International Urology and Nephrology

, Volume 46, Issue 1, pp 255–260

Use of a polysulfone hemodialysis membrane may prevent recurrent posterior reversible encephalopathy syndrome in a patient undergoing hemodialysis

Authors

    • Department of Nephrology, Graduate School of Medicine, Institute of Health BiosciencesUniversity of Tokushima
    • Shizuoka City Hospital
  • Takeshi Matsubara
    • Shizuoka City Hospital
    • Department of NephrologyKyoto University Graduate School of Medicine
  • Shuichiro Endo
    • Shizuoka City Hospital
    • Department of NephrologyKyoto University Graduate School of Medicine
  • Taichi Murakami
    • Department of Nephrology, Graduate School of Medicine, Institute of Health BiosciencesUniversity of Tokushima
    • Shizuoka City Hospital
  • Yasuki Hashimoto
    • Shizuoka City Hospital
    • Hashimoto Medical Clinic
Nephrology - Case Report

DOI: 10.1007/s11255-013-0434-y

Cite this article as:
Mima, A., Matsubara, T., Endo, S. et al. Int Urol Nephrol (2014) 46: 255. doi:10.1007/s11255-013-0434-y

Abstract

A 71-year-old woman underwent hemodialysis (HD) treatment for chronic kidney disease. During HD, she developed headache, abnormalities in visual perception, and generalized convulsion. Brain magnetic resonance imaging (MRI) showed T2-hyperintensity lesions in the posterior lobe, and an electroencephalogram showed slow waves in all areas. Twenty days later, the T2-hyperintensity lesions had vanished. Furthermore, perfusion computed tomography (CT) and single-photon emission CT with N-isopropyl[123I]-p-iodoamphetamine (IMP-SPECT) showed no significant abnormalities. The patient was diagnosed with posterior reversible encephalopathy syndrome (PRES) because she displayed typical clinical symptoms and MRI findings. Although several antihypertensive and antiseizure medications were administered, the patient experienced recurrent PRES. Therefore, we used a polysulfone dialyzer to reduce the oxidative stress and inflammation while preserving vascular endothelial function. After use of a polysulfone dialyzer membrane, the patient had no PRES episodes during the clinical course. This is the first study to demonstrate that use of a polysulfone dialyzer membrane instead of a cellulose membrane may prevent recurrent PRES.

Keywords

Posterior reversible encephalopathy syndromeHemodialysisPolysulfone dialyzer membraneEndothelial dysfunctionOxidative stressInflammation

Introduction

Posterior reversible encephalopathy syndrome (PRES) is a clinical and radiologic entity associated with severe headaches and generalized seizures [1]. Radiologically, PRES is characterized by abnormalities in the white matter of the parieto-occipital lobes [2]. Most patients with PRES have vascular endothelial dysfunction due to immunosuppressive therapy with agents such as cyclosporine, renal failure, or pregnancy [3]. Vascular endothelial dysfunction increases levels of endothelin, prostacyclin, or thromboxane A2, which induce vasoconstriction, thrombosis, and disturbance of blood flow in the brain [4, 5]. Although PRES in patients undergoing hemodialysis (HD) has been widely studied, no studies have reported use of a polysulfone dialyzer membrane for prevention of PRES. Here, we describe the first case in which PRES was prevented using a polysulfone dialyzer membrane.

Case report

A 71-year-old woman who underwent HD for the treatment for chronic kidney disease (CKD) was hospitalized because of generalized seizure consisting of loss of consciousness, tremors in upper extremities, and postictal confusion. The seizure persisted for 2 min. After recovering consciousness, the patient had no convulsions, double vision, or confusion. The patient was born at full-term by normal delivery, and there was no abnormality during infancy. She had a history of hypertension, cerebral infarction, right middle cerebral artery aneurysm, and abdominal aortic aneurysm. She never smoked or consumed alcohol and had no drug allergies. Family history was not significant. She had been in good health until she developed hearing loss at the age of 20 years.

