Prophylaxis of Thromboembolic Events in Patients with Nephrotic Syndrome

Pincus, Kathleen J; Hynicka, Lauren M.

doi:10.1345/aph.1r530

Cited by 32 publications

(35 citation statements)

References 46 publications

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“…Prophylactic treatment could include anticoagulants (for a recent review about anticoagulants in adult patients with NS, see Pincus et al [84]), but also antiplatelet agents such as acetylsalicylic acid [85]. Some early reports theoretically support the use of antiplatelet medication, showing normalization of in vitro platelet aggregation in NS during treatment with acetylsalicylic acid [23,39].…”

Section: Potential Of Antiplatelet Therapy In Nephrotic Syndromementioning

confidence: 99%

Platelet abnormalities in nephrotic syndrome

et al. 2015

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Nephrotic syndrome (NS) is a common kidney disease associated with a significantly increased risk of thrombotic events. Alterations in plasma levels of pro- and anti-coagulant factors are involved in the pathophysiology of venous thrombosis in NS. However, the fact that the risk of both venous and arterial thrombosis is elevated in NS points to an additional role for blood platelets. Increased platelet counts and platelet hyperactivity have been observed in nephrotic children. Platelet hyperaggregability, increased release of active substances, and elevated surface expression of activation-dependent platelet markers have been documented. The mechanisms underlying those platelet alterations are multifactorial and are probably due to changes in plasma levels of platelet-interfering proteins and lipid changes, as a consequence of nephrosis. The causal relationship between platelet alterations seen in NS and the occurrence of thromboembolic phenomena remains unclear. Moreover, the efficiency of prophylactic treatment using antiplatelet agents for the prevention of thrombotic complications in nephrotic patients is also unknown. Thus, antiplatelet medication is currently not generally recommended for routine prophylactic therapy.

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Section: Potential Of Antiplatelet Therapy In Nephrotic Syndromementioning

confidence: 99%

Platelet abnormalities in nephrotic syndrome

et al. 2015

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“…19 Moreover, heparin also could dissolve thrombus. 20,21 Proteinuria is one of the main characterizations of kidney diseases, the results of this study showed that low-molecularweight heparin calcium showed good curative effect on proteinuria. Fukui et al 22 conducted one controlled clinical trial in pediatric patients with moderate systems of HSP, their research also showed that intravenous administration of factor XIII concentrate, 30-50 U/kg for days, was associated with significant improvements in the severity of proteinuria and hematuria compared with a non-treated group.…”

Section: Discussionmentioning

confidence: 70%

Heparin calcium treated Henoch–Schönlein purpura nephritis in children through inhibiting hyperfibrinolysis

Tian

Liu

2015

Renal Failure

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Aim: To explore the underlying mechanism of low-molecular-weight heparin calcium therapy on Henoch-Schö nlein purpura nephritis (HSPN). Methods: Eighty-nine children with severe HSPN were randomized into control group (treated with conventional therapy, n ¼ 45) and treatment group (treated with conventional therapy plus low-molecular-weight heparin calcium, n ¼ 44). The concentrations of plasma fibrinogen (Fg), D-dimer and fibrin degradation products (FDPs) were detected before and after treatment. The urinary red blood cell (RBC) and 24 h proteinuria were determined weekly for assessing the children's kidney function. Results: Two groups were well-matched at baseline. After 8 weeks of treatment, the clinical outcomes of HSPN and outcome of proteinuria of the treatment group were better than the control group (p50.05); the content of Fg, D-dimer and FDP in plasma of the treatment group were lower than the control group (p50.05); but there was no difference about the curative effect of hematuria and the coagulation function between the two groups (p40.05). Conclusions: Fibrinolytic system may participate in the kidney injury of HSPN children and low-molecularweight heparin calcium could correct blood hypercoagulability through inhibiting hyperfibrinolysis, and thus improving the blood supply of kidney. KeywordsFibrinolytic system, Henoch-Schö nlein purpura nephritis (HSPN), low-molecular-weight heparin calcium History

