ライフサイエンスコーパス: IgA nephropathy

1 nt glycosylation of IgA1 in diseases such as IgA nephropathy.

2 he drug to the distal ileum in patients with IgA nephropathy.

3 elevated serum IgA seen in liver disease and IgA nephropathy.

4 especially in the treatment of children with IgA nephropathy.

5 sylated IgA1-containing immune aggregates in IgA nephropathy.

6 for poststreptococcal glomerulonephritis or IgA nephropathy.

7 most all of the pathologic features of human IgA nephropathy.

8 enal progression for high-risk patients with IgA nephropathy.

9 and six vascular histopathologic features of IgA nephropathy.

10 iology, diagnosis, and outcomes of recurrent IgA nephropathy.

11 ernative and lectin pathways are involved in IgA nephropathy.

12 the combined deletion of CFHR3 and CFHR1 in IgA nephropathy.

13 odies assigned salient pathogenetic roles in IgA nephropathy.

14 ephrosis, membranous glomerulonephritis, and IgA nephropathy.

15 est a role for miRNAs in the pathogenesis of IgA nephropathy.

16 is common and confers a protective effect in IgA nephropathy.

17 iferative glomerulonephritis and relapses in IgA nephropathy.

18 oviding a potential pharmacologic target for IgA nephropathy.

19 ockade, reduced proteinuria in patients with IgA nephropathy.

20 on in the hinge region of IgA1 characterizes IgA nephropathy.

21 GN could serve as an experimental model for IgA nephropathy.

22 g sporadic FSGS, minimal change disease, and IgA nephropathy.

23 alues 3 x 10(-2) to 5 x 10(-5)) but not with IgA nephropathy.

24 s, monitoring, and therapy for patients with IgA nephropathy.

25 from peripheral blood cells of patients with IgA nephropathy.

26 have implications for renal diseases such as IgA nephropathy.

27 ays an essential role in the pathogenesis of IgA nephropathy.

28 erative glomerulonephritis (23%) followed by IgA nephropathy (19%) and acute tubular injury (19%).

29 tested the efficacy of fish-oil treatment of IgA nephropathy, 2 reported beneficial effects on renal

30 geneous basement membrane abnormalities; one IgA nephropathy, 5 of 16 glomeruli globally sclerotic; o

31 tions for other Tn-related disorders such as IgA nephropathy, a condition that can result in renal fa

32 rried out a genome-wide association study of IgA nephropathy, a major cause of kidney failure worldwi

33 acute poststreptococcal glomerulonephritis, IgA nephropathy, Alport's syndrome, and membranoprolifer

34 activation has a role in the pathogenesis of IgA nephropathy, an autoimmune disease mediated by patho

35 s that have roles in human diseases, such as IgA nephropathy and cancer.

36 igen expression in human diseases, including IgA nephropathy and cancer.

37 Tg mice and kidney biopsies of patients with IgA nephropathy and CKD stages I to V, respectively.

38 istently, kidney biopsies from patients with IgA nephropathy and diabetic nephropathy exhibited subst

39 ate the association of genetic variants with IgA nephropathy and end-stage renal disease (ESRD, n = 1

40 IgA nephropathy and Henoch-Schonlein purpura nephritis a

41 Childhood IgA nephropathy and Henoch-Schonlein purpura nephritis h

42 man IgA1 and its role in the pathogenesis of IgA nephropathy and Henoch-Schonlein purpura nephritis h

43 use of immunosuppressive agents in pediatric IgA nephropathy and Henoch-Schonlein purpura nephritis,

44 IgA1 mesangial deposition is the hallmark of IgA nephropathy and Henoch-Schonlein purpura, the onset

45 diators of acute kidney injury and fibrosis, IgA nephropathy and idiopathic membranous nephropathy, a

46 In summary, lesions of TMA are frequent in IgA nephropathy and may occur in normotensive patients w

47 ibutes to the aberrant IgA1 glycosylation in IgA nephropathy and may represent a new therapeutic targ

48 t morbidity associated with diseases such as IgA nephropathy and membranoproliferative glomerulonephr

49 ion in human pIgR, A580V, is associated with IgA nephropathy and nasopharyngeal carcinoma.

50 complex-mediated GN, except two specimens of IgA nephropathy and one specimen of sclerosing membranop

51 inical intervention studies of patients with IgA nephropathy and other glomerular disorders.

