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 »  Abstract
 »  Introduction
 »  Case report
 »  Discussion
 »  References

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Year : 2000  |  Volume : 48  |  Issue : 2  |  Page : 179-81

Fulminant cerebral infarction in a patient with nephrotic syndrome.




  »  Abstract

Fulminant cerebral infarction secondary to arterial thrombosis in adults with nephrotic syndrome is rare. We report a 42 year old male with fulminant right anterior cerebral and middle cerebral artery infarction. Minimal change disease of the kidney was documented by renal biopsy. The possible pathogenesis is discussed and pertinent literature reviewed.

How to cite this article:
Pandian J D, Sarada C, Elizabeth J, Visweswaran R K. Fulminant cerebral infarction in a patient with nephrotic syndrome. Neurol India 2000;48:179


How to cite this URL:
Pandian J D, Sarada C, Elizabeth J, Visweswaran R K. Fulminant cerebral infarction in a patient with nephrotic syndrome. Neurol India [serial online] 2000 [cited 2020 Dec 3];48:179. Available from: https://www.neurologyindia.com/text.asp?2000/48/2/179/1549




   »   Introduction Top

The association between ischaemic strokes and hypercoagulable states is well recognized. Nephrotic syndrome (NS), a hypercoagulable state, has been associated with both venous and arterial thrombosis. In adults, majority of thrombosis are venous; arterial thrombosis are more common in children.[1] Cerebral infarction due to arterial thrombosis in adults associated with NS has been rarely reported.[2],[3],[4],[5],[6],[7]


   »   Case report Top

A 42 year old male was admitted for the first time to Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, in November 1998 because of sudden onset of weakness of the left upper and lower limbs and change in mental status. A diagnosis of NS and minimal change lesion had been made in 1987, elsewhere based on clinical, blood and urinary abnormalities and renal biopsy. He had three relapses, which responded to steroids. In addition, his clinical course was complicated by three episodes of deep vein thrombosis in the legs which were successfully treated with anti-coagulants elsewhere. He was hypertensive and smoked half a pack of cigarettes daily since an unspecified length of time. There was no family history of stroke, heart disease, or other thrombotic disorders. His general examination showed bilateral pedal oedema, with blood pressure of 160/90 mm of Hg. Cardiac and systemic examination were normal. Neurological examination revealed a drowsy patient, with left hemiplegia, facial weakness and right partial third nerve palsy. With in few hours of admission, he developed deep coma with bilateral Babinski's sign, dilated fixed unreactive pupils and absent brainstem reflexes.
CT scan head showed right ACA and MCA infarction, cerebral oedema with midline shift [Figure. 1]. Patient's chest roentgenogram and electrocardiogram were unremarkable. His haemotological investigations showed a markedly raised haemoglobin (22 gms%) and packed cell volume (71%). Leukocyte count was normal, however, there was thrombocytosis (4.25 lakhs/mm[3]. Blood urea nitrogen and creatinine levels were elevated to 79 mgms/dl and 4.7 mgms/dl respectively. Serum total protein and albumin concentration were 4 gms/dl and 1.5 gms/dl respectively. Serum cholesterol was markedly elevated to 960 mgms%; so was triglyceride level (225 mgms%). Hyperlipidemia was also documented in his previous medical records. Urinalysis revealed 4+ protein. Prothrombin time and activated partial thromboplastin time were within normal range. Protein-C, Protein-S, antithrombin III, fibrinogen and plasminogen estimation could not be done.
The patient rapidly deteriorated to irreversible coma and EEG showed electrocerebral silence. He succumbed to his illness on the sixth day. Partial autopsy restricted to brain and kidneys was done. Grossly, the brain showed bilateral symmetrical oedema. Thrombus was seen in the lumin of right internal carotid artery and extended to anterior and middle cerebral arteries. The renal findings were suggestive of a minimal change glomerulonephritis with acute tubulointerstitial nephritis.


