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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2016  |  Volume : 27  |  Issue : 2  |  Page : 411-414
Posterior reversible encephalopathy syndrome in a hypertensive patient with renal failure

Department of Nephrology, Dialysis and Renal Transplantation, Military Hospital Mohammed V, Hay Riad, Rabat, Morocco

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Date of Web Publication11-Mar-2016


Posterior reversible encephalopathy syndrome (PRES) is a clinical and neuroimaging entity characterized by headache, visual field deficits, changes in mentation and seizures, and by typical neuro-imaging features such as areas of sub-cortical edema, occasionally cortical, involving predominantly the occipital and parietal lobes of both hemispheres. Hypertension, uremia, immunosuppressive drugs neurotoxicity, preeclampsia or eclampsia, renal disease, and sepsis are the most common etiologies of PRES. Less common, it has been described in the setting of autoimmune disease. We report a case of PRES which was associated with hypertensive crisis in a patient with renal failure. Antihypertensive therapy and hemodialysis resulted in complete recovery.

How to cite this article:
Aatif T, El Farouki M R, Benyahia M. Posterior reversible encephalopathy syndrome in a hypertensive patient with renal failure. Saudi J Kidney Dis Transpl 2016;27:411-4

How to cite this URL:
Aatif T, El Farouki M R, Benyahia M. Posterior reversible encephalopathy syndrome in a hypertensive patient with renal failure. Saudi J Kidney Dis Transpl [serial online] 2016 [cited 2022 Jan 18];27:411-4. Available from: https://www.sjkdt.org/text.asp?2016/27/2/411/178586

   Introduction Top

Posterior reversible encephalopathy syndrome (PRES) is a clinical and radiologic entity, that is characterized by headache, variable mental status, epilepsy, visual disturbances, and typical transient changes in the posterior cerebral perfusion. [1] This is most commonly encountered in association with acute hypertension, preeclampsia or eclampsia, renal disease, sepsis, and exposure to immunosuppressants. [2],[3] Neuro-imaging features in PRES include symmetrical diffuse or focal hyper-intensity on T2weighted or fluid-attenuated inversion recovery (FLAIR) imagers, predominantly in the supratentorial white matter and especially in the posterior circulation territories. [4] We present a case of PRES in a patient with renal failure, who responded well to treatment, with improvement in clinical and radiological [conventional magnetic resonance imaging (MRI)] findings.

   Case Report Top

A 75-year-old woman, with history of pulmonary tuberculosis, was admitted to our emergency department with tonic-clonic seizures involving her arms and legs, and loss of consciousness (Glasgow Coma Scale: 7) requiring intubation. There was no focal neurological deficit and the arterial blood pressure was high at 210/110 mm Hg. Urinalysis revealed proteinuria (+2) and hematuria without leukocyturia. Laboratory tests on admission were as follows: hemoglobin, 8.3 g/dL (ref. range:≥12 g/dL); hematocrit, 24.6% (refe range: ≥36%); white blood cells and platelet counts were normal; blood urea nitrogen (BUN), 446 mg/ dL (ref. range: 15-45 mg/dL); creatinine, 22.4 mg/dL (ref. range: 0.5-1 mg/ dL); sodium, 133 meq/L (ref. range: 135-145 meq/L); potassium, 5.1 meq/L (ref. range: 3.5-5 meq/L); calcium, 77 mg/L (ref. range: 85-105 mg/L); and phosphorus, 57 mg/L (ref. range: 2.5-4.5 meq/L). The liver function tests, total protein, and albumin levels were normal. The complement C3 level was 1.10 g/L (ref. range: 0.75-1.2 g/L), and C4 was 0.25 g/L (ref. range: 0.15-mg/L). Antinuclear and anti-double-stranded DNA antibodies were negative. Ophthalmological examination showed severe hypertensive retinopathy. Renal ultrasound revealed bilateral poorly differentiated atrophic kidneys. The cerebral computerized tomography scan performed on admission was normal. The cerebral MRI showed bilateral, moderate signals on FLAIR sequences in the sub-cortical white matter of the parietal and occipital regions and diffuse cerebral atrophy [Figure 1]. On the basis of these findings, a diagnosis of hypertensive encephalopathy with cerebral edema was made. The patient was admitted in the intensive care unit, and her blood pressure was monitored and controlled. With intravenous anti-hypertensive therapy (nicardipine), anticonvulsant medication (phenobarbital), hemodialysis, and supportive care, her blood pressure came down to 130/85 mm Hg, BUN was 39 mg/dL, and creatinine was 1.3 mg/dL (after hemodialysis). There was no electrolyte imbalance. The patient was extubated and the level of consciousness rapidly resolved.
Figure 1: Cerebral magnetic resonance imaging showing bilateral, moderate signals on fluidattenuated inversion recovery sequences in the sub-cortical white matter of the parietal and occipital regions.

