Anticoagulants Are of Value in the Treatment of Renal Disease

Kincaid‐Smith, Priscilla

doi:10.1016/s0272-6386(84)80050-5

Cited by 15 publications

(1 citation statement)

References 49 publications

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“…TMA can be observed in a wide spectrum of disorders, including thrombotic thrombocytopenic purpura, hemolyticuremic syndrome, malignant hypertension, postpartum renal failure, preeclampsia, and autoimmune diseases, including antiphospholipid syndrome (APS). [2][3][4][5] Acute and/or chronic renal thrombotic manifestations are frequently observed in patients with antiphospholipid antibodies (aPLs). 6 To date, therapy for the renal involvement in TMA is limited and shows little clinical effect.…”

Section: Introductionmentioning

confidence: 99%

Role of tissue factor in a mouse model of thrombotic microangiopathy induced by antiphospholipid antibodies

Seshan¹,

Franzke

Redecha

et al. 2009

Blood

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Using different mouse monoclonal and human antiphospholipid (aPL) antibodies, we developed a new animal model of renal injury that shares many features with thrombotic microangiopathy (TMA). We found that more than 1 mechanism/signaling pathway is involved in glomerular injury induced by aPL antibodies in this model. Both complement-dependent and complementindependent pathways were identified that lead to glomerular endothelial cell damage and renal function impairment. We also found that C5a-C5aR interaction is a crucial step for the activation of the coagulation cascade and glomerular injury induced by complement-activating antibodies. In addition, our studies demonstrated complementindependent mechanisms in which reactivity with ␤ 2 glycoprotein I (␤2GPI) plays an important role in aPL-induced glomerular damage and renal failure. Independently of the mechanism responsible for aPL-induced TMA, mice that express low levels of tissue factor (TF) were protected from glomerular

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Section: Introductionmentioning

confidence: 99%

Role of tissue factor in a mouse model of thrombotic microangiopathy induced by antiphospholipid antibodies

Seshan¹,

Franzke

Redecha

et al. 2009

Blood

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Tissue‐type plasminogen activator and its inhibitor in human glomerulonephritis

Aya

Yoshioka

Murakami

et al. 1992

The Journal of Pathology

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We carried out an immunohistochemical study of tissue-type plasminogen activator (PA) and urokinase-type PA, and their inhibitors, PA inhibitor-1 and PA inhibitor-2, using renal biopsy specimens obtained from 86 patients with various forms of glomerulonephritis. The controls were four normal renal tissue specimens. On immunofluorescent observation, granular staining for tissue-type PA was found to be distributed along the glomerular capillary walls. The fluorescence was weak in the normal renal tissue and occasionally intense in the tissues of patients with IgA nephritis, minimal change nephrotic syndrome, and lupus nephritis. PA inhibitor-1 was abundant in the glomerular epithelial cells and scarce in the mesangial area and glomerular capillary lumens of the normal renal tissues. This was confirmed by immunoelectron microscopy using gold staining. The fluorescence of PA inhibitor-1 was weaker in some specimens of nephritic tissues than in the normal renal tissues. Urokinase-type PA and PA inhibitor-2 were negative within the glomeruli in all the specimens. In the glomerulonephritic tissues which were fibrin deposition-positive, tissue-type PA expression in the glomeruli tended to be strong. An association between fibrin deposition and PA inhibitor-1 staining was not clear. These data suggest that expression of tissue-type PA in the glomeruli increases in association with fibrin deposition.

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Acute and Chronic Renal Failure

Johnson¹

1992

Applied Therapeutics

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THERE are five books in this series, each dealing with a single topic or related group of topics. They seem a little expensive for their size at £5.95 each, but they have hard covers and are pleasantly produced on good quality paper. Taken together they cover renal disease in sufficient detail for anyone except the specialist nephrologist. They certainly would be adequate for preparation for the membership examination, and would be very helpful for a registrar coming to work in a renal unit. They are, however, somewhat uneven in quality. Renal Glomerular

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Anticoagulants Are of Value in the Treatment of Renal Disease

Cited by 15 publications

References 49 publications

Role of tissue factor in a mouse model of thrombotic microangiopathy induced by antiphospholipid antibodies

Role of tissue factor in a mouse model of thrombotic microangiopathy induced by antiphospholipid antibodies

Tissue‐type plasminogen activator and its inhibitor in human glomerulonephritis

Acute and Chronic Renal Failure

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