   »   Discussion Top

Haematological disorders account for upto 8% of all ischaemic strokes in different series.[8] Hypercoagulable state is reported to account for 717% of strokes in young adults.[9] Primary
hypercoagulable states are most often caused by deficiencies of physiological coagulation inhibitors and include deficiency of antithrombin III, Protein-C, Protein- S, and fibrinolytic disorders. The acquired hypercoagulable states include abnormalities of coagulation and fibrinolysis. These include diverse conditions such as malignancy, pregnancy, use of oral contraceptives, the presence of lupus anticoagulant and NS. The most common manifestation of hypercoagulable state associated with NS is renal vein thrombosis, with an incidence of 10-20%. The incidence of thrombosis at other sites averages 20%, with pulmonary embolism being the most frequent manifestation.[10]
The mechanisms that cause a hypercoagulable state in the NS are not entirely clear. One hypothesis stresses the role of renal loss of the body's own anticoagulants, such as plasminogen, antithrombin III, and proteins C and S. Another possibility is a reactively enhanced hepatic production of clotting factors.[11],[12] The patient in the current report had a hypercoagulable state which predisposed him to recurrent deep vein thrombosis in the past. In addition, he also had thrombocytosis and hypercholesterolemia which can induce arterial thrombosis. The relative polycythemia due to severe depletion of intravascular volume must have accelerated the thrombus formation. The patient outlined in the current report is the second case described with such malignant cerebral infarctions. He differs from earlier patients in that the NS had a very long protracted course and accompanied by recurrent episodes of DVT and significant relative polycythemia. All the patients reported in the literature survived and were discharged except one patient.[16] Interestingly, in 5 out of 13 patients reported so far, NS was diagnosed at the time of presentation with stroke.
Nephrotic syndrome should be considered as a contributing mechanism in any patient with ischaemic stroke and preexisting renal disease. In addition, ischaemic stroke can be the presenting manifestation of NS. Nephrotic syndrome is easy to detect by blood and urine examinations and should be considered as a contributing mechanism in stroke patients without other evident conditions predisposing to vascular disease.

 

  »   References Top

1.Cameron JS: The Nephrotic syndrome and its complications. Am J Kidney Dis 1987; 10: 151-171.   Back to cited text no. 1    
2.Miller RB, Harington JT, Ramos CP et al: Long term results of steroid therapy in adults with idiopathic nephrotic syndrome. Am J Med 1969; 46: 919-929.   Back to cited text no. 2    
3.Parag KB, Somers SR, Seedat YK et al: Arterial thrombosis in nephrotic syndrome. Am J Kidney Dis 1990; 15: 176-177.   Back to cited text no. 3    
4.Marsh EE, Biller J, Adams HP et al: Cerebral infarction in patients with nephrotic syndrome. Stroke 1991; 22: 90-93.   Back to cited text no. 4    
5.Fuh JL, Teng MMH, Yang NC et al: Cerebral infarction in young men with nephrotic syndrome. Stroke 1992; 23: 295297.   Back to cited text no. 5    
6.Chaturvedi S: Fulminant cerebral infarctions with membranous nephropathy. Stroke 1993; 24: 473-475.   Back to cited text no. 6    
7.Leno C, Pascual J, Polo MJ et al: Nephrotic syndrome, accelerated atherosclerosis and stroke. Stroke 1992; 23: 921-922.   Back to cited text no. 7    
8.Markus HS, Hambley H: Neurology and the blood; haematological abnormalities in ischemic stroke. J Neurol Neurosurg Psychiatry 1998; 64: 150-159.   Back to cited text no. 8    
9.Beevan H, Sharma K, Bradley W: Stroke in young adults. Stroke 1990; 21: 282-286.   Back to cited text no. 9    
10.Glassock JR, Coben HA, Adler SS et al: Primary glomerular diseases. In: The kidney (Ed) Brenner MB. 5th edition, Vol II, WB Saunder's company, Philadelphia. 1996; 1392-1497.   Back to cited text no. 10    
11.Llach F: Hypercoagulability, renal vein thrombosis and other thrombotic complications of nephrotic syndrome. Kidney Int 1985; 28: 429-439.   Back to cited text no. 11    
12.Shafer A: The hypercoagulable states. Ann Intern Med 1985; 102: 814-828.   Back to cited text no. 12    
13.Fritz C, Braune HJ: Cerebral infarction and nephrotic syndrome. Stroke 1992; 23: 1380-1381.   Back to cited text no. 13    

 

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