKI [13]. It is known that occurrence of CIN depends on the level of serum creatinine.…”

Section: Discussionmentioning

confidence: 99%

The Role of Serum Cystatin C in the Early Detection of Contrast-Induced Nephropathy after Coronary Intervention

Fj¹,

Mh²,

Ma³

et al. 2017

J Kidney

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Objective: Contrast induced nephropathy is the most common complication for both coronary angiography and percutaneous coronary intervention. The aim of the present study is to investigate the role of serum cystatin C among patients undergoing coronary angiography for earlier detection of contrast induced nephropathy. Materials and Methods:The study included 80 elective patients attending the cardiology center (48 males, 32 females). The study was conducted in cardiac catheterization unit at Al-Hussein Medical City/ Kerbala Health Directorate-Holy Kerbala, Iraq. Clinical examination and laboratory investigations were made before and 24 hours after angiography. These investigations include: serum creatinine, blood urea, estimated GFR and serum cystatin C.Results: According to the definition, contrast induced nephropathy occurred in 19 patients 23.8% with grade 0 to 2 of renal dysfunction. There were significant increments in serum creatinine, cystatin C and eGFR after 24 hours of angiography/angioplasty procedures p<0.001, 0.01 respectively. Receiver-operating characteristic analysis showed a higher area under the curve for creatinine 0.805 (95% CI=0.688, 0.921) p=0.001, 78.9% sensitivity and 60.7% specificity than serum cystatin C 0.777 (95% CI=0.673-0.881) P=0.001 sensitivity=78.9% and specificity=64%, a cutoff level of cystatin C>7 ng/ml. Conclusion:Cystatin C was a good biomarker for earlier diagnosis of contrast induced nephropathy when compared with blood urea and eGFR.

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“…Bu da, meduller hipoksemi ve iskemi nedenli oksidatif stres oluşmasını tetikler. KM'lerle uzun süreli olan temas, tubüler hücreler için toksiktir ve hücre ölümüne neden olur (3,(19)(20)(21)(22). Çalışmamız sırasında incelediğimiz hastalardan 42'sinin belirtilen kriterler çerçevesinde KM maruziyetinin olduğu gözlendi.…”

Section: Discussionunclassified

Cerrahi Yoğun Bakım Hastalarında Kontrast Madde Nefropatisi için Risk Faktörleri

...

2012

tybdd

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Amaç: Çalışmamızda, cerrahi yoğun bakım hastalarında kontrast madde kullanılmasına bağlı oluşabilen böbrek hasarı (CIN, Contrast Induced Nephropathy) sıklığı ve gelişimi için risk faktörlerini değerlendirmeyi amaçladık. Gereç ve Yöntem: Ocak 2001-Eylül 2006 arasında hastanemiz yoğun bakımına kabul edilen hastaların dosyaları retrospektif olarak incelendi ve kontrast madde kullanılmış hastalar çalışmaya dahil edildi. Kontrast madde (KM) verildiği dönemde renal replasman tedavisi almakta olan hastalar çalışma dışı bırakıldı. Hastalar CIN gelişen (CIN(+)) ve gelişmeyenler (CIN(-) olmak üzere iki gruba ayrıldı. CIN gelişimi için serum kreatinin seviyelerinin, KM'ye maruz kalma sonrası ilk 72 saat içerisinde bazal değerden 0,5 mg/dL veya %25 fazla olması kriter olarak kabul edildi. Bulgular: Belirtilen kriterler çerçevesinde kontrast madde kullanılan toplam 42 hastanın 17'sinde CIN gelişti. Gruplar demografik verileri, APACHE II skorları ve yoğun bakıma alınma nedenleri bakımından benzer bulundu. CIN (+) grubunda konjestif kalp yetmezliği CIN(-) grubundan daha fazla bulundu (%35'e karşın %8, p=0,045). CIN (+) grubunda, KM'ye maruz kalma öncesindeki hemoglobin düzeyi, KM'ye maruz kalma sonrasındaki parsiyel arteriyel oksijen basınçları ve diyastolik kan basıncı CIN(-) grubuna göre istatistiksel olarak anlamlı olarak düşük bulundu (Sırasıyla, 11,3±1,3'e karşın 12,7±2,5 g/dl, 66±11'e karşın 91±21 mmHg ve 59±17'ye karşın 72±19 mmHg, tüm değerler için p<0,05). Elde edilen parametrelerin çok değişkenli lojistik regresyon modelinde incelenmesiyle yalnızca arteriyel oksijen basıncının CIN gelişimi için bağımsız bir risk faktörü olduğu gözlendi (OR:0,842; CI=0,95; p=0,005

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Contrast-induced nephropathy: pathogenesis and prevention

Cited by 55 publications

References 139 publications

Aged Rats Are Susceptible to Nephrotoxicity Induced by Iodinated Contrast Media

Aged Rats Are Susceptible to Nephrotoxicity Induced by Iodinated Contrast Media

The Role of Serum Cystatin C in the Early Detection of Contrast-Induced Nephropathy after Coronary Intervention

Cerrahi Yoğun Bakım Hastalarında Kontrast Madde Nefropatisi için Risk Faktörleri

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