52 least 18 years with biopsy-confirmed primary IgA nephropathy and persistent proteinuria despite optim

53 domized 34 adult patients with biopsy-proven IgA nephropathy and proteinuria >1 g/d, maintained on an

54 an essential role for UG in preventing mouse IgA nephropathy and warrant further studies to determine

55 athies (44 with FSGS, 21 with HIVAN, 32 with IgA nephropathy, and 74 healthy controls).

56 glomerulonephritis, minimal change disease, IgA nephropathy, and diabetic nephropathy validates mult

57 S, membranoproliferative glomerulonephritis, IgA nephropathy, and membranous nephropathy), patients w

58 presenting as nephritis (postinfectious GN, IgA nephropathy, antiglomerular basement membrane and an

59 ents with end-stage kidney disease caused by IgA nephropathy are transplanted every year, and each of

60 n added to supportive care, in patients with IgA nephropathy are uncertain.

61 ined a series of 128 patients diagnosed with IgA nephropathy between 2002 and 2008 who had a mean fol

62 Thrombotic microangiopathy (TMA) occurs in IgA nephropathy, but its clinical significance is not we

63 Hematuria is a cardinal symptom in IgA nephropathy, but its influence on the risk of diseas

64 genetic contribution to the pathogenesis of IgA nephropathy, but results from genetic association st

65 ot prove the efficacy of fish oil therapy in IgA nephropathy, but suggests that an additional placebo

66 in the IgA1 hinge region are associated with IgA nephropathy, but their contribution to its pathogene

67 oadly sensitized and had a high incidence of IgA nephropathy causing end-stage renal disease.

68 entially expressed in PBMCs of patients with IgA nephropathy compared with healthy persons.

69 e supportive care in patients with high-risk IgA nephropathy did not significantly improve the outcom

70 y not requiring electron microscopy included IgA nephropathy, diffuse proliferative lupus nephritis,

71 Patients with IgA nephropathy exhibited lower C1GALT1 expression, whic

72 ns and specimens obtained from patients with IgA nephropathy, focal segmental glomerulosclerosis, min

73 We followed a cohort of 112 patients with IgA nephropathy for a mean+/-SEM period of 14+/-10.2 yea

74 IgA nephropathy frequently leads to progressive CKD.

75 anous glomerulonephritis, diabetes mellitus, IgA nephropathy, Goodpasture's syndrome, and Alport synd

76 IgA nephropathy has an impact on renal health care costs

77 interactions involved in the pathogenesis of IgA nephropathy have revealed the autoimmune nature of t

78 eserving renal function in immunoglobulin A (IgA) nephropathy have yielded conflicting results.

79 ic crescentic glomerulonephritis (RPGN/ICG), IgA nephropathy (IgA), mesangioproliferative glomerulone

80 In IgA nephropathy, IgA1 contains O-glycans that are galact

81 In IgA nephropathy, IgA1 molecules with incompletely galact

82 nsplant rates were highest for patients with IgA nephropathy (IgAN) (referent) and lower for all othe

83 efficacy in other glomerulopathies, such as IgA nephropathy (IgAN) and membranoproliferative glomeru

84 Population-based incidence data for IgA nephropathy (IgAN) are available for some countries

85 s (CICs) isolated from sera of patients with IgA nephropathy (IgAN) consist of undergalactosylated, m

86 ,131 patients with GN studied, patients with IgA nephropathy (IgAN) had the lowest mortality rates an

87 rm follow-up after renal transplantation for IgA nephropathy (IgAN) have suggested an incidence of re

88 IgA nephropathy (IgAN) is a common cause of renal failur

89 IgA nephropathy (IgAN) is a common chronic glomerular di

90 IgA nephropathy (IgAN) is a complex trait determined by

91 IgA nephropathy (IgAN) is characterized by circulating i

92 IgA nephropathy (IgAN) is characterized by mesangial cel

93 The role of immunosuppression in IgA nephropathy (IgAN) is controversial.

94 IgA nephropathy (IgAN) is the most common form of glomer

95 IgA nephropathy (IgAN) is the most common form of primar

96 IgA nephropathy (IgAN) is the most prevalent among prima

97 IgA nephropathy (IgAN) represents the leading cause of k

98 ggest treatment with corticosteroids (CS) in IgA nephropathy (IgAN) when proteinuria is persistently

99 tion have been linked to the pathogenesis of IgA nephropathy (IgAN), a kidney disease characterized b

