Persistent Decline in eGFR Observed After Anti-VEGF Treatment for DME

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Results from the 2-year retrospective cohort study showed patients with DME and extremely high or low eGFR had a greater decline in eGFR.

Yi-Ting Hsieh, MD | Image Credit: ResearchGate

Yi-Ting Hsieh, MD

Credit: ResearchGate

Long-term treatment with intravitreal anti-vascular endothelial growth factor (VEGF) therapy was associated with a continual decline in estimated glomerular filtration rate (eGFR) in patients with diabetic macular edema (DME), according to new data.1

The 2-year retrospective cohort study reported a mean decrease of 16.5% in eGFR, with patients with extremely high or low eGFR showing a greater eGFR decline and those with poor baseline rates often requiring dialysis after anti-VEGF treatment.

“For those with poor baseline renal function, a further decline in eGFR would result in the need for renal replacement therapy,” wrote the investigative team, led by Yi-Ting Hsieh, MD, from the department of ophthalmology at National Taiwan University Hospital. “Therefore, close monitoring of renal function may be necessary if these patients require long-term intravitreal anti-VEGF treatment.”

DME represents the leading cause of visual impairment in patients with diabetes, with the breakdown of the blood-retinal barrier marking a key event in the progression of the retinal disease. VEGF inhibitors have transformed the management of multiple ophthalmic diseases, showing anatomical and visual improvement in the treatment of DME.2

However, there are limited investigations into the impact of intravitreal anti-VEGF injections on renal function. As diabetic nephropathy is often comorbid with diabetic retinopathy, longitudinal changes in eGFR after anti-VEGF treatment for DME should be considered. In this analysis, Hsieh and colleagues investigated the longitudinal changes in renal function in patients receiving intravitreal ranibizumab or aflibercept for DME for up to 2 years.

A total of 108 patients were retrospectively enrolled from the National Taiwan University Hospital between January 2013 - December 2018. Investigators recorded the estimated eGFR at baseline and during the 2-year follow-up period, as well as the receipt of any renal replacement therapy, including hemodialysis and renal transplantation.

During the treatment period, a mean of 9.1 ± 3.9 injections was administered to each patient within the first year and 2.6 ± 3.0 injections administered during the second year.

After receiving intravitreal anti-VEGF therapy, a constant decline in eGFR was observed in patients with DME during the 2-year treatment period. After treatment, eGFR had a mean decline of –10.4 ± 23.2% and –16.5 ± 26.4% at months 12 and 24, respectively.

The analysis showed patients with extremely high or low eGFR had greater eGFR decline. Those in the eGFR >120 mL/min and 16–30 mL/min groups showed the greatest decline, at –32.0 ± 20.6% and –37.4 ± 30.9%, respectively. Meanwhile, patients in the 61–90 mL/min group reported the smallest decline in eGFR, at –4.3 ± 19.7%, after 2 years of treatment.

During the 2-year study period, 1 out of 52 patients (1.9%) receiving ranibizumab and 5 out of 56 patients (8.9%) receiving aflibercept started hemodialysis or peritoneal dialysis (P = .21). Regression analysis showed the baseline eGFR correlated with renal replacement therapy after intravitreal anti-VEGF treatment (hazard ratio, 0.879 per increase of 1 in eGFR; P = .018).

“To our knowledge, this is the first study to reveal long-term eGFR changes after intravitreal anti-VEGF treatment for DME,” investigators wrote.

References

  1. Fang YC, Lai IP, Lai TT, et al. Long-Term Change in Renal Function After Intravitreal Anti-VEGF Treatment for Diabetic Macular Edema: A 2-Year Retrospective Cohort Study [published online ahead of print, 2023 Aug 17]. Ophthalmol Ther. 2023;10.1007/s40123-023-00771-4. doi:10.1007/s40123-023-00771-4
  2. Das A, McGuire PG, Rangasamy S. Diabetic macular edema: pathophysiology and novel therapeutic targets. Ophthalmology. 2015;122:1375–94. https://doi.org/10.1016/j.ophtha.2015.03.024.
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