At presentation, her blood pressure was 144/92 mmHg and body temperature was 35.6 °C. Neurological examinations showed normal cranial nerve function, equal and symmetrical deep tendon reflexes, and 5/5 strength bilaterally. She did not have jugular venous distention. Her lower extremities showed muscle atrophy but no edema.

Laboratory examinations showed renal dysfunction and anemia. Serum levels of iron, albumin, and total cholesterol were decreased. Results of other peripheral blood hematology and blood chemistry tests were almost within normal limits (Table 1). Computed tomography (CT) performed immediately after convulsion showed no hemorrhage or infarction. Brain magnetic resonance imaging (MRI) showed T2-hyperintensity prominently involving the subcortical white matter of the posterior lobe (Fig. 1a). An electroencephalogram (EEG) showed slow waves (4–5 Hz) in all areas (Fig. 2a). Follow-up MRI showed significantly regressed hyperintense lesions in the posterior lobe region (Fig. 1b), and perfusion computed tomography (CT) and single-photon emission computed tomography with N-isopropyl[123I]-p-iodoamphetamine (IMP-SPECT) showed no intracranial pathology (Fig. 1c, d). A follow-up EEG also showed almost normal waves (Fig. 2b). The patient was treated with antiseizure medication (phenobarbital, 15–30 mg). However, the plasma drug concentration was below the therapeutic range. Therefore, PRES recurred several times during HD.
Table 1

Laboratory findings

Before hemodialysis

Peripheral blood

TP

3.8 g/dL

WBC

4,400/μL

Alb

2.1 g/dL

Band

0.9 %

ALP

120 IU/L

Ly

18.3 %

UA

4.4 mg/dL

Mono

2.7 %

BUN

36.6 mg/dL

Eos

3.0 %

Cr

6.97 mg/dL

RBC

263 × 104/μL

Na

139 mEq/L

Hb

8.9 g/dL

K

4.3 mEq/L

Ht

27.3 %

Glucose

93 mg/dL

Plt

9.9 × 104/μL

Fe

22 μg/dL

Blood chemistry

Ferritin

50 ng/mL

AST

6 U/L

Mg

2.0 mg/dL

ALT

5 U/L

T-cho

87 mg/dL

γ-GTP

12 U/L

TG

27 mg/dL

After hemodialysis

Peripheral blood

Blood chemistry

WBC

5,200/μL

TP

6.6 g/dL

RBC

315 × 104/μL

Alb

3.7 g/dL

Hb

10.7 g/dL

K

4.2 mEq/L

Ht

32.3 %

UA

2.9 mg/dL

Plt

13.8 × 104/μL

BUN

21.0 mg/dL

Cr

5.07 mg/dL

https://static-content.springer.com/image/art%3A10.1007%2Fs11255-013-0434-y/MediaObjects/11255_2013_434_Fig1_HTML.jpg
Fig. 1

a Brain MRI T2-weighted image obtained 7 days after seizure. b Brain MRI T2-weighted image obtained 20 days after seizure. c Perfusion CT image obtained 41 days after seizure. d IMP-SPECT image obtained 43 days after seizure

https://static-content.springer.com/image/art%3A10.1007%2Fs11255-013-0434-y/MediaObjects/11255_2013_434_Fig2_HTML.gif
Fig. 2

a EEG obtained on the day after seizure. b EEG obtained 20 days after seizure

Recent studies have shown that vascular endothelial dysfunction can induce PRES, and numerous reports have described the role of oxidative stress and inflammation in vascular endothelial dysfunction [6, 7]. Further, a dialyzer membrane prepared from modified polysulfone showed a major effect on oxidative stress and inflammation in recent studies [812]. Therefore, we replaced the cellulose dialysis membrane with a polysulfone dialyzer membrane to reduce oxidative stress and inflammation, which may induce PRES followed by vascular endothelial dysfunction. After use of the polysulfone dialyzer membrane was initiated, the patient had no PRES episodes during the clinical course (Fig. 3).
https://static-content.springer.com/image/art%3A10.1007%2Fs11255-013-0434-y/MediaObjects/11255_2013_434_Fig3_HTML.gif
Fig. 3

