Deoxyspergualin, an immunosuppressant, in patients suffering from nephropathies with crescent formation: an open-label trial to evaluate safety and efficacy

Imai, Hirokazu; Hasegawa, Osamu; Yoshimura, Mitsuhiro; Konta, Tsuneo; Tsubakihara, Yoshiharu; Miyazaki, Masanobu; Tomida, Chie; Kobayashi, Masaki; Suzuki, Satoshi; Sasaki, Hideo; Yamauchi, Atsushi; Yokoyama, Hitoshi; Nose, Masato

doi:10.1007/s10157-005-0396-1

Cited by 11 publications

(4 citation statements)

References 33 publications

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“…Patients received daily doses of 0.1 or 0.2 mg/kg (the latter dose was efficient) for four weeks along with the continuation of corticosteroid therapy. These improvements persisted during the 2-month follow-up period after the discontinuation of therapy [118]. 15-DSG was also used clinically in the therapy of renal transplant rejection and Wegener’s granulomatosis [114,119,120].…”

Section: Hspa8/hspa8 As a Therapeutic Target In Clinical Trialsmentioning

confidence: 99%

HSPA8/HSC70 in Immune Disorders: A Molecular Rheostat that Adjusts Chaperone-Mediated Autophagy Substrates

Bonam

Ruff²,

Muller

2019

Cells

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HSPA8/HSC70 is a molecular chaperone involved in a wide variety of cellular processes. It plays a crucial role in protein quality control, ensuring the correct folding and re-folding of selected proteins, and controlling the elimination of abnormally-folded conformers and of proteins daily produced in excess in our cells. HSPA8 is a crucial molecular regulator of chaperone-mediated autophagy, as a detector of substrates that will be processed by this specialized autophagy pathway. In this review, we shortly summarize its structure and overall functions, dissect its implication in immune disorders, and list the known pharmacological tools that modulate its functions. We also exemplify the interest of targeting HSPA8 to regulate pathological immune dysfunctions.

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Section: Hspa8/hspa8 As a Therapeutic Target In Clinical Trialsmentioning

confidence: 99%

HSPA8/HSC70 in Immune Disorders: A Molecular Rheostat that Adjusts Chaperone-Mediated Autophagy Substrates

Bonam

Ruff²,

Muller

2019

Cells

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“…Another open-label prospective study of deoxyspergualin in 44 patients with crescentic GN (including AAV) cited improvements in proteinuria and hematuria after 4 weeks. 231 In a murine model of AAV, deoxyspergualin was equivalent to CYC, and superior to MMF, in attenuating nephritis. 232 Additional randomized trials are required to assess the role (if any) of deoxyspergualin to treat WG.…”

Section: Deoxyspergualinmentioning

confidence: 99%

Wegener Granulomatosis (Granulomatosis with Polyangiitis): Evolving Concepts in Treatment

Lynch¹,

Tazelaar²

2011

Semin Respir Crit Care Med

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Wegener granulomatosis (WG), the most common of the pulmonary granulomatous vasculitides, typically involves the upper respiratory tract, lower respiratory tract (bronchi and lung), and kidney, with varying degrees of disseminated vasculitis. THE TERM GRANULOMATOSIS WITH POLYANGIITIS (WEGENER) WAS RECENTLY PROPOSED TO REPLACE THE OLDER TERM, WG. THE TERM GRANULOMATOSIS WITH POLYANGIITIS CAN BE ABBREVIATED TO GPA, WITH THE IDEA THAT THE EPONYM WEGENER WOULD BE OMITTED OVER TIME. Cardinal histologic features include a necrotizing vasculitis involving small vessels, extensive "geographic" necrosis, and granulomatous inflammation. Clinical manifestations of WG are protean; virtually any organ can be involved. The spectrum and severity of the disease are heterogeneous, ranging from indolent disease involving only one site to fulminant, multiorgan vasculitis. The pathogenesis of WG has not been elucidated, but both cellular and humoral components are involved. Circulating antibodies against cytoplasmic components of neutrophils [anti-neutrophil cytoplasmic antibodies (c-ANCAs)] likely play a role in the pathogenesis, and often correlate with activity of the disease. Treatment strategies are evolving. Cyclophosphamide (CYC) plus corticosteroids (CSs) is the mainstay of therapy for generalized, multisystemic WG. Historically, the combination of CYC plus CS was used for a minimum of 12 months, but concern about late toxicities associated with CYC has led to novel treatment approaches. Currently, short-course (3 to 6 months) induction treatment with CYC plus CS, followed by maintenance therapy with less toxic agents (e.g., methotrexate, azathioprine) is recommended. Further, methotrexate combined with CS may be adequate for limited, non-life-threatening WG. Recent studies suggest that rituximab may be useful for induction therapy or CYC-refractory WG. The role of other immunomodulatory agents (including trimethoprim-sulfamethoxazole) is also explored.

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“…There have been many reports on DSG-related improvements in clinical cases with severe vasculitis, which include Wegener granulomatosis and crescentic glomerulonephritis (Birck et al 2003; Shimitt et al 2005; Imai et al 2006). Researchers have also reported that all such patients showed severe vasculitis and cellular infiltration on biopsy, and remarkable improvements in these conditions after treatment with DSG.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of deoxyspergualine for antibody-mediated rejection and proteinuria after kidney transplantation

Ishida

Tanabe²

2008

TCRM

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Deoxyspergualin, an immunosuppressant, in patients suffering from nephropathies with crescent formation: an open-label trial to evaluate safety and efficacy

Abstract: Short-term treatment with DSG may be effective and tolerated in patients suffering from nephropathies with crescent formation.

Cited by 11 publications

References 33 publications

HSPA8/HSC70 in Immune Disorders: A Molecular Rheostat that Adjusts Chaperone-Mediated Autophagy Substrates

HSPA8/HSC70 in Immune Disorders: A Molecular Rheostat that Adjusts Chaperone-Mediated Autophagy Substrates

Wegener Granulomatosis (Granulomatosis with Polyangiitis): Evolving Concepts in Treatment

Efficacy of deoxyspergualine for antibody-mediated rejection and proteinuria after kidney transplantation

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