Hypercoagulation in glomerulonephritis.

Salem, Hamed; Whitworth, J. A.; Koutts, Jerry; Kincaid-Smith, P; Firkin, Barry G.

doi:10.1136/bmj.282.6282.2083

Cited by 14 publications

(17 citation statements)

References 9 publications

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“…The APTT results on the plasmas from the 117 patients investigated confirm the findings of Salem et al [10] that the plasma from a number of patients (13% in this sam ple) with renal disease contains a factor which causes shortening of the patient's APTT and of control plasma when mixed in a 1:1 ratio. The plasma from a number of other patients (3% in this sample) have nor mal APTT values but the plasma from these patients causes significant shortening of the APTT when mixed with control plasma.…”

Section: Discussionsupporting

confidence: 76%

“…Recently, Salem et al [10,11] described an activator of the coagulation acceleration factor (CAF) pathway which was present in the plasma from a number of patients with GN. CAF copurified with F.VIII coagulant activity (F.VIII:C) and is possibly an acti vated form of F. VIII:C. The presence of this activator was detected by a shortened pa tient APTT and the ability of patient plasma to shorten the APTT of control plasma by more than 5 s.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Further Investigations on the Significance of a Plasma Coagulation-Accelerating Factor in Glomerular Disease

Howard¹,

Kincaid‐Smith²,

Firkin³

et al. 1987

Pathophysiol Haemos Thromb

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The prevalence of the coagulation acceleration factor (CAF) in patients with renal disease (predominately glomerulonephritis) has been investigated. The relationship between the activated partial thromboplastin time, F.VIII:C/vWf, prekallikrein, plasminogen and the pathogenesis of glomerulonephritis was also investigated. One hundred and seventeen patients were entered into the study on the basis of admission for renal biopsy. Thirteen percent of the patients showed evidence for CAF and 15 % of patients were found to have reduced levels of plasma prekallikrein; however, no correlation was found between any of the variables measured and the type, activity or progression of glomerular disease in these patients.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Further Investigations on the Significance of a Plasma Coagulation-Accelerating Factor in Glomerular Disease

Howard¹,

Kincaid‐Smith²,

Firkin³

et al. 1987

Pathophysiol Haemos Thromb

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“…Hence, our results indicate that short APTTs are associated with activated coagulation. Enhanced plasma levels of F1+2 and FVIII in patients with short APTTs were also reported by others [9,13,18]. However, the relationship between APTTs and the level of F1+2 and FVIII:C has not been studied previously.…”

Section: Discussionmentioning

confidence: 83%

Abnormally Short Activated Partial Thromboplastin Times Are Related to Elevated Plasma Levels of TAT, F1+2, D-Dimer and FVIII:C

Boekel

Bartels²

2002

Pathophysiol Haemos Thromb

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Abnormally short activated partial thromboplastin times (APTTs) are associated with an increased risk of thrombotic disorders. We have examined the status of coagulation activity in subjects with short APTTs. In addition, the presence of the thrombotic risk factors G1691A-factor V, G20210A-prothrombin gene mutation and factor VIII coagulant activity (FVIII:C) was determined. Plasma levels of TAT, F1+2, D-dimer and FVIII:C were markedly higher in subjects with short APTTs compared with subjects with normal APTTs. APTTs were inversely related to TAT, F1+2, D-dimer and FVIII:C levels. The prevalence of G1691A-factor V and G20210A-prothrombin gene mutation between the group with short APTTs and the control group was not significantly different. Hence, these gene polymorphisms do not contribute to the increased risk of thrombosis associated with short APTTs. In conclusion, short APTTs are indicative of marked coagulation activity and elevated FVIII:C levels. Elevated FVIII:C levels may play a pathogenic role in the increased risk of thrombosis associated with abnormally short APTTs.

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“…The pres ence of fibrin deposits either in the capillary network of the glomerulus or in the Bowman's space [1][2][3][4][5] in patients suffering from the disease has been pointed out. Further more, the existence of signs of hypercoagulation as well as various alterations in the platelet function in patients suffering from GMN [6][7][8][9][10] have also been described.…”

Section: Introductionmentioning

confidence: 99%

Effects of Dipyridamole on the Short-Term Evolution of Glomerulonephritis

Cámara

Cruz

Frutos

et al. 1991

Nephron

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The aim of the present study is to evaluate the effect of dipyridamole (300 mg/day) versus placebo in a double-blind randomized trial on membranous glomerulonephritis (M-GMN), mesangial IgA glomerulonephritis (IgA-GMN), and segmentary and focal hyalinosis glomerulonephritis (SFH-GMN) during the first 3 months of treatment. In the case of M-GMN, proteinuria dropped by 60% of the basal value in patients treated with dipyridamole; in the case of IgA-GMN it dropped by 65–70%; and in the case of SFH-GMN it dropped by 40% of the basal value. Inhibition of proteinuria in M-GMN was correlated to platelet response, and above all, to the ADP-induced platelet aggregation in whole blood.

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Hypercoagulation in glomerulonephritis.

Cited by 14 publications

References 9 publications

Further Investigations on the Significance of a Plasma Coagulation-Accelerating Factor in Glomerular Disease

Further Investigations on the Significance of a Plasma Coagulation-Accelerating Factor in Glomerular Disease

Abnormally Short Activated Partial Thromboplastin Times Are Related to Elevated Plasma Levels of TAT, F1+2, D-Dimer and FVIII:C

Effects of Dipyridamole on the Short-Term Evolution of Glomerulonephritis

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