Systemic administration of agents that inhibit vascular endothelial growth factor (VEGF) and therefore vascular proliferation is often used to treat various cancers. However, these agents are associated with a number of side effects, including proteinuria and renal injury. Intravitreal injection of anti-VEGF agents has become the cornerstone of macular disease treatment. Since these agents cross the blood-retina barrier and enter the circulation, systemic side effects have been reported. We report the novel case of a 57-year-old patient who presented with macular oedema secondary to central retinal vein occlusion, underwent three monthly loading-dose injections with the anti-VEGF agent ranibizumab, and 2 weeks after the second injection presented with biopsy-verified membranoproliferative glomerulonephritis. Twelve weeks after presenting with renal failure and 10 weeks after his last anti-VEGF injection, the patient demonstrated spontaneous recovery of his kidney function. The patient had a history that promoted renal fragility, including hypertension, liver transplantation 6 years earlier for alcohol-related cirrhosis and new-onset diabetes mellitus after transplant. Our literature review and case suggest that although adverse renal events after intravitreal anti-VEGF injections are very rare, ophthalmologists and nephrologists should be aware of this risk.

OBJECTIVE: Although taxanes are a frequently used group of chemotherapy agents, they can, rarely, lead to macular oedema. The purpose of this article is to review and communicate, in an integrated way, the data of the cases previously reported in the literature, as well as to present a new case.
METHODS: Narrative review of reports of cases of macular oedema associated with taxanes, and communication of the clinical case of a 73-year-old woman who, after treatment with paclitaxel for metastatic breast cancer, developed macular oedema that disappeared after discontinuing the drug.
RESULTS: The review included 57 cases with data from 109 eyes collected in 52 articles. The large majority (76.79%) of the cases were women, and the mean age was 58.75 years. The cancer that most frequently motivated the treatment was breast cancer (60.72%), and 92.5% of cases had metastases. The most frequently associated drug was paclitaxel (52.63%). The median time to symptom development was 4.25 months. At the initial examination, 92.86% of the cases had bilateral oedema and the mean visual acuity was 0.4 (decimal scale). The mean macular thickness was 509.63 microns, and 97.83% of the eyes had no or minimal angiographic findings. In 90.57% of the cases, the treatment with taxanes was interrupted, and some other treatment was used in 43.86% of the cases, with the most widely used being acetazolamide. The outcome was favourable, to a greater or lesser extent, in 96.23% of cases.
CONCLUSIONS: Despite being a rare entity, macular oedema associated with the use of taxanes is a disorder that every oncologist and ophthalmologist should be aware of, taking into account the good outcome of the condition that usually occurs when treatment is suspended.

Cavitations in the inner nuclear layer associated with severe optic atrophy and loss of retinal ganglion cells have clinically been termed microcystic macular oedema (MME). We describe a case series of MME in patients of all ages but predominantly younger patients with a wide range of optic atrophies ranging from acute onset optic disc drusen associated ischemic optic neuropathy to slowly progressive disease as glaucoma. There were no physical distinctions between MME in different causes of optic atrophy suggesting a common causative mechanism. We reviewed the literature on MME and it appears that MME is associated with more severe visual loss, and is more common in hereditary optic neuropathies and neuromyelitis optica spectrum disease rather than in patients with optic atrophy secondary to multiple sclerosis and glaucoma. Three main causative mechanisms have been proposed, including increased vitreal traction on the macular as the ganglion cells are lost. Others have suggested that trans-synaptic loss of cells in the inner nuclear layer causes formation of empty spaces or cavities. Finally, some have hypothesized a disturbance in the fluid homeostasis of the inner retina as Müller cells are lost or their function is impaired. There are no known treatments of MME. In conclusion, MME seems to be a marker of severe optic nerve atrophy irrespective of the underlying cause.