J Korean Med Sci.  2004 Apr;19(2):315-319. 10.3346/jkms.2004.19.2.315.

Cerebral Infarction as a Complication of Nephrotic Syndrome: A Case Report with a Review of the Literature

Affiliations
  • 1Department of Internal Medicine, Hanyang University, Seoul, Korea. hjkim@hanyang.ac.kr
  • 2Department of Neurology, Hanyang University, Seoul, Korea.
  • 3Department of Thoracic and Cardiovascular Surgery, Hanyang University, Seoul, Korea.

Abstract

Arterial thrombosis is relatively rare compared with venous thrombosis in nephrotic syndrome. However, the assessment of its pathogenesis and risk factors in individual patient with nephrotic syndrome is necessary to allow appropriate prophylactic management because it is a potentially serious problem. Hereby, with review of the literature, we report a case of a 53 yr-old man with cerebral infarction associated with nephrotic syndrome due to focal segmental glomerulosclerosis during the course of treatments with diuretics and steroid. It reveals that the hypercoagulable state in nephrotic syndrome can be associated with cerebral infarction in adults. Prophylactic anticoagulants can be considered to reduce the risk of serious cerebral infarction in nephrotic patients with risk factors such as severe hypoalbuminemia and on diuretics or steroid treatment, even in young patients regardless of types of underlying glomerular diseases.

Keyword

Nephrotic Syndrome; Cerebral Infarction; Risk Factors; Anticoagulants

MeSH Terms

Cerebral Infarction/epidemiology/*etiology/pathology
Human
Male
Middle Aged
Nephrotic Syndrome/*complications/epidemiology
Risk Factors

Figure

  • Fig. 1 MR diffusion image (A) shows a hemorrhagic infarction of the right parieto-occipital area, T2 weighted image (B) shows recent infarction involving the posterior 2/3 portion of the right middle cerebral artery territory and the right head of caudate nucleus.

  • Fig. 2 MR angiography showing a focal luminal narrowing of the bifurcation site of the right middle cerebral artery and right anterior communicating artery and no flow signal intensity in the right internal carotid artery.


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