Clinical course of this patient

Discussion

PRES diagnosis is based on clinical, laboratory, and MRI findings [1, 13]. Hypertensive encephalopathy, immunosuppressive medications, and collagen vascular diseases are known causes of PRES [3]. However, only a few studies have reported recurrent PRES in patients undergoing HD [14, 15]. The main etiology of PRES includes sudden increases in blood pressure and association with HD [16]. Information about mechanisms and treatment for recurrent PRES in HD patients is limited. However, blood pressure control is a key to treatment for PRES in HD patients [17]. Our patient received strict volume control, which led to appropriate blood pressure control and improved cardiac function. Furthermore, several antihypertensive medications were administered to control blood pressure. Despite this intense and persistent therapy, the patient experienced recurrent PRES. Therefore, we believe that another mechanism induced PRES without hemodynamic changes in our case.

Two main mechanisms have been proposed in the pathophysiology of PRES. The first possible mechanism is vasospasm induced by increased blood pressure and loss of autoregulation [18]. Previous reports have suggested that vasospasm contributes to ischemia and cytotoxic cerebral edema [19]. The second mechanism is hypertension-induced hyperperfusion of the brain due to disturbances in autoregulation. Hypertension-induced dysfunction of the vascular endothelium lining the capillaries of the cerebrovasculature may cause disruption of the blood–brain barrier, resulting in increased fluid in the brain parenchyma [20]. Another important indicator of vascular endothelial dysfunction is the uremic toxins. Uremic toxins may directly reduce the availability of nitric oxide (NO), which results in vasodilatation and inhibition of smooth muscle cell growth and migration [2123]. Furthermore, uremic toxins may contribute to a general pro-oxidant and inflammatory status in patients with CKD [2426]. Recent studies have reported improvement in endothelial function after using N-acetyl cysteine (NAC) as an antioxidant in patients with chronic CKD [2729]. However, no positive efficacy in renal function has been reported in patients with CKD, although multiple trials using antioxidants such as vitamins C and E have reported beneficial effects in rodent models of CKD [30].

The polysulfone dialyzer membrane is an excellent biocompatible dialyzer. Furthermore, intriguing evidence suggests that the polysulfone dialyzer membrane reduces oxidative stress and inflammation and decreases activation of leukocytes, platelets, and monocytes [1012]. Many studies show that inhibition of oxidative stress and inflammation in vascular endothelial cells can decrease vascular endothelial dysfunction [3133], which plays a pivotal role in PRES development. We have not measured the levels of these markers yet. Therefore, further studies are required to clarify the effect of the polysulfone membrane on oxidative stress and inflammation.

Recently, it was reported that the new vitamin E–coated polysulfone membrane has greater ability to reduce oxidative stress and inflammation [8], although whole-body administration of vitamin E has no positive efficacy [34, 35]. Our observational period after initiation of polysulfone membrane use was relatively short. Long-term use of vitamin E–coated polysulfone membrane along with assessment of patient outcome is required to determine whether the risk of recurrent PRES can be further reduced.

In summary, we report the case of an HD patient with recurrent PRES. Use of polysulfone membrane could maintain vascular endothelial cell function, leading to a reduction in recurrent PRES attacks.

Acknowledgments

Preparation of this publication was supported by grants to A.M. from grant-in-aid for Scientific Research (24890148) from Japan Society for the Promotion of Science, Mochida Memorial Foundation for Medical and Pharmaceutical Research, Takeda Science Foundation, Japanese Association of Dialysis Physicians (JADP Grant 2012-03), and The Kidney Foundation, Japan (JKF13-1).

Conflict of interest

The authors declare that they have no conflict of interest.

Copyright information

© Springer Science+Business Media Dordrecht 2013