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“…The mechanism by which nephrotic syndrome causes a hypercoagulable state is unclear but is posited to be secondary to loss of proteins, including anticoagulants such as antithrombin III, plasminogen, protein C, and protein S. 11 The incidence of thromboembolism in nephrotic syndrome is not well defined but is estimated to be between 2% and 42% for venous thrombosis and between 2% and 8% for arterial thromboembolism. 12 The incidence of thromboembolism appears to be highest in the first 6 months following the diagnosis of nephrotic syndrome. 10 Patients with severe hypoalbuminemia (< 2 g/dL) and those with membranous nephropathy have the greatest risk of thromboembolic complications.…”

Section: Discussionmentioning

confidence: 99%

“…10 Patients with severe hypoalbuminemia (< 2 g/dL) and those with membranous nephropathy have the greatest risk of thromboembolic complications. 12 Although controversial, some experts recommend primary prophylaxis with anticoagulants in patients with nephrotic syndrome, particularly for those with severe hypoalbuminemia. 12 Patients with IgA nephropathy appear to have the lowest risk of thromboembolic complications.…”

Section: Discussionmentioning

confidence: 99%

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Acute Cerebellar Thrombosis in an Adult Patient with IgM Nephropathy

Adike

Cherry

Awar

2015

Methodist DeBakey Cardiovascular Journal

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A 70-year-old female with a past medical history of hypertension, type 2 diabetes, and hypothyroidism presented with a 2-month history of epigastric pain associated with abdominal distention, nausea, and generalized malaise. She also noted facial and bilateral leg swelling. Despite reporting decreased appetite, she had gained approximately 20 pounds in 1 month. She denied hematuria, fevers, night sweats, joint pain, vomiting, diarrhea, or changes in stool color or caliber. Admission vital signs were within normal range. Physical examination was remarkable for a mildly distended abdomen without evidence of ascites or peritoneal signs. Her lungs were clear and she had no jugular venous distention. There was 3+ pretibial pitting edema in her lower extremities bilaterally. Periorbital edema was also noted.Laboratory tests showed a normal electrolyte panel with a blood urea nitrogen of 2 mg/dL and creatinine of 0.7 mg/dL. Liver function tests were within normal limits. Serum albumin and protein were significantly depressed at 1.1 and 4.1 g/dL, respectively. Computed tomography of the abdomen was only remarkable for diverticulosis. Urinalysis showed 3+ protein, < 1 red blood cells, and no casts, and 24-hour urine protein was significantly elevated at 6426 mg/vol. Total cholesterol was elevated at 246 mg/dL, with an elevated triglyceride of 254 mg/dL. Hemoglobin A1c was 6.7%. Autoimmune workup was negative and systemic lupus erythematosus was excluded. Complement C3 was 126 mg/dL (normal 85-200 mg/dL) and complement C4 was 24 mg/dL (normal 17-46 mg/dL). Viral panel including acute hepatitis panel, HIV, cytomegalovirus, and herpes simplex virus was also negative. Immunoglobulin panel was checked and showed an immunoglobulin A level of 172 mg/dL (normal 85-350), immunoglobulin M (IgM) level of 99 mg/dL (normal 60-300), and immunoglobulin G level of 193 mg/dL (normal 696-1488). Doppler analysis of the renal vasculature was unremarkable. For work-up of her abdominal pain, esophagogastroduodenoscopy showed a normal esophagus and gastritis with prominent gastric folds. Gastric mucosa showed no evidence of inflammation or dysplasia but was remarkable for edema and congestion. Colonoscopy revealed diverticulosis without diagnostic mucosal alteration. Ultimately, biopsy of the left kidney was performed. Renal pathology was remarkable for mesangial proliferation and mild segmental sclerosis on light microscopy (Figure 1), diffuse IgM deposits in the mesangial area on immunofluorescence with areas of focal C1q, and diffuse C4d deposits in the mesangium (Figure 2). No light chain deposits were identified. Electron microscopy was remarkable for effacement of visceral epithelial cells (Figure 3). C A S E R E P O R T AbstractIgM nephropathy is a relatively rare cause of idiopathic nephrotic syndrome.

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Prophylaxis of Thromboembolic Events in Patients with Nephrotic Syndrome

Cited by 32 publications

References 46 publications

Platelet abnormalities in nephrotic syndrome

Platelet abnormalities in nephrotic syndrome

Heparin calcium treated Henoch–Schönlein purpura nephritis in children through inhibiting hyperfibrinolysis

Acute Cerebellar Thrombosis in an Adult Patient with IgM Nephropathy

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