Anemia and the risk of contrast-induced nephropathy in patients with renal insufficiency undergoing contrast-enhanced MDCT

https://doi.org/10.1016/j.ejrad.2013.06.004Get rights and content

Abstract

Purpose

The purpose of this study was to assess the effect of anemia on the incidence of contrast-induced nephropathy (CIN) in patients with renal impairment undergoing MDCT.

Materials and methods

Institutional review board approval was waived for this retrospective review of 843 patients with stable renal insufficiency (eGFR between 15 and 60 mL/min) who had undergone contrast-enhanced MDCT. Baseline hematocrit and hemoglobin values were measured. Serum creatinine (SCr) was assessed at the baseline and at 48–72 h after contrast administration.

Results

The overall incidence of CIN in the patient population with renal insufficiency was 6.9%. CIN developed in 7.8% (54 of 695) of anemic patients, and in 2.8% (4 of 148) of non-anemic patients (P = .027). After adjustment for confounders, low hemoglobin and low hematocrit values remained independent predictors of CIN (odds ratio 4.6, 95% CI 1.0–20.5, P = .046).

Conclusions

Anemia is associated with a higher incidence of CIN in patients with renal insufficiency. Anemia is a potentially modifiable risk factor for CIN, and has an unfavorable impact on prognosis in patients with renal insufficiency undergoing contrast-enhanced MDCT.

Introduction

Contrast-induced nephropathy (CIN) is defined as an acute form of kidney injury caused by exposure to intravascular iodinated contrast medium (CM), and usually defined as an increase in the mean serum creatinine (SCr) level of ≥.5 mg/dL (44.2 μmol/L), or ≥25% from the baseline value within 48–72 h after administration of contrast medium in the absence of other etiologies. Although CIN is mostly mild and reversible, it can occasionally lead to the need for renal replacement therapy and increase long-term mortality [1], [2], [3].

Several mechanisms of CIN have been implicated, including ischemic injury, direct cytotoxicity to renal structures, oxidative stress, apoptosis, and a decline in renal blood flow [4], [5]. Pre-existing renal insufficiency, diabetes mellitus, older age, and a higher volume of CM are well known risk factors for the development of CIN [6], [7], [8].

Anemia is a relatively frequent condition in the general population, and is often under-diagnosed and untreated. The underlying causes of anemia may include conditions such as iron, folate or B12 deficiency, malnutrition, cancer-induced blood loss, bone marrow suppression, or cytokine induction due to chronic disease [9]. Anemia is also a frequent feature of reduced kidney function, and may be related to the presence of chronic kidney disease (CKD), which is also an increasing public health problem worldwide, associated with poor outcomes. Anemia might be one of the factors responsible for worsening of renal ischemia and affect the ability of the nephrons to recover quickly from that anoxic event. The combination of anemia and CKD may be harmful in individuals who already have a reduced oxygen supply and increased oxygen demand [10], [11]. However, the significance of anemia in the development of CIN has not been reported.

In the present study, we investigated the effect of anemia on the incidence and outcomes of CIN in patients with renal insufficiency undergoing contrast-enhanced MDCT examinations.

Section snippets

Patient population

This study was HIPAA compliant, and in view of its retrospective design, institutional review board approval was waived. From the institutional database, records were obtained for all contrast-enhanced MDCT examinations performed between January and December 2009. A retrospective analysis based of the records of 10,659 patients who had undergone contrast-enhanced MDCT during this period was then conducted. The inclusion criteria were patient age ≥18 years, measurement of SCr within 7 days

Results

Of the 5536 patients, 1843 had a baseline eGFR of <60 mL/min, and only 843 of 1843 patients had SCr available within 48–72 h after administration of CM. The mean patient age was 65 ± 11 years. The overall population mean baseline SCr was .85 ± .19 mg/dL, and the corresponding mean eGFR was 48.9 ± 6.5 mL/min. Baseline clinical characteristics of the patients are presented in Table 1. In the cohort overall, the incidence of CIN in patients with stable renal insufficiency after contrast-enhanced MDCT

Discussion

Following the introduction of MDCT technology, the number of patients undergoing contrast-enhanced MDCT studies has grown steadily over the last decade. Effective prevention of CIN in patients at risk would be of significant benefit to public health, as it could potentially reduce the in-hospital mortality rate, the period of hospitalization, and the subsequent use of chronic hemodialysis.

