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Year : 2018  |  Volume : 18  |  Issue : 1  |  Page : 24-25

Fluorescein angiography and the kidney, friend or foe?

Nephrology Department, Kidney and Urology Center, Alexandria, Egypt

Date of Submission21-Nov-2017
Date of Acceptance20-Feb-2018
Date of Web Publication02-May-2018

Correspondence Address:
Dr. Mohamed E El-Rggal
23, Mohamed Safwat Street, Kafr-Abdo, Alexandria, 21529
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jesnt.jesnt_26_17

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How to cite this article:
El-Rggal ME. Fluorescein angiography and the kidney, friend or foe?. J Egypt Soc Nephrol Transplant 2018;18:24-5

How to cite this URL:
El-Rggal ME. Fluorescein angiography and the kidney, friend or foe?. J Egypt Soc Nephrol Transplant [serial online] 2018 [cited 2022 Aug 16];18:24-5. Available from: http://www.jesnt.eg.net/text.asp?2018/18/1/24/231750

Fluorescein angiography (FA) is generally accepted among the nephrology community as being kidney friendly; however, it remains unclear whether it is truly safe or not based on the available evidence. were There have been three retrospective studies [1],[2],[3] and two prospective ones [4],[5] ([Table 1]) published till now examining the effect of FA on kidney functions. When pooling data from these studies, 16 patients (of 618, 2.5%) developed acute kidney injury (AKI) [defined as an absolute increase in serum creatinine (SCr) ≥0.5 mg/dl or ≥25% increase from baseline within 24–72 h after FA]. Most of the studies reported that SCr level returned back to normal within few days without any intervention, or attributed the increase in SCr level to an associated event (e.g. concomitant nephrotoxic drug administration).
Table 1 Summary of publications examining the effect of fluorescein angiography on renal functions

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Nevertheless, these studies had many limitations, including first, the absence of long-term follow-up data. It has to be noted that the peak rise in SCr level may occur 5 days or even more after contrast exposure [6]. The second was the use of 0.5 mg/dl absolute increase in SCr as a cutoff point to define contrast induced nephropathy (CIN) rather than the 0.3 mg/dl absolute rise recommended by AKIN [7] and KDIGO [8] guidelines. Even though decreasing the threshold from 0.5 to 0.3 mg/dl may falsely identify patients with AKI owing to assay variability and day-to-day variability, early detection is more important. Third, the use of SCr and estimated glomerular filtration rate as a marker for CIN development, despite being the current accepted definition, it still got some limitations. SCr has been inferior to serum cystatin-C, urinary (or serum) neutrophil gelatinase-associated lipocalin, urinary KIM-1, and interleukin-18 in early detection of CIN [9],[10],[11],[12]. Testing these early AKI biomarkers (namely serum cystatin-C and urinary neutrophil gelatinase-associated lipocalin) after FA detected more cases with CIN rather than SCr ([Table 1]) [4].

Despite these limitation, and in the view of the current evidence and clinical practice, one cannot prohibit FA for patients at risk of CIN, especially patients with chronic kidney disease as long as it is clinically indicated. However, patients and clinicians should be aware of the absence of long-term safety data, the potential hazard of subclinical AKI and the need for further clinical trials to assess and assure the long-term safety of FA.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kameda Y, Babazono T, Haruyama K, Iwamoto Y, Kitano S. Renal function following fluorescein angiography in diabetic patients with chronic kidney disease. Diabetes Care 2009; 32:e31.  Back to cited text no. 1
Chung B, Lee CS. Renal function following fluorescein angiography. Invest Ophthalmol Vis Sci 2014; 55:258.  Back to cited text no. 2
Lee JH, Chung B, Lee SC, Kim SS, Koh HJ, Lee CS. Lower incidence of contrast-induced nephropathy in patients undergoing fluorescent angiography. BMC Ophthalmol 2017; 17:46.  Back to cited text no. 3
Almalki W, Abdalla A, Elkeraie A, Abdelhadi A, Elrggal M, Elrggal M. Effect of fluorescein angiography on renal functions in type 2 diabetes patients: a pilot study. Saudi J Kidney Dis Transplant 2017; 28:491.  Back to cited text no. 4
Alemzadeh-Ansari MJ, Beladi-Mousavi SS, Feghhei M. Effect of fluorescein on renal function among diabetic patients. Nefrologia 2011; 31:612–613.  Back to cited text no. 5
Burns KEA, Chu MWA, Novick RJ, Fox SA, Gallo K, Martin CM et al. Perioperative N-acetylcysteine to prevent renal dysfunction in high-risk patients undergoing cabg surgery: a randomized controlled trial. JAMA 2005; 294:342–350.  Back to cited text no. 6
Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG et al. Acute kidney injury network: report of an initiative to improve outcomes in acute kidney injury. Crit Care 2007; 11:R31.  Back to cited text no. 7
[No authors listed]. Section 4: contrast-induced AKI. Kidney Int Suppl (2011) 2012; 2:69–88.  Back to cited text no. 8
Alharazy SM, Kong N, Saidin R, Gafor AHA, Maskon O, Mohd M et al. Serum neutrophil gelatinase-associated lipocalin and cystatin C are early biomarkers of contrast-induced nephropathy after coronary angiography in patients with chronic kidney disease. Angiology 2013; 65:436–442.  Back to cited text no. 9
Malyszko J, Bachorzewska-Gajewska H, Poniatowski B, Malyszko JS, Dobrzycki S. Urinary and serum biomarkers after cardiac catheterization in diabetic patients with stable angina and without severe chronic kidney disease. Ren Fail 2009; 31:910–919.  Back to cited text no. 10
Duan SB, Liu GL, Yu ZQ, Pan P. Urinary KIM-1, IL-18 and Cys-c as early predictive biomarkers in gadolinium-based contrast-induced nephropathy in the elderly patients. Clin Nephrol 2013; 80:349–354.  Back to cited text no. 11
Ebru AE, Kilic A, Korkmaz FS, Seker R, Sasmaz H, Demirtas S et al. Is cystatin-C superior to creatinine in the early diagnosis of contrast-induced nephropathy?: a potential new biomarker for an old complication. J Postgrad Med 2014; 60:135–140.  Back to cited text no. 12
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