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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
ORIGINAL ARTICLE  
Year : 2017  |  Volume : 28  |  Issue : 3  |  Page : 491-498
Effect of fluorescein angiography on renal functions in type 2 diabetes patients: A pilot study


1 Department of Pharmacology, Umm Al-Qura University, Makkah, Saudi Arabia
2 Department of Internal Medicine and Nephrology, Alexandria University, Alexandria, Egypt
3 Department of Ophthalmology, Alexandria University, Alexandria, Egypt
4 Department of Clinical Pharmacy, College of Pharmacy, Umm-Al-Qura University, Makkah, Saudi Arabia
5 Kidney and Urology Center, Alexandria, Egypt

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Date of Web Publication18-May-2017
 

   Abstract 

Fluorescein angiography (FA) is an important tool for the diagnosis and management of diabetic retinopathy. However, the safety of fluorescein sodium on renal functions is not fully understood. One hundred type 2 diabetes patients, within the Ophthalmology Outpatient Clinic at Alexandria Main University Hospital, Egypt, were enrolled in this prospective observational study to determine the safety of FA on renal function. Serum creatinine and cystatin C were measured pre- and 2 days post-FA. Urinary neutrophil gelatinase-associated lipocalin (uNGAL) was measured pre- and 4 hours post-FA. Renal injury was defined as a 25% increase in serum creatinine, cystatin C, or uNGAL. The study included 71 females and 29 males, with a mean age of 55.73 ± 7.29 years. Baseline serum cystatin C and uNGAL were 0.89 ± 0.34 mg/L and 21.7 ± 2.39 ng/mL, respectively. Serum cystatin C and uNGAL significantly increased after FA to 0.95 ± 0.36 and 27 ± 2.81, respectively (P <0.001). Eleven patients (11%) experienced more than a 25% rise in serum cystatin C from baseline, whereas 40 patients (40%) experienced more than a 25% increase in uNGAL levels after FA. However, the mean serum creatinine level did not change significantly after FA (P = 0.061). Only one patient experienced more than a 25% rise in serum creatinine from baseline. FA showed a significant increase in early sensitive acute kidney injury biomarkers (as serum cystatin C and uNGAL) in substantial number of patients, suggesting but still not proving, a potential harmful effect of FA on kidney functions. These findings were not demonstrated using ordinary serum creatinine.

How to cite this article:
Almalki WH, Abdalla AN, Elkeraie AF, Abdelhadi AM, Elrggal M, Elrggal ME. Effect of fluorescein angiography on renal functions in type 2 diabetes patients: A pilot study. Saudi J Kidney Dis Transpl 2017;28:491-8

How to cite this URL:
Almalki WH, Abdalla AN, Elkeraie AF, Abdelhadi AM, Elrggal M, Elrggal ME. Effect of fluorescein angiography on renal functions in type 2 diabetes patients: A pilot study. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2017 Nov 23];28:491-8. Available from: http://www.sjkdt.org/text.asp?2017/28/3/491/206444

   Introduction Top


Five hundred and ninety-two million people worldwide are projected to have diabetes by 2035 according to the International Diabetes Federation.[1] Diabetes complications such asdiabetic kidney disease (DKD), diabetic retino- pathy (DR), diabetic neuropathy, vasculopathy, and an increased risk for cerebrovascular and cardiovascular diseases have major implications on health resources and medical expenditure. According to the American Diabetes Association, the total estimated cost of diagnosed diabetes in 2012 is $245 billion, of which 18% (about 44 billion) were used to treat diabetes complications.[2] DR and DKD are two of the most common microvascular complications of DM, representing the leading cause of blindness[3] and end-stage renal disease (ESRD)[4] worldwide, respectively. The concordance rate between these two complications is very high among both type 1 and type 2 diabetic patients.[5],[6]

Fluorescein angiography (FA) is the current gold standard for visualizing retinal vascula- ture. It allows staging of DR, identification of areas of nonperfusion, macular edema, ischemia, and microaneurysms.[7] Although optical coherence tomography is a noninvasive rapid tool that allows visualization and assessment of retinal thickness and morphology, it cannot replace FA, especially in ischemic diabetic maculopathy.[8] Both tools are required for accurate detection of macular edema that might be missed if either of them was used alone[9] and also during planning for laser photocoagulation.[10]

Fluorescein sodium dye is metabolized by the kidneys and eliminated through the urine within 48–72 h of administration.[11] FA is a relatively safe procedure compared to other intravenous radiocontrast media angiography with few reported adverse drug reactions (among which the most common were nausea and vomiting, with no reported serious adverse drug reactions or deaths).[12],[13]

Regarding fluorescein sodium (as a non- iodinated dye) effect on renal function, very few studies have been published with conflicting results.[14],[15],[16] Two studies showed no effect of FA on renal functions;[14],[16] however, one study demonstrated significant rise in serum creatinine in nine (out of 44) patients.[15] None of these studies used sensitive new biomarkers for the detection of possible kidney injury following FA.

