Saudi Journal of Kidney Diseases and Transplantation

: 2014  |  Volume : 25  |  Issue : 3  |  Page : 615--620

Central serous chorioretinopathy following kidney transplantation

Kianersi Farzan1, Leila Rezaei2, Heshmatollah Ghanbari1, AliReza Dehghani1,  
1 Department of Ophthalmology, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Ophthalmology, Kermanshah University of Medical Sciences, Kermanshah, Iran

Correspondence Address:
Dr. Leila Rezaei
Department of Ophthalmology, Kermanshah University of Medical Sciences, Kermanshah


A lesser known complication of long-term corticosteroid therapy is chronic central serous chorioretinopathy (CSCR). Although idiopathic CSCR is known to be mild with spontaneous improvement and minimal effects on the vision, chronic CSCR is different and may cause irreversible visual loss. We report four patients with CSCR on corticosteroid therapy after kidney transplant. The interesting point about these patients is that they were of a younger age group compared with classic CSCR cases, and there were two females among the patients. Organ transplantation and corticosteroid therapy are the risk factors for CSCR. We should discontinue or at least reduce corticosteroid dosage. Knowledge about this rare complication after kidney transplantation (even in unusual age and sex) is important.

How to cite this article:
Farzan K, Rezaei L, Ghanbari H, Dehghani A. Central serous chorioretinopathy following kidney transplantation.Saudi J Kidney Dis Transpl 2014;25:615-620

How to cite this URL:
Farzan K, Rezaei L, Ghanbari H, Dehghani A. Central serous chorioretinopathy following kidney transplantation. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2021 Dec 4 ];25:615-620
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Full Text


Central serous chorioretinopathy (CSCR) is an idiopathic condition characterized by the development of a serous detachment of the sensory retina. CSCR occurs primarily in healthy men between 25 and 55 years of age. Most patients are asymptomatic unless the central macula is affected. Symptomatic patients describe the sudden onset of blurred and dim vision, micropsia (objects appear smaller than they are), metamorphopsia (objects appear distorted), para-central scotomata or decreased color vision. In rare cases, these symptoms are accompanied by a migraine-like headache. Certain personality types, including type A personality, hypochondria, hysteria and conversional neurosis, have been associated with CSCR [1] as well as psychiatric medication use.

Patients with elevated levels of corticosteroids due to either corticosteroid administration (inhaled, topical or systemic) or Cushing syndrome are at an increased risk of developing CSCR. The development of serous detachment of the sensory retina results from altered barrier and deficient pumping functions at the level of the retinal pigment epithelium (RPE). We present four cases of CSCR secondary to long-term steroid therapy following kidney transplantation to illustrate this potentially blinding complication and the importance of being aware of this complication after kidney transplantation.

 Case Reports

Case 1

A 24-year-old woman presented with diminution of vision in the left eye (OS). She did not have symptoms of flashes of light, floaters and photophobia. She had undergone kidney transplantation 2.5 years earlier, with the underlying native kidney disease being systemic lupus erythematosus (SLE) nephropathy. Her medications included cyclosporine A and prednisolone 15 mg/day. She had a past history of similar attack in her right eye (OD), which improved gradually. Best-corrected visual acuities were 10/10 in her right eye and 3/10 in the left one. Pupils were equal and reactive to light, with negative afferent pupillary defect (RAPD) in both eyes (OU).

The intraocular pressure was 16 mm Hg (OU). Fundus evaluation showed serous macular detachment of the left eye and old macular pigmentary changes of the right one. With a clinical suspicion of CSCR, we decided to seek assistance from ancillary tests such as fluorescein angiography (FA) and optical coherence tomography (OCT). FA showed pinpoint focus of early macular dye leakage of the left eye that increased in size intensity as the angiogram progressed. OCT showed a serous detachment of the macula with no break in the retinal pigment epithelium [Figure 1]. The FA and OCT findings confirmed the diagnosis of CSCR. After consultation with a nephrologist, prednisolone was tapered as it was the culprit drug.{Figure 1}

At the three-month follow-up, the vision of OS improved to 9/10. The serous detachment got completely resolved with some residual pigmentary changes. During the subsequent years of follow-up, she had multiple attacks of CSCR. After eight years, she underwent cataract surgery of both eyes. Her final visual acuity was 3/10 in the right eye and 1/10 in the left one. The cause of her visual impairment was severe pigmentary changes of the macula.

