Ocular Complications of Renal Cancer

A 61-year-old male patient was referred for the management of ocular hypertension and the assessment of neurologic visual field defects. He had undergone brain surgery 3 months earlier to have a renal cell carcinoma (RCC) metastatic tumor resected. His medical history was positive for hypertension, gastric reflex disease, hypothyroidism, seizure, chronic pain, kidney removal secondary to RCC, and adrenal insufficiency secondary to kidney removal with subsequent Cushing disease due to overtreatment with oral prednisone. His medication regimen included vitamin B1, vitamin D3, niacin, metoprolol, pantoprazole, levothyroxine, prednisone, hydrocodone/acetaminophen, gabapentin, ondansetron, levetiracetam, and pembrolizumab.

EXAMINATION FINDINGS

The patient’s BCVA was 20/20 OD and 20/25 OS with significant myopic correction. Pupil testing was equal, round, and reactive to light without an afferent pupillary defect. Extraocular motilities were full OU without diplopia or nystagmus. Confrontation visual fields suggested left-sided hemianopic visual field defects. Cover testing at distance was ortho and 2 prism diopters of exophoria at near with his habitual spectacle prescription. Anterior segment examination was unremarkable, except for age-appropriate mild nuclear sclerosis bilaterally. Goldmann applanation tonometry measured IOP of 30 mm Hg OU. Gonioscopy was unremarkable OU.

Pachymetry was 535 µm OU. Dilated fundus examination showed scattered punched-out lesions of the retina with peripapillary atrophy/scarring consistent with presumed ocular histoplasmosis syndrome and chorioretinal scarring without evidence of choroidal neovascular membrane formation (Figure 1). Formal threshold automated perimetry testing confirmed left-sided homonymous hemianopias (Figure 2). OCT of the retinal nerve fiber layer and ganglion cell-inner plexiform layer showed changes consistent with glaucoma (Figures 3 and 4).

Neuroimaging showed that the RCC intracranial metastatic lesion was located on the right side of the patient’s brain near the parietotemporal-occipital lobe junction involving the right-sided optic radiations of the visual pathway (Figure 5). It correlated with the patient’s left-sided homonymous hemianopsias.

DISCUSSION

Intracranial metastases occur in approximately 170,000 people per year in the United States.¹ Lung cancer (40-52%) and breast cancer (17%) are the two most common intracranial metastases.¹ The third most common is kidney cancer, occurring in approximately 3% to 11% of intracranial metastatic cases, as in this case.¹

The patient was diagnosed with adrenal insufficiency (ie, Addison disease) post-removal of his kidney secondary to RCC. Because his remaining kidney was not able to produce adequate levels of cortisol, he was started on oral prednisone. With chronic prednisone use, his cortisol levels increased to higher-than-normal levels, which led him to develop Cushing syndrome. His prednisone use had to be titrated back down to normal levels over time.

The patient also had presumed ocular histoplasmosis syndrome—first described in 1942 by Reid et al²—which is associated with increased risk of Addison disease.^3,4 Ocular findings typically include discrete atrophic choroidal scars with sharp borders and peripapillary atrophy without ocular inflammation.² The causative organism is the fungus Histoplasma capsulatum, which gains access to the retina through the choroidal circulation, causing subclinical choroiditis.² Choroidal neovascular membranes and macular involvement secondary to scarring are the main causes of symptomatic vision changes and vision loss.² The patient’s macular area was unaffected, so I chose to monitor his retina findings.

I opted to treat the patient’s elevated IOP with a glaucoma medication so he could remain on oral prednisone to avoid slipping into Addisonian crisis (ie, acute adrenal insufficiency), which would be life-threatening. He was started on latanoprost ophthalmic solution 0.005% (Xalatan, Viatris) and asked to return in 4 to 6 weeks.

The patient was educated on his visual field defects secondary to his intracranial metastasis and was counseled against driving. A low vision evaluation was discussed at length and recommended, but he declined. He was encouraged to follow up with his other medical specialists (ie, oncology, nephrology, and neurosurgery) in the meantime.

IT’S ALL IN THE HISTORY

Taking a comprehensive case history is one of the most important things we can do for our patients as clinicians. In this case, the patient’s history of kidney cancer helped guide his ocular care from start to finish and pointed me in several directions I may not have otherwise looked. Don’t overlook this important step of gathering a thorough case history; it can make all the difference for you and the comprehensive and continued care of your patients.