Diagnosis of contrast-induced (CI) nephro- pathy [or CI acute kidney injury (AKI)] depends mainly on serum creatinine (as an increase by 0.5 mg/dL or >25% from baseline). However, serum creatinine lacks sensitivity to rapid glomerular filtration rate changes seen in AKI, and its elevation occurs usually two to three days following renal insult.[17] Several biomarkers including neutrophil gelatinase-associated lipocalin (NGAL),[18] cystatin-C,[19] Urinary Kim-1,[20] and interlukin- 18[21] have been proposed to diagnose CI-AKI earlier than serum creatinine. This earlier detection was demonstrated both in patients with normal renal functions[18] and chronic kidney disease (CKD).[22],[23] However, there are no published studies comparing cystatin C or urinary NGAL (uNGAL) before and after FA.

Therefore, the aim of our study was to test the safety of FA using sensitive early AKI biomarkers such as uNGAL and serum cystatin C.


   Materials and Methods Top


This is a pre- and post-study design using a single group that was conducted from January 1, 2014, to July 1, 2014. The primary outcome was to test the FA safety using uNGAL and serum cystatin C.

The patients were selected from the Ophthalmology Outpatient clinic at Alexandria Main University Hospital, Egypt.

The Faculty of Medicine’s Ethics Committee at Alexandria University approved the study. Written consents were obtained from all patients before sampling and following a thorough explanation of the procedure according to Helsinki Declaration.[24]

All type 2 diabetic patients, of any age and gender, with stable kidney functions over the past three months before enrolling in the study who have signs of DR referred to the clinic for FA assessment were included in the study. Patients with recent AKI, recent use of nonsteroidal anti-inflammatory drugs, steroids, or angiotensin-converting enzyme inhibitors or angiotensin receptor blockers within two weeks, thyroid dysfunction, pregnancy and lactation, use of contrast media within two weeks of study entry, history of hyper- sensitivity reaction to contrast media, and known familial nephropathies such as auto- somal dominant polycystic kidney disease were excluded from the study. Patients were examined by a nephrologist and ophthalmologist for inclusion and exclusion criteria including patient history, clinical examination, and laboratory investigations. The first 100 consecutive patients who met our inclusion criteria were selected in this prospective observational study.

Urine (for urinary albumin/creatinine ratio UACR and uNGAL) and serum samples (for creatinine and cystatin C) were collected just before FA. Five milliliters of 5% fluorescein sodium were injected as a bolus into a peripheral vein[25],[26] and retinal photography started. Four hours later, the uNGAL measurement was repeated from a second urine sample. Serum creatinine and cystatin C measurements were then repeated 48 h later.

Biochemical analysis

Serum cystatin C assays were performed using the latex particle-enhanced nephelo- metric immunoassay on a BN II nephelometer (SIEMENS ®). For uNGAL, the BioVendor® Human Lipocalin-2/NGAL ELISA kit was used.

Acute kidney injury definition

According to the European Society of Urogenital Radiology (2011), CI-AKI is defined as an increase of 25% or more in serum creatinine or an absolute increase of 0.5 mg/dL or more from baseline value at 48–72 h following the exposure to intravascular contrast media (CM).[27],[28] This definition was criticized by lack of sensitivity and non-inclusion of urine output changes, as used in RIFLE,[29] AKIN,[30] and KDIGO [1] definitions. However, it is still the most acceptable one and it has the advantage of being widely used as an end point in many clinical trials, thus allowing comparison between different trials’ results. Similarly, a 25% increase in serum cystatin C or uNGAL was considered a marker for renal injury. Few studies tested a 25% increase in serum cystatin C or uNGAL for earlier diagnosis of CI- AKI.[32],[33] In one study, defining CI-AKI as 25% increase in serum cystatin C increased prevalence of diagnosed cases than when a 25% increase in serum creatinine was used (44% vs. 11%, respectively), with 78% sensitivity and 81% specificity.[32] Another study proved that a 25% increase in uNGAL 8 h after contrast administration was able to identify cases with CI-AKI with a 94.1% sensitivity and 97.7% specificity at the time when creatinine level did not show statistically significant changes (P = 0.11) until 48 h after contrast material administration.[33] Thereby, we adopted a 25% increase in serum cystatin C and uNGAL as markers of kidney injury following FA.


