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 Table of Contents  
SYMPOSIUM
Year : 2018  |  Volume : 5  |  Issue : 2  |  Page : 47-50

Contrast Induced Nephropathy in ICU settings


Consultant Pediatric Intensivist, Associate Professor, Department of Pediatrics, S.N.Medical College & HSK Hospital, Bagalkot-587103, Karnataka, India

Date of Submission19-Jan-2018
Date of Acceptance07-Mar-2018
Date of Web Publication30-Apr-2018

Correspondence Address:
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Source of Support: None, Conflict of Interest: None


DOI: 10.21304/2018.0502.00373

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  Abstract 


Contrast-Induced Nephropathy (CIN) is defined as acute deterioration of renal function after the administration of Radio-contrast materials, mostly within a period of 24 to 48 hours. Most of cases are non-oliguric and reversible and rarely associated with adverse outcomes. The diagnosis of CIN is based upon the clinical presentation, including the characteristic rise in serum creatinine concentration beginning with the first 24 to 48 hours after contrast exposure, and the exclusion of other causes of acute kidney injury (AKI). Incidence of CIN varies widely depending on the definition of AKI, the presence or absence of risk factors, the amount and type of agent administered, and the type of radiologic procedure. Biomarkers Cystatin C, Neutrophil gelatinase-associated lipocalin (NGAL) in urine and plasma, 2 hr after contrast administration have been shown to be predictive biomarkers of CIN. Most cases of CIN are self-limited. Management is conservative as with any other case of AKI and dialysis is rarely required. Adequate hydration, use of low doses of contrast media especially low-osmolar or iso-osmolar type , will reduce the risk of CIN.

Keywords: Acute Kidney Injury, biomarkers, Contrast induced nephropathy, Pediatrics, Prognosis, Risk factors


How to cite this article:
Vanaki R. Contrast Induced Nephropathy in ICU settings. J Pediatr Crit Care 2018;5:47-50

How to cite this URL:
Vanaki R. Contrast Induced Nephropathy in ICU settings. J Pediatr Crit Care [serial online] 2018 [cited 2020 Mar 29];5:47-50. Available from: http://www.jpcc.org.in/text.asp?2018/5/2/47/281120




  Introduction: Top


The increasing application of iodinated contrast media(CM) for diagnostic and interventional procedures have made CIN the third most common cause of hospital-acquired AKI. AKI is reversible in most cases, but its development rarely associated with adverse outcomes.[1]

Iodinated CM are either ionic or non-ionic and vary in their osmolality relative to plasma. High-osmolality CM (ionic) is more nephrotoxic than low-osmolality ionic or non-ionic CM, in at-risk patients.[2] CIN is defined as serum creatinine (SCr) elevation of 0.5 mg/ dl or of 25 % within 48 h after exposure to CM.[3] SCr is a relatively crude measure of glomerular filtration rate (GFR), and it has been suggested that creatinine clearance should be used to identify at-risk patients, as it provides better indication of renal function.[4]

Incidence:

Incidence of CIN varies widely depending on the definition of AKI, the presence or absence of risk factors, the amount and type of agent administered, and the type of radiologic procedure. Recently the risk of renal failure, injury to the kidney, failure of kidney function, loss of kidney function and end stage renal disease (RIFLE) criteria have been regarded as a more sensitive tool for detecting AKI. CIN may affect as little as 3 % of low-risk patients and as many as 25% of patients with risk factors, such as preexisting renal dysfunction, diabetes, advanced age, or concurrent nephrotoxic drug exposure.[3] Only limited data is available in pediatric setting. A recent study reported a CIN incidence ranging from 5 to 10 % in a population of 128 pediatric patients undergoing contrast-enhanced multidetector computer tomography (MDCT) with intravenous injection of low osmolar or an iso-osmolar iodinated CM.[4] In another prospective study, involving 80 children undergoing cardiac angiography, comparison of two non-ionic CM, iopromide and iohexol, was done in terms of complications ( in relation to the type and dosage of CM and the presence of cyanosis). Using the RIFLE classification applied for the diagnosis of CIN, the incidence was 18.75%.[5]

