Thromb Haemost 1984; 52(03): 253-255
DOI: 10.1055/s-0038-1661190
Original Article
Schattauer GmbH Stuttgart

Abnormal Haemostasis and Blood Viscosity in Malignant Hypertension

C Isles
The University Department of Medicine and Renal Unit, Glasgow Royal Infirmary and the MRC Blood Pressure Unit and Department of Haematology, Glasgow Western Infirmary, U.K
,
G D O Lowe
The University Department of Medicine and Renal Unit, Glasgow Royal Infirmary and the MRC Blood Pressure Unit and Department of Haematology, Glasgow Western Infirmary, U.K
,
B M Rankin
The University Department of Medicine and Renal Unit, Glasgow Royal Infirmary and the MRC Blood Pressure Unit and Department of Haematology, Glasgow Western Infirmary, U.K
,
C D Forbes
The University Department of Medicine and Renal Unit, Glasgow Royal Infirmary and the MRC Blood Pressure Unit and Department of Haematology, Glasgow Western Infirmary, U.K
,
N Lucie
The University Department of Medicine and Renal Unit, Glasgow Royal Infirmary and the MRC Blood Pressure Unit and Department of Haematology, Glasgow Western Infirmary, U.K
,
A F Lever
The University Department of Medicine and Renal Unit, Glasgow Royal Infirmary and the MRC Blood Pressure Unit and Department of Haematology, Glasgow Western Infirmary, U.K
,
A C Kennedy
The University Department of Medicine and Renal Unit, Glasgow Royal Infirmary and the MRC Blood Pressure Unit and Department of Haematology, Glasgow Western Infirmary, U.K
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Publikationsverlauf

Received 06. Juni 1984

Accepted 16. August 1984

Publikationsdatum:
19. Juli 2018 (online)

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Summary

We have previously shown abnormalities of haemostasis suggestive of intravascular coagulation in patients with malignant hypertension, a condition associated with retinopathy and renal fibrin deposition. To determine whether such abnormalities are specific to malignant hypertension, we have measured several haemostatic and haemorheological variables in 18 patients with malignant hypertension (Group 1), 18 matched healthy controls (Group 2), and 18 patients with non-malignant hypertension (Group 3) matched for renal pathology, blood pressure and serum creatinine with Group 1. Both Groups 1 and 3 had increased mean levels of fibrinogen, factor VIIIc, beta-thrombo- globulin, plasma viscosity and blood viscosity (corrected for haematocrit); and decreased mean levels of haematocrit, antithrombin III and platelet count. Mean levels of fast antiplasmin and alpha2-macroglobulin were elevated in Group 1 but not in Group 3. We conclude that most blood abnormalities are not specific to malignant hypertension; are also present in patients with non-malignant hypertension who have similar levels of blood pressure and renal damage; and might result from renal damage as well as promoting further renal damage by enhancing fibrin deposition. However increased levels of fibrinolytic inhibitors in malignant hypertension merit further investigation in relation to removal of renal fibrin.