   Statistical Analysis Top


Data were analyzed using descriptive frequencies and percentages. Statistical analysis was performed using PASW Statistics version 18 (SPSS-IBM Co, Chicago, Illinois, USA). After testing for normality using Kolmogorov- Smirnov test, paired t-test was applied to compare the different periods. Pearson correlation was done to find the degree of association between serum creatinine and serum cystatin C. P <0.05 was considered statistically significant for all the results.


   Results Top


Clinical characteristics of patients presenting for FA are summarized in [Table 1]. Participants included 71 females and 29 males, with a mean age of 55.73 ± 7.29 years. Sixty-four patients had a history of hypertension. Fifty- two patients had DM for more than 10 years; 34 patients had DM between 5 and 10 years; and 14 patients had DM <5 years. UACR levels ranged from 4.13 to 610 mg/g.

Before FA, serum creatinine showed positive correlation with serum cystatin (r = 0.67, P <0.001; [Figure 1]). This correlation was also noticed 48 h after FA (r = 0.685, P<0.001).uNGAL and either serum creatinine (r = 0.034, P = 0.74) or cystatin-C (r = 0.113, P = 0.264). Forty-eight hours after FA, we observec a nonsignificant rise in serum creatinine with a corresponding significant decrease in estimated GFR (eGFR) using Modification of Diet in Renal Disease, and CKD-Epi creatinine equations were also noticed [Table 2]. However, a significant increase in uNGAL (4 h after FA) and serum cystatin C (48 h after FA) was observed, with a corresponding significant decrease in cystatin C-based eGFR after FA [Table 2].
Table 1: Baseline characteristics in patients undergoing fluorescein angiography.

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Table 2: Changes in creatinine, eGFR, Cystatin C, and urinary NGAL after FA.

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Figure 1: Correlation between serum creatinine and serum cystatin C.

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A 25% increase in biomarkers from baseline was considered an AKI as per our definition. Only one patient experienced a >25% (i.e., 32.5%) increase in serum creatinine from baseline, whereas 11 patients had more than a 25% increase in cystatin C. Meanwhile, 40 cases showed increases in uNGAL by more than 25% from baseline, with 33 of them experiencing more than 50% increase.


   Discussion Top


In our study, we found that FA caused significant increases in uNGAL (4 h after FA) and cystatin C (48 h after FA). However, serum creatinine and eGFR did not change significantly (48 h after FA).

Similar results were observed by Kameda et al[14] using eGFR and Chung and Lee[16] using serum creatinine. Kameda et al found no effect of FA on renal functions.

There was no significant correlation between using eGFR.[14] Furthermore, Chung and Leereported no significant change in serum crea- tinine after FA in 186 patients retrospectively. Four patients developed AKI that was explained by authors to be due to unrelated reasons.[16] On the other hand, Alemzadeh- Ansari et al demonstrated a 25% rise in serum creatinine following FA in nine out of 44 diabetic patients which was not specified by the authors to be significant or not.[15]

Both serum cystatin C and uNGAL have been established in different previous trials as novel biomarkers for early diagnosis and detection of CI-AKI.

When defining renal injury as 25% increase in cystatin C, 11 patients (11%) were diagnosed to have FA-induced renal injury compared to only one patient using 25% rise in serum creatinine.

Ideally, serum cystatin C should have been measured 24 h after the procedure (not 48 h as we did). However, this pilot study was conducted to test the possible occurrence of fluorescein-induced renal injury, rather than the equivocal early detection. Furthermore, in other studies, cystatin C measured at 48 h following contrast administration detected CI- AKI (45 patients - 37.2%) better than crea- tinine (20 patients - 16.5%) and Mehran risk scoring correlated more strongly with a cys- tatin C increase.[19] Moreover, it was more convenient for patients to come only once after 48 h for both creatinine and cystatin C measurements. Serum cystatin C significantly increased 48 h after FA (P >0.001). Moreover, when calculating eGFR using the 2012 CKD- Epi Cystatin C and CKD-Epi Creatinine- Cystatin-C equations, eGFR significantly decreased after FA (P <0.001).

