Hyperuricemia may be related to contrast-induced nephropathy after percutaneous coronary intervention

Demırkol, Sait; Balta, Şevket; Akgül, Emin Özgür; Cakar, Mustafa; Sarlak, Hakan; Kurt, Ömer

doi:10.6061/clinics/2013(07)28

Cited by 3 publications

(3 citation statements)

References 6 publications

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“…Although the pathophysiology of CIN is not completely understood, vasoconstriction of renal vessels, oxidative stress, free radical damage and endothelial dysfunction may play a role in CIN development [2][3][4][5]. However, the available body of evidence is still not sufficient, and there are ongoing efforts to clarify the pathophysiology of the CIN development [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Contribution of platelets indices in the development of contrast-induced nephropathy

Şahin

Karabulut

Avcı

et al. 2015

Blood Coagulation &Amp; Fibrinolysis

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Contrast-induced nephropathy (CIN) accounts for 10% of hospital-acquired renal failure, causes a prolonged in-hospital stay and represents a powerful predictor of poor clinical outcome. The underlying mechanism of the CIN development remains unclear and seems to be multifactorial. The potential link between platelet indices such as mean platelet volume (MPV) and platelet distribution width (PDW) with CIN is unknown. Herein, we aimed to investigate the correlation between MPV and PDW levels with the development of CIN. The incidence of CIN (20.5%) was prospectively evaluated in 430 patients with diagnosis of acute coronary syndrome. Initial creatinine (1.13 ± 0.25 vs. 1.05 ± 0.27 mg/dl, P = 0.01) and PDW (40.1 ± 20.2 vs. 34.5 ± 19.9%, P = 0.02) levels and the total volume of contrast media used (121 ± 61 vs. 94 ± 42 ml, P = 0.01) were higher in patients who developed CIN. MPV was similar between the two groups (P = 0.80). In a univariate regression analysis, age, increased creatinine, uric acid, phosphate, PDW levels and higher total volume of contrast media used were significantly correlated with CIN incidence. However, in a multivariate analysis, only total volume of CM used [odds ratio (OR) 1.011, 95% confidence interval (CI) 1.006-1.016; P = 0.01], increased age (OR 1.026, 95% CI 1.00-1.052; P = 0.05) and increased PDW levels (OR 1.009, 95% CI 1.00-1.022; P = 0.04) remained as the independent predictors of CIN. Among platelet indices, PDW, but not MPV, was associated with CIN development. The clinical significance of such link remains unclear, but may indicate involvement of platelet activation in CIN pathogenesis.

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Section: Introductionmentioning

confidence: 99%

Contribution of platelets indices in the development of contrast-induced nephropathy

Şahin

Karabulut

Avcı

et al. 2015

Blood Coagulation &Amp; Fibrinolysis

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“…These parameters are assessed in the clinical setting, predominantly due to easy accessibil-ity and lower cost, although superior markers are available, including cystatin C and neutrophil gelatinase associated lipocalin (NGAL) [3,4]. Other simple laboratory predictors, for instance uric acid levels, are also under investigation to define novel determinants of CIN development [5][6][7]. Serum alkaline phosphatase (ALP) levels have been shown to have a promoting effect on vascular calcification [8][9][10], and a correlation of ALP with chronic renal failure is also well-established.…”

Section: Introductionmentioning

confidence: 99%

Impact of serum alkaline phosphatase level on the pathophysiologic mechanism of contrast-induced nephropathy

et al. 2014

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CIN was observed in 20.5% of patients. Advanced age, male gender, elevated creatinine, uric acid and phosphate levels, and low glomerular filtration rate were correlated with the development of CIN. Correlation analysis also showed a significant association between the ALP level and the development of CIN (126.1 ± 144.9 vs. 97.2 ± 46.9, p = 0.004). Univariate regression analysis also showed the impact of ALP on the development of CIN (OR 1.004, 95% CI 1.001–1.007, p = 0.02). Conclusions: Our outcomes indicate a possible active role of ALP in the mechanism of CIN. An elevated ALP level may predict the development of CIN.

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“…Other risk factors for CIN are salt depletion, dehydration, estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m 2 , left ventricular ejection fraction <45%, diabetes mellitus, age >70 years, concurrent use of nephrotoxic drugs and higher contrast agents dose, and a previous history of hypotension, anemia, emergency percutaneous coronary intervention and/or myocardial infarction [2,][3]. In addition, hyperlipidemia, impaired fasting glucose, smoking and alcohol consumption may be associated with CIN [4]. The type of radiocontrast agent used may also be connected with the higher incidence of CIN.…”

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confidence: 99%

The Relation between Renin-Angiotensin-Aldosterone System Blockade and Contrast-Induced Nephropathy: An Unresolved Issue

Balta

Aparcı

2014

Cardiology

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Hyperuricemia may be related to contrast-induced nephropathy after percutaneous coronary intervention

Cited by 3 publications

References 6 publications

Contribution of platelets indices in the development of contrast-induced nephropathy

Contribution of platelets indices in the development of contrast-induced nephropathy

Impact of serum alkaline phosphatase level on the pathophysiologic mechanism of contrast-induced nephropathy

The Relation between Renin-Angiotensin-Aldosterone System Blockade and Contrast-Induced Nephropathy: An Unresolved Issue

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