Case 2

A 29-year-old woman presented with decreased vision in the left eye nine years after she underwent kidney transplantation. Her medications included Cyclosporine A and prednisolone 5 mg/day. Best-corrected visual acuity was 10/10 in OD and 5/10 in OS. Anterior segment examination was normal. Fundus examination revealed a small serous macular detachment in her left eye. FA showed a small point of dye leakage that was followed by late pooling [Figure 2]. OCT confirmed a serous macular detachment and CSCR diagnosis. At the two-month follow-up, the patient's visual acuity improved to 10/10 and serous retinal detachment resolved without any intervention. During six years of follow-up, she had two similar attacks of CSCR that improved with tapering or cessation of corticosteroid; however, her final visual acuity is 6/10.{Figure 2}

Case 3

A 23-year-old man was referred to us with severe visual loss in his right eye. He had undergone kidney transplantation two years ago and was on Cyclosporine and prednisolone (15 mg/day). His right eye vision was 1/10 and left one was 10/10. Anterior segment was normal. Fundus examination showed three sites of serous detachment in the right eye (one site in the macula and two sites in the superior and inferior aspects of the retina). OCT showed three small sites of serous retinal detachment [Figure 3]; however, because of the history of the post-transplant BUN/Cr abnormality, FA was not performed. With the clinical and OCT-assisted diagnosis of multiple CSCR and after consultation with a nephrologist, prednisolone was tapered. The patient was followed-up at regular intervals. At the four-month follow-up, the final visual acuity improved to 5/10.{Figure 3}

Case 4

A 16-year-old man presented with decreased vision in his left eye for one week. He had undergone kidney transplantation five years ago for renal failure of unknown etiology. He was on cyclosporine A and 7.5 mg/day prednisolone for immunosuppression. Vision of the OD was 10/10 and OS was 5/10. Fundus examination showed a serous macular detachment in the left eye. OCT showed a site of serous macular detachment of the retina associated with a site of retinal pigmented epithelial (RPE) detachment underneath the retinal detachment [Figure 4].{Figure 4}

Serous retinal detachment resolved after four months and vision improved to 8/10.


Central serous chorioretinopathy is defined as a detachment of the sensory retina. The condition typically has a male predominance of 8:1 to 10:1 over females. Usually, one eye is involved, but bilateral involvement occurs in approximately 20% of patients. [1],[2],[3],[4],[5]

The anterior segment and vitreous are unaffected. The detached sensory retina is usually transparent and of normal thickness, and the subretinal fluid is clear. In some cases, an area of RPE detachment may be seen corresponding to the site of subretinal fluid leakage. Serous RPE detachments are reported frequently in conjunction with central serous chorioretinopathy. The development of serous detachment of the sensory retina result from altered barrier and deficient pumping functions at the level of the RPE. [3],[6],[7]

The PubMed Database of the United States National Library of Medicine has in excess of nine million citations of Medline and Pre Medline Articles. This database listed 13 articles about CSCR development after corticosteroid therapy of the organ transplantation such as post-bone marrow or cardiac transplantation; however, only five articles of these 13 (included 17 cases) were about CSCR in renal transplant recipients. [8],[9],[10],[11],[12],[13],[14],[15],[16],[17]

We report an additional four cases of CSCR after a low dosage of corticosteroid therapy. In addition, relatively younger age of these present cases was quiet interesting, especially in the fourth case. Also, two of our patients were females, unusual for this disease because CSCR is reported to be rarer in young females. All of these cases suffered from diminution of vision and CSCR developed with a low dosage of maintenance corticosteroid therapy. Many of the kidney transplant recipients are concurrently treated with corticosteroid along with other immunosuppressive therapies. Determining the etiology of these conditions is made more complex because of the known link of CSCR to immunosuppressive agents [18] or, maybe, the organ transplantation process increases the susceptibility of a patient to CSCR development.

CSCR can be confirmed with several imaging modalities. In FA, an expansile dot of hyper fluorescence is the most common presentation. The dot represents a small, focal hyperfluorescent leak from the choroid through the RPE. Other imaging modalities for CSCR include OCT, an excellent, non-invasive method to use for diagnosing and following the resolution of the sub-retinal fluid. The retinal pigment epithelial layer, which appears as a band, red in color, on OCT because of its high reflectivity may present with focal damage at the site of fluid leakage. The sensory retina has less reflectivity and has a blue-green appearance, and is separated by an optically empty space from the red band of the RPE. [9]

Corticosteroids are known to produce catecholamine-mediated vasoconstriction in several organs, and glucocorticoids are known to cause an increase in catecholamine release. Therefore, CSCR could be induced by both increasing the catecholamine levels and by making the choroidal vasculature more susceptible to its effects. [5],[19]

The visual prognosis of CSC is usually good, except in chronic, recurrent cases and in cases of bullous CSCR. [1] Most eyes with CSCR (80-90%) undergo spontaneous resorption of the subretinal fluid within three to four months; recovery of visual acuity usually follows, but can take up to one year. Some eyes may suffer permanently diminished visual acuity, and many (40-50%) experience one or more recurrences. A small subset of patients has poor visual outcomes. [1]

Current treatment guidelines suggest that patients may be observed for at least three to four months (average time for spontaneous recovery) in most first episodes of unilateral CSCR. Laser photocoagulation may be considered in persistent or recurrent instances.


Once it is determined to be CSCR, the best management for patients is observation alone. If the CSCR is steroid induced, a modification of the medication should be recommended to the patient's physician.


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