ライフサイエンスコーパス: glomerulopathy

1 y (or exclusion of it in cases of collapsing glomerulopathy).

2 complex-mediated or complement-mediated (C3 glomerulopathy).

3 change/FSGS, membranous nephropathy, and C3 glomerulopathies).

4 al-change-type lesions to FSGS or collapsing glomerulopathy.

5 ased serum C3 levels in a murine model of C3 glomerulopathy.

6 ther it restores complement regulation in C3 glomerulopathy.

7 s erythematosus (SLE) -associated collapsing glomerulopathy.

8 (C3GN) are widely recognized subtypes of C3 glomerulopathy.

9 n at 81 days and developed chronic xenograft glomerulopathy.

10 walls, albeit at lower intensity than in C3 glomerulopathy.

11 and clinical biopsies that had no transplant glomerulopathy.

12 diabetic kidney disease and is a hallmark of glomerulopathy.

13 effect on renal endothelial dysfunction and glomerulopathy.

14 IV-1 transgenic mouse, a model of collapsing glomerulopathy.

15 ty to experimental doxorubicin hydrochloride glomerulopathy.

16 rocess effacement, proteinuria and FSGS-like glomerulopathy.

17 orts of patients with and without transplant glomerulopathy.

18 indicative of fibrosis/atrophy or transplant glomerulopathy.

19 ntibodies common to patients with transplant glomerulopathy.

20 lant and strongly associated with transplant glomerulopathy.

21 cts graft loss when combined with transplant glomerulopathy.

22 nail-patella syndrome and collagen type III glomerulopathy.

23 F-A/VEGF receptor (VEGFR) system in diabetic glomerulopathy.

24 e development of thrombotic microangiopathic glomerulopathy.

25 reverses the established lesions of diabetic glomerulopathy.

26 is, fibrointimal hyperplasia, and transplant glomerulopathy.

27 rastructure similar to that of immunotactoid glomerulopathy.

28 lipidemia, type II diabetes, proteinuria and glomerulopathy.

29 ix protein accumulation are seen in diabetic glomerulopathy.

30 c markers and the development of sickle cell glomerulopathy.

31 ts; one of them developed de novo collapsing glomerulopathy.

32 lonephritis and 33 to 45 nm in immunotactoid glomerulopathy.

33 ted association of HCV with acute transplant glomerulopathy.

34 ant form of glomerular injury was transplant glomerulopathy.

35 pared with 51 human biopsies with transplant glomerulopathy.

36 There is no effective treatment for C3 glomerulopathy.

37 sement membrane GN, monoclonal Ig GN, and C3 glomerulopathy.

38 and of a special subset of human transplant glomerulopathy.

39 te that this approach should be tested in C3 glomerulopathy.

40 ction with glomerular thrombi and transplant glomerulopathy.

41 ody-mediated rejection, and early transplant glomerulopathy.

42 ld proteinuria at 18-24 wk due to membranous glomerulopathy.

43 ed with more rapid progression to transplant glomerulopathy.

44 GN but is absent or minimally detected in C3 glomerulopathy.

45 odocyte depletion associated with transplant glomerulopathy.

46 glomerulopathies such as FSGS or collapsing glomerulopathy.

47 ameliorate manifestations of early diabetic glomerulopathy.

48 reventing ABMR and development of transplant glomerulopathy.

49 eculizumab patients had almost no transplant glomerulopathy.

50 ed rejection (AMR) and subsequent transplant glomerulopathy.

51 a useful biomarker for the treatment of some glomerulopathies.

52 hat these are general features of collapsing glomerulopathies.

53 hemolytic uremic syndrome (aHUS) and related glomerulopathies.

54 gulated in hyperglycemic and immune-mediated glomerulopathies.

55 ular injury in diabetes and other sclerosing glomerulopathies.

56 ot observed in a variety of non-Alport human glomerulopathies.

57 gial matrix deposition of diabetic and other glomerulopathies.

58 ell (MC) proliferation is a hallmark of many glomerulopathies.

59 d complement-activation disorders, including glomerulopathies.

60 n, the primary treatment of choice for these glomerulopathies.

61 ion, in particular, cancer and proliferative glomerulopathies.

62 , atypical hemolytic uremic syndrome, and C3 glomerulopathies.