To date, no single study has evaluated FA- induced AKI using cystatin C. However, it has been used for the early detection of iodinated CM-induced AKI in many studies. Rickli et al[34] found elevated cystatin C 24 h after radiocontrast media administration, whereas crea- tinine was elevated after 48 h. Ebru et al[19] detected CI-AKI using cystatin-C (45 patients - 37.2%) better than creatinine (20 patients - 16.5%) when both were measured 48 h after diagnostic coronary angiography. Briguori et al[35] measured serum creatinine and cystatin C at 24 and 48 h after angiography, and followed up those patients for 12 months later regarding major adverse events (including death of any cause and dialysis). A cutoff cystatin C increased concentration of >10% at 24 h after CM exposure had a negative predictive value of 100% and a positive predictive value of 39% and was found to be a more reliable marker for the early diagnosis and prognosis of CI-AKI, as it more strongly correlated with major adverse events at 12 months.

When defining renal injury as 25% increase in uNGAL, prevalence of FA-induced renal injury increased to 40% (P <0.001). Previous studies detecting CI-AKI reported similar results following iodinated CM administration. Hirsch et al[36] found that 2 h uNGAL was a powerful independent predictor of CI-AKI after cardiac catheterization and angiography in children with congenital heart disease. Moreover, Bachorzewska-Gajewska et al[32] showed that NGAL levels were significantly higher 2 h after the percutaneous coronary intervention (PCI) (with serum NGAL) and 4 h after the PCI (with uNGAL). Researchers concluded that urinary NGAL could be used as an early sensitive biomarker of renal impairment after PCI.

The percentage of change in uNGAL from baseline to diagnose CI-AKI has been different in previous research. Bachorzewska- Gajewska et al[32] found that a 25% variation in uNGAL concentration was sufficient as a predictor of contrast nephropathy. However, Souza et al[37] found that an increase of 50% from baseline values in uNGAL was predictive of early stages of AKI (creatinine >0.3 mg/dL) with 60% sensitivity and 81% specificity. In our study, 40 cases had a >25% increase in uNGAL level from baseline, of which 33 cases had an increase of >50% from baseline, which may draw an attention to the possibility of FA-induced renal injury.

Although we had patients with significant increases in biomarkers after FA, we did not follow up to identify any potential reversible or irreversible loss of kidney function. This omission warrants consideration in future studies. However, we cannot overlook the significant increase in biomarkers, which have been proven to be early sensitive detectors of CI-AKI. Furthermore, NGAL has been demonstrated in many studies to be useful in predicting the prognosis and outcome of AKI, even in the absence of a diagnostic rise in serum creatinine.[38] When analyzing pooled data from 2322 critically ill patients from 10 prospective observational studies of NGAL, Haase et al found significant increase in subsequent renal replacement therapy initiation and hospital mortality in the group of patients who had a rise in NGAL levels without an increase in serum creatinine level.[38] These researchers concluded that NGAL detects sub- clinical AKI and a subsequent increased risk of adverse outcomes in the absence of diagnostic increases in serum creatinine.

More recently, Claudio Ronco et al discussed the potential occurrence of a subclinical AKI. The authors clearly stated that if a biomarker- positive, creatinine-negative patient is observed, then he/she has probably received an “injury” to his/her kidney. However, this patient may still be in a preclinical (according to crea- tinine) phase.

These findings together with our results should draw the attention to the possibility of FA-induced renal injury. However, our study was not powered enough to detect and prove such a finding. Therefore, patients undergoing FA should be carefully monitored for any potential kidney injury, and alternative retinal imaging techniques may be preferably used to avoid the risk of AKI.

Limitations of our study include the absence of long-term follow-up of the patients, using single point measurement of biomarkers following FA instead of serial measurements, non-inclusion of more advanced CKD who might be more vulnerable to CI-AKI and the use of a small sample of patients. These limitations should be addressed in future studies.


   Conclusion Top


FA may not be as safe, for the kidneys, as it was previously assumed. The use of newly discovered biomarkers, such as serum cys- tatin-C and uNGAL, revealed a possible form of subclinical AKI that was not previously demonstrated using traditional renal function tests.

Further studies addressing the same issue with larger cohort and sufficient follow-up periods to detect any possible degrees of kidney damage are needed. Until more data are available, other non-fluorescein-based retinal examination techniques may be recommended for diabetic patients with high-risk factors for CI-AKI.


   Acknowledgment Top


The authors would like to thank the “Institute of Scientific Research and Revival of Islamic Heritage (ISRRIH), Umm Al-Qura University, Saudi Arabia” (Project: 43410015) for their financial support.

Conflict of interest: None declared.

 
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Correspondence Address:
Mohamed E Elrggal
Kidney and Urology Center, Alexandria
Egypt
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DOI: 10.4103/1319-2442.206444

PMID: 28540884

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