Posterior Reversible Encephalopathy Syndrome in a Patient with Severe Uremia without Hypertension

Abstract

A 28-year-old man was admitted to our hospital with nausea, headache and weakness of the left hand. He had severe uremia without hypertension due to recurrent/chronic pyelonephritis. Brain magnetic resonance imaging showed reversible vasogenic edema in the brainstem and bilateral frontal centrum semiovale. All of his neurological symptoms immediately improved after the introduction of hemodialysis. When a patient with uremia presents with neurological symptoms, posterior reversible encephalopathy syndrome should be considered in the differential diagnosis even if high blood pressure is not observed. Brain magnetic resonance imaging may be helpful in such a case, and an appropriate therapy could be subsequently initiated.

The nature, consequences, and management of neurological disorders in chronic kidney disease

“…The subcortical white matter changes usually improve or disappear with control of hypertension. Although posterior reversible encephalopathy in patients with kidney failure is usually attributed to hypertensive encephalopathy, it has been reported sometimes in patients with kidney disease in the absence of hypertension, implicating the role of uremia itself in white matter edema . Improvement in kidney function often results in improvement of encephalopathy and abnormal posterior MRI signals (Figure ).…”

<p>Posterior Reversible Encephalopathy Syndrome Due to Acute Water Intoxication in a Patient with Schizophrenia</p>

“…Factors leading to the onset of PRES include sudden blood pressure fluctuations, renal failure, autoimmune disorders, eclampsia, septicemia, and use of drugs such as immunosuppressants administered after organ transplantation or anti-cancer drugs. 6,7 Background factors for PRES are hypertension, immunosuppressant drug use, anti-cancer drug use, eclampsia, collagen disorders, and electrolyte abnormalities. In this disease state, sudden increases in blood pressure or the effects of cytokines cause vascular endothelial injury, resulting in transient cerebral edema (vasogenic edema).…”

Posterior Reversible Leukoencephalopathy Syndrome: Clinical Case and Literature Overview

“…Определенная роль в патогенезе СЗОЛ отводится некоторым лекарственным препаратам, изменяющим состояние гематоэнцефалического барьера или путем прямого токсического действия на эндотелий сосудов, или опосредованно, за счет стимулирования синтеза цитокинов, которые, в свою очередь, индуцируют повреждение клеток-мишеней [1,5,6]. В частности, иммуносупрессивные или цитотоксические препараты (например, метотрексат) способны служить триггерами развития СЗОЛ даже через несколько месяцев после завершения их приема [2,22].…”

“…Стойкий остаточный неврологический дефицит, в основе которого лежит развитие кистозно-атрофических изменений головного мозга, описан в 5-30% случаев СЗОЛ [4,8,22]. Описано персистирование гемипареза, судорожного синдрома, зрительных нарушений, головокружения [2].…”