June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Increases in markers of renal damage in patients with diabetic maculopathy receiving intravitreal Avastin
Author Affiliations & Notes
  • Emily Han Shao
    ophthalmology, Imperial College London, London, United Kingdom
  • Shenzhen Tempest-Roe
    ophthalmology, Imperial College London, London, United Kingdom
  • Simon R Taylor
    ophthalmology, Imperial College London, London, United Kingdom
  • Footnotes
    Commercial Relationships Emily Shao, None; Shenzhen Tempest-Roe, None; Simon Taylor, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 1502. doi:
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      Emily Han Shao, Shenzhen Tempest-Roe, Simon R Taylor; Increases in markers of renal damage in patients with diabetic maculopathy receiving intravitreal Avastin. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):1502.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract
 
Purpose
 

Monocyte chemoattractant protein 1 (MCP1) is a key chemokine that regulates migration and infiltration of monocytes/ macrophages. It also mediates acute ischaemic and toxic kidney injury and is a major marker of acute kidney injury. Vascular endothelial growth factor (VEGF) has become a major target for the treatment of retinal disease. However, the systemic effects of intraocular administration of anti-VEGF drugs remain controversial and this may be particularly important in patients with coexistent diabetic maculopathy and nephropathy, as VEGF is essential for the maintenance of normal renal function.<br /> <br /> In this study we analysed systemic changes in VEGF and MCP-1 systemic levels in diabetic patients with diabetic macular oedema who was treated with a course of bevacizumab injections for diabetic macular oedema.

 
Methods
 

Serum samples were obtained from six patients with diabetic macular oedema who were treated with 3 bevacizumab injections over a period of 3 months. Peripheral venous blood samples were taken at each visit and centrifuged at 3,000 rpm for 10 minutes followed by being stored at - 70°C until analysis. Serum VEGF 165 and MCP-1 levels were determined using enzyme-linked immunosorbent assay (R&D systems, UK) both pre and post immunodepletion to remove complexed VEGF.

 
Results
 

Serum VEGF 165 levels was suppressed by intravitreal bevacizumab. Serum MCP-1 levels conversely increased with intravitreal Bevacizumab, after the end of the first course of three injections. Patients with poorer initial renal function had a significantly greater increase in systemic MCP-1 levels following intravitreal Bevacizumab relative to patients with normal baseline renal function.

 
Conclusions
 

These results suggest that repeated intravitreal Bevacizumab injections lead to a decrease in systemic VEGF levels, with corresponding increase in MCP-1 levels in diabetic patients. Patients with poor baseline renal function were the most affected, suggesting that the systemic decrease in VEGF levels with intravitreal Bevacizumab may be of particular significance in diabetic patients with coexistent nephropathy.  

 
Figure 1. Decrease in systemic VEGF levels with intravitreal Bevacizumab.
 
Figure 1. Decrease in systemic VEGF levels with intravitreal Bevacizumab.
 
 
Figure 2. Increase in MCP-1 with intravitreal Avastin is significantly greater in patients with low baseline eGFR compared to patients with normal baseline eGFR.
 
Figure 2. Increase in MCP-1 with intravitreal Avastin is significantly greater in patients with low baseline eGFR compared to patients with normal baseline eGFR.

 
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