Thrombosis of the pulmonary arteries and the nephrotic syndrome.

Levin, S. E.; Zamit, R.; Schmaman, A

doi:10.1136/bmj.1.5533.153

Cited by 32 publications

(10 citation statements)

References 9 publications

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“…PTE is a serious and sometimes fatal complication of childhood nephrotic syndrome [5,8,9,14]. As in this case, it may not be possible to distinguish an embolic event from local thrombosis.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary thrombo-embolism in nephrotic syndrome treated with tissue plasminogen activator

Reid

Segal²

1997

European Journal of Pediatrics

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Section: Discussionmentioning

confidence: 99%

Pulmonary thrombo-embolism in nephrotic syndrome treated with tissue plasminogen activator

Reid

Segal²

1997

European Journal of Pediatrics

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“…Pulmonary artery thrombosis has been reported gnosis of minimal change disease, which could not be mainly in nephrotic children; most of these cases occur confirmed histologically because of the necessity of at the time of massive generalized oedema or during continuing anticoagulant treatment. Spiral CT angiog-the phase of steroid treatment and intensive diuretic raphy follow-up showed progressive decrease of the therapy [6][7][8]. This condition is very rare in adults occlusive thrombus of the left pulmonary artery.…”

Section: Casementioning

confidence: 99%

Multiple venous thrombosis and massive pulmonary artery thrombus as the presenting features of steroid-responsive nephrotic syndrome

Peces

Pobes²,

Rodríguez³

et al. 1999

Nephrology Dialysis Transplantation

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“…Patients with nephrotic syndrome are apt to develop venous or even pulmonary artery thrombosis (Levin et al, 1967), especially when given steroid therapy. This tendency has been attributed to raised levels of plasma fibrinogen and of inhibitors of fibrinolysis found in the increased a2-globulin and f8-globulin fractions.…”

Section: Introductionmentioning

confidence: 99%

Study of Proteins and Fibrinolysis in Patients with Glomerulonephritis

Wardle¹,

Menon²,

Rastogi³

1970

BMJ

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Evidence is accumulating to substantiate the view that the oxytocic effects of E prostaglandins on uterine myometrium are much more pronounced than those of the Fa prostaglandins. In the induction of labour at term the available evidence suggests that the effective dose range for F2a is about 5 to 10 times that for E2 (Karim et al., 1969; Embrey, 1970). So far personal experience of the F prostaglandins in early pregnancy extends to only six cases. The dose range was 2-5 Ag./min. and the total amount infused varied from 820 to 3,150 ILg. Only in one case (receiving the largest dose) was abortion successfully induced, clearly indicating the superiority of prostaglandin E2 in early pregnancy too. These observations are not at variance with those of Karim and Filshie (1970). They have just reported successful induction of abortion with F2a in 14 out of 15 cases, but they used a very much higher dosage (infusion rate 50 ,ug./min.; infusion time about 4 to 27 hours) and there were frequent sideeffects (diarrhoea and vomiting). No noticeable side-effects could be ascribed to the infusion in any of the cases in this series. The patients were composed and symptom-free. Two vomited, but in each instance only when abortion was well advanced. No significant or constant changes in pulse or blood pressure were recorded in the cases.It would be unwise, on such limited experience, to make extravagant claims for the use of E prostaglandins in the termination of pregnancy. Nevertheless, the results so far are encouraging. The Journal, 1970, 2, 260-263 Summary: Plasma and urine fibrinolysis were studied in 36 patients with glomerulonephritis and proteinuria. In 40% of these plasma fibrinolytic activator activity was moderately reduced and fibrinolytic inhibitors were increased. Globulins with antiplasmin effect were raised, particularly in the earlier months. Both the serum cholesterol and the plasma fibrinogen were related to the level of serum albumin, and those patients with high fibrinogen levels were also those with poor plasma fibrinolytic activator and those showing a steady deterioration. Urinary fibrinolysis was greatly reduced in most patients and bore no relation to plasma fibrinolysis levels. Hence urokinase is not derived from circulating plasminogen activator.

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Thrombosis of the pulmonary arteries and the nephrotic syndrome.

Cited by 32 publications

References 9 publications

Pulmonary thrombo-embolism in nephrotic syndrome treated with tissue plasminogen activator

Pulmonary thrombo-embolism in nephrotic syndrome treated with tissue plasminogen activator

Multiple venous thrombosis and massive pulmonary artery thrombus as the presenting features of steroid-responsive nephrotic syndrome

Study of Proteins and Fibrinolysis in Patients with Glomerulonephritis

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