Abstract

Consequent to the extended use of intravenous iodinated contrast media, increased adverse effects have been recognized, with Contrast-Induced Nephropathy (CIN) constituting one of the most serious of these adverse effects. The purpose of the current study was to investigate a prophylaxis strategy for reducing the effect of intravenous contrast on the development of CIN. Data were collected from 120 patients who received intravenous iodinated contrast agents during CT procedures. CIN was defined as a relative increase of more than 25% or an absolute increase of ≥ 0.5 mg/dL (44 µmol/L) in serum creatinine levels within 48-72 hours post-CT. Our prophylaxis strategy involved intravenous administration of 500 ml normal saline within one hour before the CT procedure and 3 liters of oral hydration within 12 hours post-CT. Additionally, the volume of administered low osmolality contrast media was based on the weight of the patient. A paired t-test revealed no statistically significant differences in creatinine (t = 0.07, P = 0.942) or urea (t = 0.52, P = 0.608) pre-CT vs. post intravenous iodinated contrast media-enhanced CT. Use of low osmolality contrast media and good hydration pre and post intravenous iodinated contrast administration are effective approaches to the prevention of CIN.

Highlights

  • Contrast-Induced Nephropathy (CIN) is defined as a deterioration of renal function as measured by an increase in serum creatinine of more than 25% or 44 μmol/L within three days of intravascular administration of contrast media (CM) in the absence of other etiology such as nephrotoxins, hypotension, urinary obstruction, or atheromatous emboli [1,2]

  • Several different definitions are used in the literature, most relying on the measurement of serum creatinine concentrations

  • The American College of Radiology suggests using the term postcontrast acute kidney injury (PC-AKI) rather than CIN as the literature points to an association but not causality [4]

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Summary

Introduction

Contrast-Induced Nephropathy (CIN) is defined as a deterioration of renal function as measured by an increase in serum creatinine of more than 25% or 44 μmol/L within three days of intravascular administration of contrast media (CM) in the absence of other etiology such as nephrotoxins, hypotension, urinary obstruction, or atheromatous emboli [1,2]. Contrast-induced acute kidney injury (CI-AKI) has been described in which injury or damage to the kidney has taken place, but is subclinical in that no measurable reduction in renal filtration is apparent [3]. The American College of Radiology suggests using the term postcontrast acute kidney injury (PC-AKI) rather than CIN as the literature points to an association but not causality [4]. Standardization of evidence-based best practices in nursing care may reduce the incidence of acute kidney injury due to contrast material by standardized fluid orders, patient education about oral hydration, and by limiting the volume of contrast material [5]. The type and volume of contrast used correlate with the risk of CIN [10]

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