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 glomerular destabilization and transplant glomerulopathy.

5 ody-mediated rejection, and early transplant glomerulopathy.

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

7 ed with more rapid progression to transplant glomerulopathy.

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

9 odocyte depletion associated with transplant glomerulopathy.

10 glomerulopathies such as FSGS or collapsing glomerulopathy.

11 ameliorate manifestations of early diabetic glomerulopathy.

12 reventing ABMR and development of transplant glomerulopathy.

13 eculizumab patients had almost no transplant glomerulopathy.

14 ed rejection (AMR) and subsequent transplant glomerulopathy.

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

16 ther it restores complement regulation in C3 glomerulopathy.

17 s erythematosus (SLE) -associated collapsing glomerulopathy.

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

19 n at 81 days and developed chronic xenograft glomerulopathy.

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

21 and clinical biopsies that had no transplant glomerulopathy.

22 effect on renal endothelial dysfunction and glomerulopathy.

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

24 ty to experimental doxorubicin hydrochloride glomerulopathy.

25 rocess effacement, proteinuria and FSGS-like glomerulopathy.

26 orts of patients with and without transplant glomerulopathy.

27 indicative of fibrosis/atrophy or transplant glomerulopathy.

28 ntibodies common to patients with transplant glomerulopathy.

29 sclerosis with features of healed collapsing glomerulopathy.

30 lant and strongly associated with transplant glomerulopathy.

31 ical hemolytic uremic syndrome (aHUS) and C3 glomerulopathy.

32 cts graft loss when combined with transplant glomerulopathy.

33 nail-patella syndrome and collagen type III glomerulopathy.

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

35 e development of thrombotic microangiopathic glomerulopathy.

36 reverses the established lesions of diabetic glomerulopathy.

37 is, fibrointimal hyperplasia, and transplant glomerulopathy.

38 rastructure similar to that of immunotactoid glomerulopathy.

39 lipidemia, type II diabetes, proteinuria and glomerulopathy.

40 ix protein accumulation are seen in diabetic glomerulopathy.

41 c markers and the development of sickle cell glomerulopathy.

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

43 lonephritis and 33 to 45 nm in immunotactoid glomerulopathy.

44 ted association of HCV with acute transplant glomerulopathy.

45 ant form of glomerular injury was transplant glomerulopathy.

46 occur in patients with IgA nephropathy or C3 glomerulopathy.

47 an intact Factor H gene are described in C3 glomerulopathy.

48 features associated with cases of transplant glomerulopathy.

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

50 diabetic kidney disease and is a hallmark of glomerulopathy.

51 pared with 51 human biopsies with transplant glomerulopathy.

52 There is no effective treatment for C3 glomerulopathy.

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

54 and of a special subset of human transplant glomerulopathy.

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

56 ction with glomerular thrombi and transplant glomerulopathy.

57 , atypical hemolytic uremic syndrome, and C3 glomerulopathies.

58 a useful biomarker for the treatment of some glomerulopathies.

59 hat these are general features of collapsing glomerulopathies.

60 hemolytic uremic syndrome (aHUS) and related glomerulopathies.

61 gulated in hyperglycemic and immune-mediated glomerulopathies.

62 ular injury in diabetes and other sclerosing glomerulopathies.

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

64 gial matrix deposition of diabetic and other glomerulopathies.

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

66 substantial albumin leakage, as observed in glomerulopathies.

67 entify new potential therapeutic targets for glomerulopathies.

68 lay an important role in the pathogenesis of glomerulopathies.

69 to cure or delay FSGS and potentially other glomerulopathies.

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

71 d complement-activation disorders, including glomerulopathies.

72 ion, in particular, cancer and proliferative glomerulopathies.

73 ge disease, 2 were diagnosed with membranous glomerulopathy, 1 was diagnosed with crescentic transfor

74 ney biopsy, 5 were diagnosed with collapsing glomerulopathy, 1 was diagnosed with minimal change dise

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

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

77 r versus children with hypocomplementemic C3 glomerulopathy (31 of 34 [91%] versus 4 of 28 [14%], res

78 Transplant glomerulopathy, a common glomerular lesion observed afte

79 It shares clinicopathologic features with C3 glomerulopathy, a complement-mediated glomerulopathy tha

80 patients, biopsies have revealed collapsing glomerulopathy, a distinct form of glomerular injury tha

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

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

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

84 EGFR kinase activity, males had progressive glomerulopathy, albuminuria, loss of podocytes, and tubu

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

86 Many adult-onset glomerulopathies also feature alterations in Nephrin exp

87 y is fundamental to the manifestations of C3 glomerulopathy, although terminal pathway dysregulation

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

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

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

91 146a(-/-)) showed accelerated development of glomerulopathy and albuminuria upon streptozotocin (STZ)

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

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

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

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

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

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

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

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

100 from the National French Registry who had C3 glomerulopathy and persistent hypocomplementemia.

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

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

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

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

105 Genotyping of three patients with collapsing glomerulopathy and the patient with minimal change disea

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

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

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

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

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

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

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

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

114 lar basement membrane glomerulonephritis, C3 glomerulopathy, and monoclonal immunoglobulin-associated

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

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

117 plement gene mutations can cause familial C3 glomerulopathy, and studies have reported rare variants

118 diagnosed chronic glomerulopathy, such as C3 glomerulopathy, and to help determine therapy.

119 stologic parameters revealed five transplant glomerulopathy archetypes characterized by distinct func

120 The C3 glomerulopathies are a group of rare kidney diseases cha

121 Nonimmune glomerulopathies are an area of significant research.

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

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

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

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

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

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

128 and 24% (4/13) of cases developed transplant glomerulopathy (Banff cg score > 0).

