Femoral arterial thrombosis in nephrotic syndrome.

Cameron, J. S.; Ogg, C S; Ellis, F.R.; Salmon, M

doi:10.1136/adc.46.246.215

Cited by 15 publications

(8 citation statements)

References 9 publications

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“…Steroids alter the coagulation state by increasing factor VIII and other serum proteins, and by decreasing the fibrinolytic activity. Cameron et al 3 recommended that steroid therapy should be replaced by cyclophosphamide therapy. Table 2 4-8 summarizes the reported cases of lower extremity arterial thrombosis in adult patients with nephrotic syndrome.…”

Section: Discussionmentioning

confidence: 99%

Acute arterial thrombosis with antithrombin III deficiency in nephrotic syndrome: Report of a case

et al. 2000

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Nephrotic syndrome frequently causes venous thromboembolic complications. Arterial thrombosis has rarely been reported and is mainly observed in children. Only six cases of lower extremity arterial thrombosis in adults have been reported in the literature. The outcome in these cases was unsatisfactory because of the high rates of limb loss and recurrence of thrombosis. We report successful treatment of a 39-year-old man who suffered from right lower extremity arterial thrombosis associated with decreased levels of serum antithrombin III. He was admitted to our hospital with severe pain in his right foot. No pulse was palpable in his right dorsalis pedis or posterior tibial arteries. His right foot was cold and mottled, with a reduced sensation and motor activity. The laboratory data revealed a serum total protein concentration of 3.9g/dl and an albumin concentration of 1.5 g/dl. The coagulation profile showed a fibrinogen level of 879 mg/dl and antithrombin III value of 9.5%. Right lower extremity arteriography showed a complete occlusion of the right deep femoral artery and popliteal artery, and a filling defect in the common femoral artery. An emergency thrombectomy was performed under general anesthesia. The patient was treated successfully, and surgical treatment was followed by anticoagulant therapy with 1,000 units of antithrombin III. A renal biopsy revealed histologic evidence of minimal change of glomerulonephritis. He was discharged 3 months later, and no recurrence of thrombosis has yet been observed.

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Section: Discussionmentioning

confidence: 99%

Acute arterial thrombosis with antithrombin III deficiency in nephrotic syndrome: Report of a case

et al. 2000

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“…Since then thrombotic complications have frequently been observed in nephrotic patients in both venous and arterial systems [14,15,31,39,45,50]. The association of the nephrotic syndrome with renal vein thrombosis has been found to be particularly frequent [23,26,33,39,45] and it is now generally considered to be a complication, while in the past was regarded as a cause of the nephrotic syndrome [30,32], The tendency of nephrotic patients to thrombotic episodes has been attributed to a hypercoagulable state.…”

Section: Introductionmentioning

confidence: 99%

Comprehensive Study of Haemostasis in Nephrotic Syndrome

Panicucci

Sagripanti

Vispi

et al. 1983

Nephron

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A comprehensive study of haemostasis has been performed in a homogeneous group of 20 patients with nephrotic syndrome without renal failure. We have found unchanged number of platelets and a significant increase of platelet adhesiveness and aggregation; increased levels of activity and related antigen of fibrinogen, of factor VIII, of activity of factors II, VII and X and of antigens of factors XIII. Antithrombin III was unchanged in plasma and was detected in the urine. Euglobulin lysis times were decreased, and levels of plasminogen and its activators were increased after a venous occlusion test. At the same time urokinase inhibitors and antiplasmins were increased not only after, but also before a venous occlusion test. Fibrinogen degradation products have been found in the urine of all our patients but not in their sera.

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“…Untreated nephrotic syndrome may cause numerous complications, such as hypovolemia, hypertension, hyperlipidemia, hypercoagulability, growth and developmental delays, and anemia. 8,13,14 Total plasma cholesterol and low-density lipoprotein cholesterol levels are elevated in most patients. [15][16][17] Decreased bone mineral content and impaired linear height attainment appear to resolve with resolution of immunosuppressant therapy and seem to be related more to therapy than underlying disease state.…”

Section: Complications Of Untreated Nephrotic Syndromementioning

confidence: 99%

“…Subsequent changes in fluid status may lead to oliguria and increased blood urea nitrogen and risk of thrombosis even in those with normal glomeruli. 9,13 Hypercoagulability may occur due to thrombocytosis; elevated concentrations of plasma fibrinogen factors V, VII, VIII, and X; increased platelet aggregation; and accelerated thromboplastin generation. 20,21 Increased coagulation may cause renal vein and deep vein thrombosis or central venous sinus thrombosis, and thus renal necrosis and damage.…”

Section: Complications Of Untreated Nephrotic Syndromementioning

confidence: 99%

Management of Nephrotic Syndrome in Children

et al. 2003

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Idiopathic childhood nephrotic syndrome generally has a favorable long-term prognosis. Prompt administration of and improved guidelines for monitoring therapy have decreased morbidity and mortality. The treatment goal is to induce prompt remission while minimizing complications and adverse events. Aggressive therapy induces remission and decreases the frequency of relapse in most patient populations; however, such treatment often results in unnecessary toxicity. We critically assessed the current clinical evidence that supports each pharmacologic therapy. For each drug regimen, the risks and monitoring parameters required to reduce complications and optimize therapy are discussed. Some of the treatments are the common corticosteroid approaches, cytotoxic therapies (chlorambucil, cyclophosphamide), cyclosporine, less frequently used drugs (e.g., levamisole), and experimental therapies. Further studies are needed to identify the most effective and least toxic therapeutic regimens for inducing and maintaining remission in children with nephrotic syndrome.

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Femoral arterial thrombosis in nephrotic syndrome.

Cited by 15 publications

References 9 publications

Acute arterial thrombosis with antithrombin III deficiency in nephrotic syndrome: Report of a case

Acute arterial thrombosis with antithrombin III deficiency in nephrotic syndrome: Report of a case

Comprehensive Study of Haemostasis in Nephrotic Syndrome

Management of Nephrotic Syndrome in Children

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