63 , subnephrotic proteinuria, and less nodular glomerulopathy (18 versus 100%; P < 0.0001).

64 ight microscopy (transplant arteriopathy and glomerulopathy); (3) widespread C4d deposits in PTC by i

65 Thus, in fH mutation-related C3 glomerulopathy, additional factors that impact the activ

66 gical reasons and one failed from transplant glomerulopathy after 5.8 yr with no histological evidenc

67 nd in 8 of 51 human biopsies with transplant glomerulopathy after rigorous exclusion of immune comple

68 In minimal change disease and membranous glomerulopathy, all mature podocyte markers were retaine

69 recognized to be distinct from immunotactoid glomerulopathy, an entity characterized by glomerular de

70 elp identify patients at risk for collapsing glomerulopathy, an entity with a poor prognosis that is

71 ng the end point was higher in children with glomerulopathies and increased with age, blood pressure,

72 146a(-/-)) showed accelerated development of glomerulopathy and albuminuria upon streptozotocin (STZ)

73 ogic normoglycemia in diabetic patients with glomerulopathy and avoid or delay the onset of diabetic

74 ost half of the surviving grafts do not have glomerulopathy and avoiding antibodies against donor cla

75 ve changes and matrix remodeling (transplant glomerulopathy and capillaropathy); (b) EC procoagulant

76 h histopathologic findings of minimal change glomerulopathy and FSGS, respectively.

77 identifying patients at risk for transplant glomerulopathy and graft loss.

78 er allograft injury with increased allograft glomerulopathy and interstitial fibrosis/tubular atrophy

79 ly valuable model of mesangial proliferative glomerulopathy and its resolution.

80 Coupled with absent transplant glomerulopathy and low rates of progressive IF/TA on ear

81 for miR-146a in protecting against diabetic glomerulopathy and podocyte injury.

82 These abnormalities and the associated glomerulopathy and proteinuria were prevented by adminis

83 n renal allograft recipients with transplant glomerulopathy and seem to be under the regulation of fu

84 the coexistence of idiopathic minimal-change glomerulopathy and SLE.

85 ng atypical hemolytic uremic syndrome and C3 glomerulopathies, and age-related macular degeneration.

86 ypical hemolytic uremic syndrome, C3 and C1q glomerulopathies, and preeclampsia.

87 females with gonadal dysgenesis, progressive glomerulopathy, and a significant risk of gonadoblastoma

88 for antibody-mediated rejection, transplant glomerulopathy, and allograft loss (P<0.0001).

89 ibrosis, tubular atrophy, chronic transplant glomerulopathy, and chronic vascular rejection changes a

90 associations with C4d deposition, transplant glomerulopathy, and graft failure.

91 mmation, were more likely to have transplant glomerulopathy, and had worse graft outcome.

92 expression, decreased albuminuria, decreased glomerulopathy, and inhibition of expression of markers

93 y negative in 24 (80%) of 30 specimens of C3 glomerulopathy, and only trace/1+ C4d staining was detec

94 bined presence of C4d positivity, transplant glomerulopathy, and serum creatinine of >2.3 mg/dl at bi

95 Nonimmune glomerulopathies are an area of significant research.

96 orts the underlying hypothesis that these C3 glomerulopathies are diseases of fluid-phase complement

97 The causes of age-dependent glomerulopathy are multifactorial and include an imbalan

98 lled microcysts with hallmarks of collapsing glomerulopathy, as well as extensive effacement of podoc

99 ared with minimal change disease, membranous glomerulopathy, as well as normal adult and fetal human

100 essive effect in acute phases or relapses of glomerulopathies associated with MC proliferations.

101 ays an important role in the pathogenesis of glomerulopathy associated with type 2 diabetes and could

102 om baseline) or had minimal or no transplant glomerulopathy (Banff cg0-1).