Pathophysiology:

CM used for radiologic procedures are tri-iodinated benzene derivatives that rely on iodine for their radio-opacity. Iodinated CM may be either ionic or non-ionic. Due to risk of CIN, iso-osmolar CM are preferred over high or low-osmolar CM.[2],[4],[5] Pathogenesis although not completely understood, CIN is most likely due to Acute Tubular Necrosis (ATN), related to vasoconstriction and cytotoxic effects from CM , possible contributions from prerenal factors or intratubular obstruction. Unlike other types of ATN, in CIN there is relatively rapid recovery of renal function and hence AKI improves rapidly after early and effective intervention.[1],[2]

Table 1 : Major risk factors

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Clinical Features:

Onset of AKI occurs within minutes after exposure to CM. The major clinical manifestations of CIN are an increase in the SCr and less commonly, oliguria. Most patients are non-oliguric and the increased creatinine is generally observed within 24 to 48 hours after contrast exposure and is mild. SCr usually starts to decline within three to seven days. Other manifestations of AKI may be present, including hyperkalemia, acidosis, and hyperphosphatemia. The diagnosis of CIN is based upon the clinical presentation, including the characteristic rise in SCr concentration beginning with the first 24 to 48 hours after contrast exposure, and the exclusion of other causes of AKI.

Biomarkers Cystatin C, Neutrophil gelatinase- associated lipocalin (NGAL) in urine and plasma, 2 hr after contrast administration have been shown to be predictive biomarkers of CIN but these results remain unvalidated. These could be allowed for earlier identification and intervention to avoid bad outcomes associated with CIN.[6],[7]

The urinary sediment may show classic findings of ATN, including muddy brown granular and epithelial cell casts and free renal tubular epithelial cells without evidence of glomerular disease (such as dysmorphic red blood cells or red blood casts) or interstitial nephritis (such as white cells or white cell casts). Protein excretion on presentation is absent or mild. If urine is tested and proteinuria is detected, the test should be repeated at least 48 hours after contrast exposure to exclude a false-positive result due to iodinated CM.

The fractional sodium excretion (FENa) is often <1% in patients with CIN. There are no characteristic radiographic features of CIN.A prolonged nephrogram may be seen among patients with established CIN who undergo a contrast enhanced CT scan. Role for ultrasound study and renal biopsy is limited.[2],[8]

Management and Prognosis:

Most cases of CIN are self-limited. Management is conservative as with any other case of AKI. In most cases, SCr starts to decline within three to seven days, and returns to baseline renal function.[2],[3]

Table 2. Conservative management of CIN

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Dialysis rarely required. Acute and maintenance dialysis is indicated in an estimated 1% of cases of CIN.[9] The indications of dialysis are the same as in other forms of AKI. The risk is higher with severe, underlying CKD, in which residual renal dysfunction may persists even after SCr returns to baseline. Adult studies have shown that CIN leads to prolonged hospital stay and added economic burden in addition to increased mortality risk. The 30-day, one-year, and five-year mortality risks are higher among patients who developed CIN.[10]

Table 3 : Other pharmacological & non-pharmacological interventions

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Preventive Strategies:

Table 4. Prevention of CIN[2]

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There are no randomized trials that have been proven that specific interventions to prevent CIN, or prevent morbidity or mortality.

Volume Expansion: Ensure adequate hydration with isotonic saline prior to contrast administration reduces risk of CIN. (Grade 2C) 2-6

Start Isotonic Saline at 1ml/kg/hr at least 2 hours prior to contrast administration and continue for 6-12 hours following the procedure.