100 IgA nephropathy (IgAN), characterized by mesangial IgA1

101 tients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membranoproliferative GN (MPGN)

102 In IgA nephropathy (IgAN), serum IgA1 with abnormal O-glyco

103 In IgA nephropathy (IgAN), serum IgA1 with abnormal O-glyco

104 in about 6-8% of the disease heritability of IgA nephropathy (IgAN), suggesting that there are still

105 ed a genome-wide association study (GWAS) of IgA nephropathy (IgAN), the most common form of glomerul

106 The hallmark of IgA nephropathy (IgAN), the most common form of glomerul

107 IgA nephropathy (IgAN), the most common primary glomerul

108 athway has a key role in the pathogenesis of IgA nephropathy (IgAN).

109 1 may contribute to pathogenic mechanisms in IgA nephropathy (IgAN).

110 racellular matrix lead to the progression of IgA nephropathy (IgAN).

111 osylated hinge region O-glycans characterize IgA nephropathy (IgAN).

112 Many of the alleles that protect against IgA nephropathy impart increased risk for other autoimmu

113 rogression of renal disease in patients with IgA nephropathy in a multicenter, placebo-controlled, ra

114 rving renal function in patients with severe IgA nephropathy in a randomized, open-label, parallel-gr

115 d their fragments may serve as biomarkers of IgA nephropathy in serum, urine, or renal tissue.

116 on susceptibility alleles that predispose to IgA nephropathy in the European population.

117 miR-148b function in PBMCs of patients with IgA nephropathy increased C1GALT1 mRNA and protein level

118 ed EBV-immortalized cells from patients with IgA nephropathy indicated a decrease in beta1,3-galactos

119 IgA nephropathy is a chronic kidney disease defined by d

120 proteinuria in diabetes (types 1 and 2) and IgA nephropathy is related to the degree of podocyte dep

121 IgA nephropathy is the most common glomerular disease wo

122 IgA nephropathy is thought to be associated with mucosal

123 We now know that IgA nephropathy leads to progressive renal destruction i

124 re/grade/class for disease entities, such as IgA nephropathy, lupus nephritis, and ANCA GN; and addit

125 ases affecting the glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nephropat

126 r understanding of the role of complement in IgA nephropathy may provide potential targets and ration

127 imab, at least at this stage and severity of IgA nephropathy, may reflect a failure of rituximab to r

128 patients with a single underlying diagnosis: IgA nephropathy (n = 5), diabetes (n = 7), or lupus neph

129 ferative glomerulonephritis type 1 (n = 12), IgA nephropathy (n = 7), and mesangial glomerulonephriti

130 ntains genes that seem to influence familial IgA nephropathy, obesity, BP, insulin resistance, and ty

131 a may have a significant favorable effect on IgA nephropathy outcomes.

132 nal function loss in high-risk patients with IgA nephropathy, particularly those with moderately adva

133 nd IL-5 by peripheral blood lymphocytes from IgA nephropathy patients might result in the production

134 cludes poststreptococcal glomerulonephritis, IgA nephropathy, rapidly progressive glomerulonephritis

135 y, but not in those with lupus membranous or IgA nephropathy, recognized PLA(2)R.

136 other autoimmune or infectious diseases, and IgA nephropathy risk allele frequencies closely parallel

137 derived from patients with sporadic forms of IgA nephropathy (see the related article beginning on pa

138 e-wide analysis in a cohort of patients with IgA nephropathy selected from the UK Glomerulonephritis

139 ive Therapy for the Treatment of Progressive IgA Nephropathy (STOP-IgAN) Trial, 162 patients with IgA

140 ould become the first specific treatment for IgA nephropathy targeting intestinal mucosal immunity up

141 Immunoglobulin A (IgA) nephropathy, the most common form of glomerulonephr

142 molecular mechanism(s) of immunoglobulin A (IgA) nephropathy, the most common primary renal glomerul

143 s involving altered O-glycosylation, such as IgA nephropathy, Tn syndrome, Henoch-Schonlein purpura,

144 splants) with end-stage renal disease due to IgA nephropathy were performed at the University of Cali

145 ed 141 Caucasian patients with biopsy-proven IgA nephropathy who had minor abnormalities at presentat

146 g-term prognosis for Caucasian patients with IgA nephropathy who present with minor urinary abnormali

147 The long-term outcome of patients with IgA nephropathy who present with normal renal function,

148 tcome from a dataset of 148 individuals with IgA nephropathy who underwent renal biopsy at our instit