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Follow-up MRI, performed two weeks after the initial presentation, was normal. At this time, the patient's condition was clinically normal. She did not experience any further seizures. The clinical improvement allowed her to be transferred to a nephrology medical unit for treatment of the persistent renal failure.

   Discussion Top

PRES is characterized by mental impairment, headache, epilepsy, and visual disturbances. Seizures are the most common clinical presentation and renal failure (either acute or chronic) is present in approximately 57% of patients presenting with PRES. A history of autoimmune disease is present in 45% of patients and among these, three fourths are female. [3] The lesions generally disappear with appropriate treatment. Hypertensive encephalopathy, preeclampsia or eclampsia, renal disease with hypertension, infection, immunosuppressive and cytotoxic medications, collagen vascular disease, thrombotic thrombocytopenic purpura, human immunodeficiency virus infection, acute intermittent porphyria, and organ transplantation are among the known conditions associated with PRES. [3],[4],[5] Our patient presented with both seizures and uremia. There was no history of autoimmune disease and immunological investigations were negative.

Two possible mechanisms have been proposed to explain the pathophysiology of PRES. The first is vasospasm due to acutely increased blood pressure; it has been suggested that vasospasm contributes to ischemia and cytotoxic edema in regions of the arterial border zone. [6] The second mechanism is loss of autoregulation; this is supported by diffusion images suggesting that dilatation develops in cerebral arterioles due to autoregulatory failure. The objective of cerebral autoregulation is to keep blood flow constant, and to protect the brain during changes in blood pressure; however, sudden and severe increases in blood pressure can impair autoregulation, and such impairment can, in turn, lead to arteriolar vasodilatation and endothelial dysfunction. The association of PRES in patients with autoimmune disorders may support the theory that PRES is in part caused by endothelial dysfunction, a process in which the host autoimmune response is essential. [3] In this condition, plasma and red blood cells migrate from the intravascular to the extravascular space, resulting in vasogenic edema. [7] The predominant involvement of posterior cerebral regions is a recognized hallmark of PRES. [8] It has been proposed to be the result of regional differences in the distribution of intracranial adrenergic receptors. [9] Vessels of the posterior circulation have sparse sympathetic innervention and are therefore, poorly equipped to initiate protective vasoconstriction in response to sudden increase in arterial blood pressure, resulting in disruption of the blood-brain barrier and passive extravasations of fluid into the interstitium. [10]

Uremic encephalopathy is due to elevated levels of BUN from acute or chronic renal failure. Neurological deficit from simple uremia is not a frequent occurrence, and the pathophysiology of this entity is not well known. It has been suggested that a breakdown of the blood-brain barrier due to endothelial injury (as in the kidney) leads to an increased concentration of uremic toxins in the brain parenchyma and associated neurological abnormalities. [11] In our patient, both chronic uremia and acute hypertension were present, and as such, we cannot confirm which condition induced the neurological and morphological changes, but can only suppose that both may be responsible.

Many authors have accepted that PRES is caused by an acute increase in blood pressure. [12] The risk of developing hypertensive encephalopathy is high in patients who experience a sudden increase in blood pressure to a level 30% greater than that of the normal blood pressure for persons of that age. However, no association has been found between the severity of hypertension and the prognosis in PRES; the findings of leukoencephalopathy are found to improve in most patients in 1-2 weeks. [12]

Despite the absence of neurological sequelae attributable to PRES in our patient, corticomedullary malacia was seen, probably due to elderly age and chronic kidney disease. Cerebral atrophy is seen frequently in patients with uremia, and may manifest as cortical or subcortical atrophy, or a combination of both. It may be related to chronic anemia and a decrease in tissue oxygenation due to hypertensive heart failure. Vascular calcification due to hyperparathyroidism and/or dyslipidemia and systemic hypertension may also contribute to the development of atrophy via compromise of vasculature of the brain. [13]