103 sgenesis, whereas her sister has progressive glomerulopathy but a 46,XX karyotype and normal female d

104 es associates with HIV-associated collapsing glomerulopathy, but it is unknown whether these risk all

105 genase levels between those with and without glomerulopathy, but the mean arterial pressure was highe

106 A second subset developed glomerulopathy by an average of 10 years after transplan

107 r DSA by C1q is more specific for transplant glomerulopathy (C1q: 81%, 95% CI 0.57-0.94; IgG: 67%, 95

108 C3 glomerulopathies (C3G) are a group of severe renal disea

109 The complement-mediated renal diseases C3 glomerulopathy (C3G) and atypical hemolytic uremic syndr

110 s alternative pathway complement-mediated C3 glomerulopathy (C3G) and immune complex-mediated membran

111 oclonal gammopathy in adult patients with C3 glomerulopathy (C3G) emphasizes the role of monoclonal i

112 C3 glomerulopathy (C3G) is a severe kidney disease for whic

113 In C3 glomerulopathy (C3G), the alternative pathway of complem

114 reports support the use of eculizumab in C3 glomerulopathy (C3G).

115 antly complement-driven etiology, such as C3 glomerulopathy (C3G).

116 ar degeneration (AMD) and associates with C3 glomerulopathy (C3G).

117 e thrombotic microangiopathies (TMAs) and C3 glomerulopathies (C3Gs) include a spectrum of rare disea

118 Collapsing glomerulopathy can arise in renal allografts as a de nov

119 Patients affected by C3 glomerulopathy can develop neovascular membranes as reti

120 Collapsing glomerulopathy (CG) has become an important cause of end

121 Collapsing glomerulopathy (CG) has become an important cause of ESR

122 Collapsing glomerulopathy (CG) is associated with disorders that ma

123 ), and a trends toward a higher mean chronic glomerulopathy (cg) score (1.65 +/- 0.93 vs 1.11 +/- 0.9

124 Chronic allograft injury (transplant chronic glomerulopathy [cg] or chronic lesion score CLS]) were a

125 Kidneys of Bru mice have peripheral glomerulopathy characterized by hypertrophy and hyperpla

126 C3GN is a subtype of C3 glomerulopathy characterized by predominant C3 deposits

127 nt in apoJ/clusterin developed a progressive glomerulopathy characterized by the deposition of immune

128 D developed a severe mesangial proliferative glomerulopathy, characterized by enlarged glomeruli and

129 progressive renal insufficiency in SSA is a glomerulopathy, clinically detected by the presence of m

130 rom crescents of patients with proliferative glomerulopathies confirmed the translational relevance o

131 cantly higher prevalence of acute transplant glomerulopathy (Ctrl, 6%; R-HCV, 55%, P<.0001; D-HCV 40%

132 ents with proliferative and nonproliferative glomerulopathies, dysregulated CD133(+)CD24(+) progenito

133 nephrotic syndrome in patients with diverse glomerulopathies, even those resistant to steroids.

134 Transplant glomerulopathy-free survival was also inferior in the TR

135 ssociation with alternative pathway-mediated glomerulopathies (GP).

136 contrast, patients who developed transplant glomerulopathy had 10- to 20-fold increased levels of po

137 te antigens type II (DSA II+) and transplant glomerulopathy has been clearly established, its role in

138 rillary glomerulonephritis and immunotactoid glomerulopathy have features that overlap with cryoglobu

139 3-1; C1q: 88%, 95% CI 0.62-0.98), transplant glomerulopathy (IgG: 100%, 95% CI 0.73-1; C1q: 100%, 95%

140 se cytokines were associated with transplant glomerulopathy (IL-1beta, P=0.019; IL-6, P=0.015; and TN

141 At variance, in most patients with C3 glomerulopathies/immune complex-associated membranoproli

142 stent infection may result in development of glomerulopathies in these patients.

143 ion scanning microscopy (HIM) to examine the glomerulopathy in a Col4a3 mutant/Alport syndrome mouse

144 rulonephritis and two cases of immunotactoid glomerulopathy in association with HCV infection.

145 There was no transplant glomerulopathy in biopsies from either group.

146 tical ultrastructural characteristics of the glomerulopathy in Col4a3 mutant mice.

147 ssociated with the development of transplant glomerulopathy in independent validation sets.

148 trastructural characteristics of proteinuric glomerulopathy in mice with CD2-associated protein (CD2A

149 es in 21% (including overlap with collapsing glomerulopathy in one patient).