129 who presented with a diagnosis of transplant glomerulopathy (Banff cg score >=1 by light microscopy),

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

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

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

133 x have less inflammation and less transplant glomerulopathy, but most chronic histologic changes were

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

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

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

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

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

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

140 C3 glomerulopathy (C3G) and immune-complex membranoprolifer

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

142 C3 glomerulopathy (C3G) is a heterogeneous group of chronic

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

144 C3 glomerulopathy (C3G) is characterized by the alternative

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

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

147 damage is a key mechanism of pathology in C3 glomerulopathy (C3G).

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

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

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

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

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

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

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

155 Collagenofibrotic glomerulopathy (CG) is a rare disease characterized by t

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

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

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

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

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

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

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

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

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

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

166 The two major subgroups of C3 glomerulopathy - dense deposit disease (DDD) and C3 glom

167 ent of other renal complications (such as C3 glomerulopathy) despite sustained dysregulation of C3.

168 he median time from transplant to transplant glomerulopathy diagnosis was 33.18 months.

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

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

171 tis, rituximab, diabetes, v score, allograft glomerulopathy, fibrous intimal thickening, tubular atro

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

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

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

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

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

177 3-1; C1q: 88%, 95% CI 0.62-0.98), transplant glomerulopathy (IgG: 100%, 95% CI 0.73-1; C1q: 100%, 95%

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

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

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

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

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

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

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

185 tient reports have also described collapsing glomerulopathy in COVID-19.

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

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

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

189 Reports of collapsing glomerulopathy in patients of African ancestry and high-

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

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

192 APOL1 high-risk patient developed collapsing glomerulopathy in the engrafted kidney, which was transp

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

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

195 tive glomerulonephritis and acute transplant glomerulopathy in transplanted kidneys.

196 samples (from 385 patients) with transplant glomerulopathy (incidence of 6.7%).

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

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

199 as significantly upregulated in common human glomerulopathies, including diabetic nephropathy, IgA ne

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

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

202 Transplant glomerulopathy increased over time after transplantation

203 -4 production, transforming a mild mesangial glomerulopathy into a severe systemic immune complex dis

204 Collapsing glomerulopathy is a devastating renal disease that prima

205 C3 glomerulopathy is a recently described form of CKD.

206 Collapsing glomerulopathy is a recently described form of glomerula

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

208 C3 glomerulopathy is associated with complement alternative

209 Transplant glomerulopathy is associated with poor prognosis, indepe

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

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

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

213 roliferative GN, including complement 3 (C3) glomerulopathy, is a rare, untreatable kidney disease ch

214 n ( COL4A3, COL4A4 , and COL4A5 ) leading to glomerulopathy, kidney failure, hearing loss, and eye ab

215 19, recurrent anemia, and de novo collapsing glomerulopathy leading to allograft failure developed in

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

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

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

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

220 he regenerative nature of hantavirus-induced glomerulopathy may generate new therapeutic approaches f

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

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

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

224 In the human glomerulopathies minimal-change nephrosis and membranous

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

226 positive SARS-CoV-2 PCR revealed collapsing glomerulopathy (n = 1), acute tubular injury (n = 1), an

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

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

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

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

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

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

233 Morphologic criteria for acute transplant glomerulopathy or proliferative glomerulonephritis were

234 osits are minimal in patients with either C3 glomerulopathy or thrombotic microangiopathy).

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

236 ssociated AKI with podocytopathy, collapsing glomerulopathy, or both.

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

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

239 iabetic nephropathy (DN) and obesity-related glomerulopathy (ORG), while the frequencies of minimal c

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

241 in atypical hemolytic uremic syndrome and C3 glomerulopathy, over the past decade, a rapidly accumula

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

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

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

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

246 C3 glomerulopathy refers to renal disorders characterized b

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

248 C3 glomerulopathy results from deposition of C3 and other c

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

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

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

252 receptors is preferentially associated with glomerulopathies such as minimal change disease and FSGS

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

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

255 kidney biopsy to avoid misdiagnosed chronic glomerulopathy, such as C3 glomerulopathy, and to help d

256 0-26 ng/ml (n=2) developed chronic allograft glomerulopathy, suggesting 35 ng/ml as the threshold blo

257 Upregulation of Gprc5b in human glomerulopathies suggests that it may play a role in the

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

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

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

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

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

263 Transplant glomerulopathy (TG) is a major cause of late allograft l

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

265 ubular capillary inflammation and transplant glomerulopathy (TG).

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

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

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

269 ith C3 glomerulopathy, a complement-mediated glomerulopathy that, unlike acute postinfectious GN, has

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

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

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

273 C4d positivity and transplant glomerulopathy together portended exceptionally poor gra

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

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

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

277 Transplant glomerulopathy was diagnosed by surveillance and clinica

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

279 model of the alternative pathway disease C3 glomerulopathy was established to evaluate the potential

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

281 .7% vs. 88.0%, p < 0.01) and chronic injury (glomerulopathy) was present in 54.5% of surviving grafts

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

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

284 (aged 18-60 years) with biopsy-confirmed C3 glomerulopathy were enrolled from 35 hospitals or medica

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

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

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

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

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

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

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

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

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

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

295 2 (CR2) and FH (CR2-FH) in two models of C3 glomerulopathy with either preexisting or triggered C3 d

296 merular lesions resembling a noninflammatory glomerulopathy with extensive extracapillary proliferati

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

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

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

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