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The Significance of Microangiopathic Haemolytic Anaemia in Accelerated Hypertension
Author(s) -
Sevitt L. H.,
Naish P.,
Baker L. R. I.,
Bulpitt C. J.,
Archer D. F. J.,
Nelson D. A.,
Peters D. K.
Publication year - 1973
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1973.tb01676.x
Subject(s) - microangiopathic hemolytic anemia , fibrinogen , fragmentation (computing) , red cell , medicine , fibrin , red blood cell , endocrinology , pathology , chemistry , platelet , immunology , biology , thrombotic thrombocytopenic purpura , ecology
S ummary . Twenty‐two patients with accelerated hypertension and varying degrees of renal involvement have been studied in order to assess the significance of microangiopathic haemolytic anaemia (MAHA) and the possible pathogenic role of intravascular fibrin deposition in this condition. Vascular damage was assessed by retinal photography including fluorescein angiography. Haematological investigations including examination of peripheral films and assessment of red cell fragmentation were carried out. Fibrinogen catabolism was measured using radio‐iodine labelled fibrinogen. No correlation between the degree of vascular damage in the retinal vessels and the blood pressure, degree of red cell fragmentation or evidence of renal damage was found. There was a significant increase in red cell fragmentation when the creatinine clearance was 20 ml/min or less. Fibrinogen derivatives were demonstrated in the serum in the minority and in the urine of the majority of those patients with MAHA. Fibrinogen catabolism was normal in all cases. The significance of microangiopathic haemolytic anaemia in accelerated hypertension is discussed. It is suggested from these data that the red cell fragmentation occurs predominantly within the kidney and that there is no evidence that fibrinogen deposition plays an important role in red cell damage, or that it is an important pathogenic factor in producing accelerated hypertension.