150 r Myh9 podocyte deletion predisposed mice to glomerulopathy in response to injury by doxorubicin hydr

151 We determined the onset of the glomerulopathy in the embryonic stage.

152 There was more chronic glomerulopathy in the splenectomy-alone and eculizumab-a

153 rked contrast to severe renal impairment and glomerulopathy in the wild-type mice given HFD.

154 tive glomerulonephritis and acute transplant glomerulopathy in transplanted kidneys.

155 deficiency occurs in multiple human primary glomerulopathies including sporadic FSGS, minimal change

156 of mouse develops proteinuria and a distinct glomerulopathy including mesangiolysis but little inters

157 have implicated Nox1, -2, and -4 in several glomerulopathies, including diabetic nephropathy, little

158 n has been implicated in certain unexplained glomerulopathies, including minimal change nephrosis, me

159 Transplant glomerulopathy increased over time after transplantation

160 -4 production, transforming a mild mesangial glomerulopathy into a severe systemic immune complex dis

161 Collapsing glomerulopathy is a devastating renal disease that prima

162 C3 glomerulopathy is a recently described form of CKD.

163 Collapsing glomerulopathy is a recently described form of glomerula

164 In conclusion, ADCK4-related glomerulopathy is an important novel differential diagno

165 C3 glomerulopathy is associated with complement alternative

166 Transplant glomerulopathy is associated with poor prognosis, indepe

167 These findings indicate that obesity-induced glomerulopathy is associated with upregulation of key in

168 egree of anemia, suggesting that sickle cell glomerulopathy is not solely related to hemodynamic adap

169 ted rejection, the significance of C4d in C3 glomerulopathy is undetermined.

170 19, recurrent anemia, and de novo collapsing glomerulopathy leading to allograft failure developed in

171 ted with accelerated development of diabetic glomerulopathy lesions in type 1 diabetic patients.

172 layed increased proteinuria, more transplant glomerulopathy lesions, and lower glomerulitis, but simi

173 cations for podocyte dysfunction in diabetic glomerulopathy, manifesting as GBM thickening and altere

174 Notably, glomerulopathies may account for about 40% of failed kid

175 Eculizumab might benefit C3 glomerulopathies mediated by dysregulation of the altern

176 Membranous glomerulopathy (MG) is one of the most common glomerulon

177 antation, mean arterial pressure, transplant glomerulopathy, microcirculation inflammation, and de no

178 In the human glomerulopathies minimal-change nephrosis and membranous

179 interstitial nephropathies (n = 92 [10.2%]), glomerulopathies (n = 69 [7.7%]), postischemic CKD (n =

180 ), and HIV-negative patients with collapsing glomerulopathy (n = 8) were analyzed in this study.

181 assessed whether similar changes occur with glomerulopathy/nephrotic syndrome, in which high-circula

182 d G2 alleles and to better understand "APOL1 glomerulopathy," no data prove that these APOL1 sequence

183 The collapsing glomerulopathy of HIV-associated nephropathy (HIVAN) is

184 ed in glomerular podocytes in the collapsing glomerulopathy of HIV-associated nephropathy (HIVAN).

185 had higher rates of inflammation and chronic glomerulopathy on both 1- and 5-year biopsies.

186 Morphologic criteria for acute transplant glomerulopathy or proliferative glomerulonephritis were

187 ssociated with the development of transplant glomerulopathy (OR=10.7, 95% CI=3.1-37.1, P<0.01).

188 tients who had no C4d deposition, transplant glomerulopathy, or microcirculation inflammation had a 1

189 ucose and/or fatty acids, in obesity-related glomerulopathy (ORG) and diabetic nephropathy (DN).

190 al glomerulosclerosis coined obesity-related glomerulopathy (ORG).

191 odds of developing SLE-associated collapsing glomerulopathy (P<0.001).

192 ly associated with SLE-associated collapsing glomerulopathy (P<0.001).