In addition, sudden changes in blood pressure during hemodialysis in hypertensive patients with volume overload may lead to brain injury. [14] Although aluminum is no longer a component of dialysate solution, previous intoxication from this compound remains one of the major causes of cerebral atrophy in patients undergoing hemodialysis. [13]

Early diagnosis and treatment of PRES is important. Without prompt treatment, the syndrome may lead to permanent brain injury or neurological sequelae such us epilepsy. The diagnosis may be difficult. The presence of diagnosis criteria is helpful [Table 1]. [15]
Table 1: Diagnostic criteria for posterior reversible encephalopathy syndrome (PRES).[15]

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First-line treatment of PRES is to control the blood pressure. The mean arterial pressure should be reduced by 20-25%, or diastolic pressure should be lowered to 100 mm Hg within the first 1-2 h. Rapid decrease in blood pressure should be avoided due to the risk of hypoperfusion and consequent cerebral infarction or impairment of organ function. [13]

In this report, we present a case of PRES in a patient with both renal failure and hypertension crisis, who responded well to treatment.

Conflict of interest: None declared.

   References Top

Hinchey J, Chaves C, Appignani B, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494-500.  Back to cited text no. 1
Port JD, Beauchamp NJ Jr. Reversible intracerebral pathologic entities mediated by vascular autoregulatory dysfunction. Radiographics 1998;18:353-67.  Back to cited text no. 2
Fugate JE, Claassen DO, Cloft HJ, Kallmes DF, Kozak OS, Rabinstein AA. Posterior reversible encephalopathy syndrome: associated clinical and radiologic findings. Mayo Clin Proc 2010;85:427-32.  Back to cited text no. 3
Ay H, Buonanno FS, Schaefer PW, et al. Posterior leukoencephalopathy without severe hypertension: utility of diffusion-weighted MRI. Neurology 1998;51:1369-76.  Back to cited text no. 4
Garg RK. Posterior leukoencephalopathy syndrome. Postgrad Med J 2001;77:24-8.  Back to cited text no. 5
Naidu K, Moodley J, Corr P, Hoffmann M. Single photon emission and cerebral computerized tomographic scan and transcranial doppler sonographic findings in eclampsia. Br J Obstet Gynaecol 1997;104:1165-72.  Back to cited text no. 6
Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet 2000;356:411-7.  Back to cited text no. 7
Schwartz RB, Jones KM, Kalina P, et al. Hypertensive encephalopathy: findings on CT, MR imaging, and SPECT imaging in 14 cases. AJR Am J Roentgenol 1992;159:379-83.  Back to cited text no. 8
Beausang-Linder M, Bill A. Cerebral circulation in acute arterial hypertension - protective effects of sympathetic nervous activity. Acta Physiol Scand 1981;111:193-9.  Back to cited text no. 9
Benziada-Boudour A, Schmitt E, Kremer S, et al. Posterior reversible encephalopathy syndrome: a case of unusual diffusion-weighted MR images. J Neuroradiol 2009;36:102-5.  Back to cited text no. 10
Lecouvet FE, Duprez TP, Raymackers JM, Peeters A, Cosnard G. Resolution of early diffusion-weighted and FLAIR MRI abnormalities in a patient with TIA. Neurology 1999;52:1085-7.  Back to cited text no. 11
Prasad N, Gulati S, Gupta RK, Kumar R, Sharma K, Sharma RK. Is reversible posterior leukoencephalopathy with severe hypertension completely reversible in all patients? Pediatr Nephrol 2003;18:1161-6.  Back to cited text no. 12
Ergün T, Lakadamyali H, Yilmaz A. Recurrent posterior reversible encephalopathy syndrome in a hypertensive patient with end-stage renal disease. Diagn Interv Radiol 2008;14:182-5.  Back to cited text no. 13
Kwon S, Koo J, Lee S. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Pediatr Neurol 2001;24:361-4.  Back to cited text no. 14
Ahn KJ, You WJ, Jeong SL, et al. Atypical manifestations of reversible posterior leukoencephalopathy syndrome: findings on diffusion imaging and ADC mapping. Neuroradiology 2004;46:978-83.  Back to cited text no. 15

Correspondence Address:
T Aatif
Department of Nephrology, Dialysis and Renal Transplantation, Military Hospital Mohammed V, Hay Riad, Rabat
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DOI: 10.4103/1319-2442.178586

PMID: 26997402

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