Summary & Recommendations:

  • CIN is generally reversible type of AKI that occurs after the administration of CM
  • Pathogenesis although not completely understood, CIN is most likely due to ATN, related to vasoconstriction and cytotoxic effects from CM with possible contributions from prerenal factors or intratubular obstruction.
  • CIN presents with increase in SCr within 24- 48hrs after CM exposure and less commonly with oliguria. AKI is usually mild and responds to conservative measures and declines by 3-7days and rarely requires dialysis
  • The diagnosis is based upon the clinical presentation and the exclusion of other causes of AKI. The absence of other findings on urinalysis such as white blood cells (WBCs), WBC casts, dysmorphic red blood cells (RBCs), or RBC casts generally excludes other causes of AKI such as interstitial nephritis and glomerular diseases.
  • Levels of Cystatin C, NGAL in urine and plasma have been shown to be promising predictive biomarkers of CIN.
  • For all at-risk patients, use low-osmolar or iso- osmolar CM with preferred low dose and avoid repetitive studies.
  • Adequate hydration with isotonic saline prior to and continued for several hours after contrast administration prevents CIN
  • For all at risk patients, acetylcysteine not be given orally or intravenously as it has not shown alter outcomes compared to placebo.(Grade 2B)


Source of Funding - Nil

Conflict of Interest - Nil



 
  References Top

1.
Maliborski A, Zukowski P, Nowicki G, Boguslawska R. Contrast-induced nephropathy - a review of current literature and guidelines. Med Sci Monit 2011;17(9):199-204.  Back to cited text no. 1
    
2.
Verghese P. Contrast nephropathy in children. J Pediatr Intensive Care 2015;3(2):45-52.  Back to cited text no. 2
    
3.
Cantais A, Hammouda Z, Mory O, Patural H, Stephan JL, Gulyaeva L, et al. Incidence of contrast-induced acute kidney injury in a pediatric setting: a cohort study. Pediatr Nephrol 2016;31(8):1355-62.  Back to cited text no. 3
    
4.
Zo’o M, Hoermann M, Balassy C, Brunelle F, Azoulay R, Pariente D, et al. Renal safety in pediatric imaging: Randomized, double-blind phase IV clinical trial of iobitridol 300 versus iodixanol 270 in multidetector CT. Pediatr Radiol 2011;41(11):1393-400.  Back to cited text no. 4
    
5.
Ajami G, Derakhshan A, Amoozgar H, Mohamadi M, Borzouee M, Basiratnia M, et al. Risk of nephropathy after consumption of nonionic contrast media by children undergoing cardiac angiography: A prospective study. Pediatr Cardiol. 2010;31(5):668-73.  Back to cited text no. 5
    
6.
Benzer M, Alpay H, Baykan Ö, Erdem A, Demir IH. Serum NGAL, cystatin C and urinary NAG measurements for early diagnosis of contrast-induced nephropathy in children. Ren Fail 2016;38(1):27-34.  Back to cited text no. 6
    
7.
Ribitsch W, Schilcher G, Quehenberger F, Pilz S, Portugaller RH, Truschnig-Wilders M, et al. Neutrophil gelatinase- associated lipocalin (NGAL) fails as an early predictor of contrast induced nephropathy in chronic kidney disease (ANTI-CI-AKI study). Sci Rep 2017;7:1-9.  Back to cited text no. 7
    
8.
Chao C-T. Epidemiology, Clinical Features and Diagnosis of Contrast Induced Nephropathy: A Brief Review. Gen Med 2013;1(1):1-5.  Back to cited text no. 8
    
9.
Rudnick MR, Goldfarb S, Wexler L, Ludbrook PA, Murphy MJ, Halpern EF, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: A randomized trial. Kidney Int 1995;47(1):254-61.  Back to cited text no. 9
    
10.
From AM, Bartholmai BJ, Williams AW, Cha SS, McDonald FS. Mortality associated with nephropathy after radiographic contrast exposure. Mayo Clin Proc 2008;83(10):1095-100.  Back to cited text no. 10
    
11.
Weisbord SD, Gallagher M, Jneid H, Garcia S, Cass A, Thwin S-S, et al. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine. N Engl J Med 2018; 378(7):603-61.  Back to cited text no. 11
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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