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| Year : 2010 | Volume
: 21
| Issue : 5 | Page : 957-958 |
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| Posterior reversible encephalopathy syndrome |
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Kamal F Akl1, Osama A Samara2
1 Department of Pediatrics, Jordan University Hospital, College of Medicine, University of Jordan, P. O. Box 831373, Amman 11183, Jordan
2 Department of Radiology, Jordan University Hospital, College of Medicine, University of Jordan, P. O. Box 831373, Amman 11183, Jordan
Click here for correspondence address and email
| Date of Web Publication | 31-Aug-2010 |
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How to cite this article:
Akl KF, Samara OA. Posterior reversible encephalopathy syndrome. Saudi J Kidney Dis Transpl 2010;21:957-8 |
To the Editor,
We read with great interest the paper by Saeed et al. [1] A similar case was reported in an adult patient. [2] Out of 130 patients with the nephrotic syndrome, seen at a tertiary care center from 2002 to 2008, we encountered 13 cases (10%) of focal and segmental glomerulosclerosis (FSGS), who were resistant to steroids and calcineurin inhibitors. One of these patients had recurrent posterior reversible encephalopathy syndrome (PRES) and one other had PRES like syndrome with normal imaging.
 Case 1 | |  |
A nine-year-old female with the nephrotic syndrome secondary to FSGS, developed hypertension, seizures, headache, loss of vision, aphasia, and decreased level of consciousness while on steroid monotherapy, that lasted for three weeks. Computerized axial tomography (CAT) scan and magnetic resonance imaging (MRI) of the brain were consistent with PRES. Since that episode, the patient had poor school performance. A second episode associated with hypertension, and manifesting as headache and decreased level of consciousness, occurred eight months later. Serum sodium and albumin were 118 mEq/L and 1 g/dL respectively. After one dose of intravenous furosemide, the symptoms were aborted and never recurred.
| Case 2 | | |
A three-year-old male with the nephrotic syndrome secondary to FSGS, while on steroids and cyclosporine, developed hypertension, seizures, blindness, aphasia, and decreased level of consciousness that lasted for around three weeks. CAT scan and MRI of the brain were normal. A similar episode recurred after seven months. Following recovery, the patient became aggressive.
The case of Saeed et al, de Oliveira et al and our cases suggest that the nephrotic state in general, [3],[4] and FSGS in particular, predispose patients to PRES. Cyclosporine is just one of several triggering factors amongst others, such as hyponatremia, sepsis, and hypoalbuminemia.
| References | | |
| 1. | Saeed B, Abou-Zor N, Amer Z, Kanani I, Hilal M. Cyclosporine-A induced posterior reversible encephalopathy syndrome. Saudi J Kidney Dis Transpl 2008:19(3):439-42.  |
| 2. | De Oliveira RA, Fechine LM, Neto FC, et al. Posterior reversible encephalopathy syndrome (PRES) induced by cyclosporine use in a patient with collapsing focal glomerulosclerosis. Int Urol Nephrol 2008;40(4):1095-8. |
| 3. | Ishikura K, Ikeda M, Hamasaki Y, et al. Nephrotic state as a risk factor for developing posterior reversible encephalopathy syndrome in pediatric patients with nephrotic syndrome. Nephrol Dial Transpl 2008;23(8):2531-6. |
| 4. | Ikeda M, Yata N, Kamei K, et al. Posterior leuko-encephalopathy syndrome in pediatric patients with kidney disease. Pediatr Nephrol 2002;17(1):71. |
Correspondence Address:
Kamal F Akl
Department of Pediatrics, Jordan University Hospital, College of Medicine, University of Jordan, P. O. Box 831373, Amman 11183
Jordan
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PMID: 20814143 
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