193 significantly higher in IF+i and transplant glomerulopathy patients compared with normal histology a

194 ction with reversible, mild microangiopathic glomerulopathy, probably associated with preformed antib

195 C3 glomerulopathy refers to renal disorders characterized b

196 merular structure, resulting in a collapsing glomerulopathy resembling those in human disease, includ

197 C3 glomerulopathy results from deposition of C3 and other c

198 ovo donor-specific antibodies and transplant glomerulopathy showed higher risk of graft loss compared

199 athogenesis of podocyte injury in sclerosing glomerulopathies such as focal segmental glomerulosclero

200 d how podocyte injury evolves to progressive glomerulopathies such as FSGS or collapsing glomerulopat

201 Cyclosporine's efficacy in other glomerulopathies, such as IgA nephropathy (IgAN) and mem

202 cyte injury is the inciting event in primary glomerulopathies, such as minimal change disease and pri

203 0-26 ng/ml (n=2) developed chronic allograft glomerulopathy, suggesting 35 ng/ml as the threshold blo

204 eyond diabetes, studies in other settings of glomerulopathies support a critical RAGE-dependent pathw

205 transplant recipients who develop transplant glomerulopathy (TG) and those who do not.

206 Graft survival and time to transplant glomerulopathy (TG) development were estimated in surviv

207 Transplant glomerulopathy (TG) is a diagnostic criterion for chroni

208 Transplant glomerulopathy (TG) is a histopathologic entity of kidne

209 s and predicts the development of transplant glomerulopathy (TG).

210 ubular capillary inflammation and transplant glomerulopathy (TG).

211 associated with allograft loss in transplant glomerulopathy (TGP) patients.

212 Searching for models of glomerulopathy that display strong gene-environment inte

213 ephropathy is a unique pattern of sclerosing glomerulopathy that ranges in prevalence from 1 to 10% o

214 In contrast to other glomerulopathies, the development of systemic hypertensi

215 ition have been associated with a variety of glomerulopathies, the pathogenic mechanisms by which com

216 normoalbuminuric patients may have advanced glomerulopathy, the selection of slow-track patients bas

217 C4d positivity and transplant glomerulopathy together portended exceptionally poor gra

218 Transplant glomerulopathy (TxGN; cg>/=1) developed in 47% of patien

219 Transplant glomerulopathy (TxGN; cg>/=1) developed in 47% of patien

220 segmental glomerulosclerosis (not collapsing glomerulopathy variant), pauci-immune crescentic glomeru

221 ing and podoprotective effect in proteinuric glomerulopathies via MC1R-independent mechanisms.

222 Transplant glomerulopathy was diagnosed by surveillance and clinica

223 Transplant glomerulopathy was diagnosed in 73 patients (12%) during

224 Transplant glomerulopathy was present in 25.0% of biopsies and resu

225 .7% vs. 88.0%, p < 0.01) and chronic injury (glomerulopathy) was present in 54.5% of surviving grafts

226 on by mesangial cells are characteristics of glomerulopathies, we propose that SPARC is one of the fa

227 ologic mechanisms associated with transplant glomerulopathy, we examined the expression of acidic fib

228 Five cases of de novo collapsing glomerulopathy were identified (0.6% of biopsies; 3.2% s

229 erexpressing mice had a milder proliferative glomerulopathy, whereas the mice overexpressing PDGF-C a

230 Regardless of the histologic pattern, C3 glomerulopathy, which includes dense deposit disease and

231 c patients with proteinuria have established glomerulopathy, which is more advanced in those with nod

232 Ds) in a woman affected by Complement 3 (C3) glomerulopathy, which represents a spectrum of glomerula

233 s with SLE identified 26 cases of collapsing glomerulopathy, which we genotyped for APOL1 risk allele

234 ion, specifically avoidance of patients with glomerulopathies whose recurrence may obscure potential

235 mals for the absence or presence of diabetic glomerulopathy with a high degree of precision.

236 r subtype) in 79% of patients and membranous glomerulopathy with atypical features in 21% (including

237 The renal disorder C3 glomerulopathy with dense deposit disease (C3G-DDD) patt

238 2 (CR2) and FH (CR2-FH) in two models of C3 glomerulopathy with either preexisting or triggered C3 d

239 merular lesions resembling a noninflammatory glomerulopathy with extensive extracapillary proliferati

240 ular disease in five cases, and a membranous glomerulopathy with mesangial proliferative features in

241 grafts exhibited thrombotic microangiopathic glomerulopathy with multiple platelet-fibrin microthromb

242 died before postnatal day 3 (P3) from severe glomerulopathy with podocyte effacement and segmental gl

243 with sickle cell anemia (SCA) may develop a glomerulopathy with proteinuria and progressive renal in