Incidence and Main Determinants of Contrast-Induced Nephropathy following Coronary Angiography or Subsequent Balloon Angioplasty

Abstract

Background/Aims: Patient assessment by imaging studies using contrast media is currently replacing open procedures, especially in high-risk patients. However, the use of such contrast media might result in acute events and injuries after the procedure. In the present study, we first determined the incidence of contrast-induced nephropathy (CIN) in a sample of Iranian patients who candidated for coronary angiography and/or angioplasty, and then assessed major risk factors predicting the appearance of CIN following these procedures. Methods: Two hundred and fifty consecutive, eligible patients scheduled for coronary angiography and/or angioplasty at the Afshar Hospital in Yazd between January 2009 and August 2010 were considered for enrollment. Renal function was measured at baseline and 48 h after the intervention, and CIN was defined by an increase in creatinine of >0.5 mg/dl or 25% of the initial value. The predictive role of potential risk factors was determined in a multivariate model adjusted for comorbidities, preexisting renal impairment, and angiographic data. Results: CIN following coronary angiography or angioplasty appeared in 12.8% of the cases. A myocardial infarction before the procedure (OR = 2.121, p = 0.036) and a prior history of hypertension (OR = 2.789, p = 0.025) predicted the appearance of acute renal failure following angiography or subsequent angioplasty. A low estimated glomerular filtration rate at baseline slightly predicted CIN after these interventions. Conclusion: Transient acute renal dysfunction occurred in 12.8% of the patients within 48 h after angiography or subsequent angioplasty and could be predicted by a myocardial infarction before the procedure or by a prior history of systolic hypertension.

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

“…Apart from a direct toxic effect of contrast agent, disturbances in the renal blood flow, vasoconstriction of renal vessels, oxidative stress, free radical damage and endothelial dysfunction are thought to be major mechanism in the development of CIN [2][3][4][5]. Apart from a direct toxic effect of contrast agent, disturbances in the renal blood flow, vasoconstriction of renal vessels, oxidative stress, free radical damage and endothelial dysfunction are thought to be major mechanism in the development of CIN [2][3][4][5].…”

“…More than half of CIN cases are diagnosed after cardiac catheterization accounting for at least 10-15% of extra hospitalizations due to acute renal failure [2,3]. 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].…”

Coronary Atherosclerosis Imaging

“…A potentially serious complication is the contrast-induced nephropathy (CIN), defined as an acute rise in serum creatinine of ≥0.5 mg/dl (0.04 mmol/L) or 25% above the baseline value, occurring during the first 72 hours after the procedure [127]. In patients undergoing coronary angiography the incidence of CIN is between 2% and 15%, strongly related to preexisting clinical conditions such as renal insufficiency, diabetes, advanced age, extent of CAD, and congestive heart failure [128][129][130][131][132][133][134]. Although CIN is usually transient, few patients may develop persistent renal damage and an increased risk of cardiovascular events [135,136].…”

Contrast- Induced Nephropathy after Coronary Angiography

“…An Iranian study published in 2013 (36) found that there is a transient acute renal dysfunction occurred in 12.8% of patients within 48 h after angiography or subsequent angioplasty and could be predicted by a myocardial infarction before the procedure or by a prior history of systolic hypertension.…”