The incidence of CIN in the present study was 6.9%. Since 1000 patients had not measured had not measured

Conclusions

In our present cohort, the overall incidence of CIN in patients with renal insufficiency after contrast-enhanced MDCT examination was 6.9%. Anemic patients showed a significantly higher incidence of CIN than non-anemic patients. Anemia is a potentially modifiable risk factor for CIN, and has an unfavorable impact on prognosis in patients with renal insufficiency undergoing contrast-enhanced MDCT. A prospectively designed trial to clarify the value of anemia correction in such patients is

Conflict of interest

The authors have no conflicts of interest to declare. The authors alone were responsible for the content and writing of the paper.

References (30)

  • S.A. Nguyen et al.

    Iso-osmolality versus low-osmolality iodinated contrast medium at intravenous contrast-enhanced CT: effect on kidney function

    Radiology

    (2008)
  • C. Haller et al.

    Cytotoxicity of radiocontrast agents on polarized renal epithelial cell monolayers

    Cardiovascular Research

    (1997)
  • P. Liss

    Effects of contrast media on renal microcirculation and oxygen tension. An experimental study in the rat

    Acta Radiologica. Supplementum

    (1997)
  • P.S. Parfrey et al.

    Contrast material-induced renal failure in patients with diabetes mellitus, renal insufficiency, or both. A prospective controlled study

    New England Journal of Medicine

    (1989)
  • S.G. Albert et al.

    Analysis of radiocontrast-induced nephropathy by dual-labeled radionuclide clearance

    Investigative Radiology

    (1994)
  • Cited by (24)

    • Contrast-associated acute kidney injury: An update of risk factors, risk factor scores, and preventive measures

      2021, Clinical Imaging
      Citation Excerpt :

      The authors concluded that renal transplantation should not be regarded as a contraindication to coronary angiography [37]. Anemia is a risk factor for CA-AKI because it can increase renal tissue hypoxia [38]. Therefore, clinicians should correct underlying anemia as much as possible before operation and use of a contrast agent.

    • Contrast induced nephropathy in vascular surgery

      2016, British Journal of Anaesthesia
      Citation Excerpt :

      Where patients are admitted on the day of surgery they should be instructed to drink oral fluids liberally the night before. Preoperative anaemia should be sought and treated where time permits, as anaemia is correlated with the incidence of CIN.106–108 One should be aware that patients taking beta blockers are more likely to develop anaphylactoid reactions to CM and are, in turn, potentially more resistant to treatment.109

    • Preventing Acute Kidney Injury

      2015, Critical Care Clinics
      Citation Excerpt :

      Monitoring of urine output and body weight is a simple and inexpensive way to prevent fluid overload and can be implemented in all ICUs. The KDIGO AKI guidelines using protocol-based methods for optimization of hemodynamics and oxygenation should be interpreted with flexibility, according to particular aspects of the patient, the medical staff, and the health care infrastructure, and should be monitored for efficacy and changed as necessary.17,34–39 The avoidance of drugs and nephrotoxins that cause AKI, and the appropriate dose adjustment for kidney function medications, are important for AKI management.40

    • International Society of Nephrology's 0by25 initiative for acute kidney injury (zero preventable deaths by 2025): A human rights case for nephrology

      2015, The Lancet
      Citation Excerpt :

      Randomised trials to compare different vasopressors in AKI and assessment of the parameters to assess haemodynamics are necessary. Low haematocrit has been associated with AKI development.134–137 Although no evidence-based data are available, elective procedures to correct low haematocrit levels and prevent AKI might be useful in high-risk patients or in those about to undergo planned interventions that could cause AKI.

    • Association of admission hemoglobin levels and acute kidney injury among myocardial infarction patients treated with primary percutaneous intervention

      2015, Canadian Journal of Cardiology
      Citation Excerpt :

      Local renal hypoxia can therefore be aggravated among patients with low hemoglobin levels after exposure to contrast media; hence, the combination of contrast-induced vasoconstriction and anemia might decrease oxygen delivery, sufficiently to cause renal medullary hypoxia. Previous studies have shown that anemia increases the risk of CIN in various patient populations.14-16 Nikolsky et al., in a large cohort of patients who underwent percutaneous coronary intervention, demonstrated that patients with the lowest eGFR and hematocrit had the highest rates of CIN.14

    View all citing articles on Scopus
    View full text