Immunohistological Study of Endothelin-1 and Endothelin-A and B Receptors in Two Patients with Scleroderma Renal Crisis

Kobayashi, Hill Hiroki; Nishimaki, Tomoe; Kaise, Shunji; Suzuki, Tomohiro; Watanabe, Keita; Kasukawa, Reji

doi:10.1007/s100670050132

Cited by 61 publications

(39 citation statements)

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“…This particular sensitivity is because ET-1 receptors occur in higher density on vascular smooth cells of all renal resistance vessels (33) and, through an autocrine loop, may amplify ET-1 expression (34). The observation of increased ET-1 expression in the kidneys in this GVH SSc model supports the proposed pathophysiologic role of ET-1 in the development of renal crisis in human SSc (35)(36)(37). Our observations of morphologic changes in smooth muscle cells surrounding vessels, as well as increases in ET-1 expression around vessels and in kidney tubules in the GVH-induced scleroderma model, provide further evidence that vascular changes contribute to contractility of the vessels and possibly promote increased extracellular matrix deposition.…”

Section: Resultssupporting

confidence: 84%

A modified model of graft‐versus‐host–induced systemic sclerosis (scleroderma) exhibits all major aspects of the human disease

Ruzek¹,

Jha²,

Ledbetter³

et al. 2004

Arthritis & Rheumatism

110

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Objective. Diffuse systemic sclerosis (SSc; scleroderma) is a debilitating disease characterized by excessive dermal fibrosis with later progression to internal organs. In addition to the fibrotic component, major aspects of the disease include vascular or circulatory involvement and immune dysregulation evidenced by inflammatory cells in affected tissues and production of autoantibodies. Many animal models resembling this disease have been studied, including genetic models in mice and chickens, challenge with chemicals such as bleomycin or vinyl chloride to induce fibrosis, and models of graft-versus-host (GVH)-induced disease using certain strains of mice with differences in minor histocompatibility loci. The present studies were undertaken to determine if alteration of the induction of GVH-induced scleroderma could result in a model that more fully represented the human condition. Methods. Disease was induced by injection of spleen cells from B10.D2 mice into BALB/c mice deficient in mature T and B cells (recombination-activating gene 2 targeted). Dermal thickening, collagen deposition, vasoconstriction, and parameters of immunity were analyzed.Results. Similar to the human disease, this modified GVH model of SSc demonstrated evidence of dermal thickening, particularly in the extremities, progressive fibrosis of internal organs, vasoconstriction and altered expression of vascularity markers in skin and internal organs, early immune activation, inflammation in skin and internal organs, and autoantibody generation.Conclusion. This modified model of GVH-induced SSc exhibits all major components of human disease and is likely to contribute to better understanding of the disease mechanisms and, ultimately, improved treatments for patients.

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Section: Resultssupporting

confidence: 84%

A modified model of graft‐versus‐host–induced systemic sclerosis (scleroderma) exhibits all major aspects of the human disease

Ruzek¹,

Jha²,

Ledbetter³

et al. 2004

Arthritis & Rheumatism

110

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“…Zbiti also reported a normocytic normochromic anemia with hemoglobin of 6g/dL [5]. High-dose corticosteroid therapy longer than 3 months is considered as a powerful risk factor of SRC [6,[8][9][10][11] as evidenced by case No 1 who developed a SRC after 4 months treatment with 40 mg of prednisone per day .Hypertension, usually malignant (DBP ≥ 130 mm Hg) was found in approximately 87% of patients [6,8] in its typical form. In our study 2 patients had malignant hypertension one a BP of 230 / 140mmHg and hypertensive retinopathy (case NO 1) and the other with a BP of 250 / 130mmHg and low consciousness level (case NO 2).…”

Section: Discussionmentioning

confidence: 99%

Scleroderma renal crisis in tropical region, two senegalese cases

MM¹,

AKO²,

SM³

et al. 2015

Clin Case Rep Rev

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Scleroderma renal crisis (SRC) is defined as the new onset of accelerated arterial hypertension and /or rapidly progressive oliguric renal failure during the course of systemic sclerosis. It is a rare but life-threatening complication. This formerly serious complication has got a considerable brighter outlook since the introduction of angiotensin converting enzyme inhibitors (ACE) however the mortality is still remaining high. We report two cases of SRC which to our knowledge are the firsts described in Dakar. They were two women aged 45 and 32 years, one of them was previously following for systemic sclerosis. Both of them had malignant hypertension associated with rapidly progressive renal failure, the other was put under corticosteroid therapy four months before SRC occurrence. The histological and laboratory finding showed thrombotic microangiopathy. The height blood pressure returned to normal value after treatment with ACE inhibitors. The final outcome was undesirable with the death of one after two months due to the hemodialysis discontinuation and persistence of renal failure in the other.

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“…Higher serum ET-1 levels were detected in SSc compared to healthy controls (Vancheeswaran et al, 1994). In kidney specimens, overexpression of ET-1 and ET type B receptors were described in two patients who died following SRC (Kobayashi et al, 1999). Mouthon et al extended the aforementioned observations by studying the pattern of ET-1 expression in kidney biopsies utilizing the immunoperoxidase technique (Mouthon et al).…”

Section: Pathophysiologymentioning

confidence: 99%