These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: [Carotid artery thrombosis and myocardial infarction in nephrotic syndrome].
    Author: Nigond J, Grolleau-Raoux R.
    Journal: Arch Mal Coeur Vaiss; 1990 Jan; 83(1):105-8. PubMed ID: 2106297.
    Abstract:
    The authors report the case of a 18 year old man with a chronic corticosteroid-refractory nephrotic syndrome complicated by carotid artery thrombosis and myocardial infarction. Thromboembolism is one of the most serious complications of the nephrotic syndrome. Serious clotting factor disturbances are observed: changes in platelet function (hyperaggregability) increased plasma zymogens and cofactors, increased plasma fibrinogen, abnormalities of the fibrinolytic system and acquired deficiencies of coagulation inhibitors. The respective role of each of these abnormalities have not been clearly established, but it is likely that increased platelet aggregation and antithrombin III deficiency are important factors in producing a hypercoagulable state in the nephrotic syndrome. Hyperlipidemia is also a characteristic feature of the nephrotic syndrome: these is a wide spectrum of lipoprotein patterns with increased low density lipoproteins (LDL) or very low density lipoproteins (VLDL) or both; contradictory results have been reported with respect to the high density lipoproteins (HDL): decreased, normal or even increased plasma levels have been observed. In addition, changes in the distribution and composition of LDL and VLDL subclasses have been detected. Most of these changes have an atherogenic potential but controversy still surrounds the question of the prevalence of ischaemic heart disease in the nephrotic syndrome; it is unlikely that nephrotic syndromes of short duration have any influence on the incidence of coronary events, but patients with chronic heavy protein urea and long-term exposure to abnormalities of haemostasis and lipid profiles appear to have a significant risk of developing cardiovascular disease and may require long-term anticoagulant therapy.
    [Abstract] [Full Text] [Related] [New Search]