ライフサイエンスコーパス: FSGS

1 FSGS as a cause of pediatric end-stage renal disease lea

2 FSGS associated with two APOL1 risk alleles associated w

3 FSGS is a CKD with heavy proteinuria that eventually pro

4 FSGS is a clinical disorder characterized by focal scarr

5 FSGS is a clinicopathologic entity characterized by neph

6 FSGS is a common glomerular disorder that has a high pro

7 FSGS is characterized by podocyte injury and depletion a

8 FSGS is characterized by segmental scarring of the glome

9 FSGS is characterized by the presence of partial scleros

10 FSGS is the most common primary glomerular disease under

11 FSGS recurrence is highest in young, white children, whe

12 FSGS results from podocyte injury, yet the mechanistic d

13 FSGS, the most common primary glomerular disorder causin

14 variants in the APOL1 gene on chromosome 22 {FSGS odds ratio = 10.5 [95% confidence interval (CI) 6.0

15 In addition, FSGS-linked ACTN4 mutants not only mislocalized to the c

16 isease, motivating our search for additional FSGS genes.

17 In contrast, an FSGS-linked ACTN4 mutant, K255E, which has increased act

18 to a murine embryonic stem cell line with an FSGS-susceptible genetic background that allows shRNA-me

19 second cohort of patients with DN (n=19) and FSGS (n=21).

20 as the pathological uPAR is circulating and FSGS can recur even after a damaged kidney is replaced w

21 veness, presence of a genetic diagnosis, and FSGS or diffuse mesangial sclerosis on initial biopsy as

22 erulosclerosis (FSGS), a kidney disease, and FSGS+Charcot-Marie-Tooth neuropathy.

23 lasia of the patellae, nails, and elbows and FSGS with specific ultrastructural lesions of the glomer

24 indings of minimal change glomerulopathy and FSGS, respectively.

25 with HIV-associated nephropathy (HIVAN) and FSGS.

26 ogenesis of NFAT-induced podocyte injury and FSGS.

27 meruli with mesangial expansion, injury, and FSGS at study end.

28 ing of the glomerular basement membrane, and FSGS-like lesions.

29 subgroups (children, adults, MCD/MesGN, and FSGS; P<0.01).

30 sociated with HIV-associated nephropathy and FSGS in African Americans.

31 diseases, such as membranous nephropathy and FSGS, persistent injury often leads to irreversible stru

32 ing foot process effacement, proteinuria and FSGS-like glomerulopathy.

33 mice also caused progressive proteinuria and FSGS.

34 cess architecture results in proteinuria and FSGS.

35 lytical ultracentrifugation of wild-type and FSGS mutant ABDs (Lys255Glu, Ser262Pro, and Thr259Ile) a

36 lves to progressive glomerulopathies such as FSGS or collapsing glomerulopathy.

37 t diseases affecting the glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nep

38 for glomerular disease, and APOL1-associated FSGS occurs earlier and progresses to ESRD more rapidly.

39 echanisms underlying ACTN4 mutant-associated FSGS are not completely understood.

40 GS: 70 patients from the North America-based FSGS clinical trial (CT) and 94 patients from PodoNet, t

41 Our data provide the first link between FSGS-linked ACTN4 mutants and transcriptional activation

42 Unexpectedly, in both FSGS and HIVAN but not normal kidneys, the media of medi

43 In both FSGS patients and PAN-treated rats, miR-30s were downreg

44 rovides a tool to rapidly evaluate candidate FSGS-associated genes.

45 Nine candidate FSGS susceptibility genes were identified in our patient

46 The same TRPC6 mutants can cause FSGS, but whether this involves an NFAT-dependent mechan

47 ions in this podocyte-expressed formin cause FSGS emphasizes the importance of fine regulation of act

48 suPAR as a circulating factor that may cause FSGS.

49 Identification of genes causing FSGS has improved our understanding of disease mechanism

50 GN), and nephrotic syndrome (minimal change/FSGS, membranous nephropathy, and C3 glomerulopathies).

51 5D, de novo) in a sporadic case of childhood FSGS using next generation sequencing.

52 on profiles of patients with primary classic FSGS, collapsing FSGS (COLL), minimal change disease (MC

53 pathy (HIVAN) is characterized by collapsing FSGS.

54 tients with primary classic FSGS, collapsing FSGS (COLL), minimal change disease (MCD), and normal co

55 H-ESKD; OR 5.7; P = 9 x 10(-27) for combined FSGS and HIVAN, recessive.

56 Consequently, FSGS-linked ACTN4 mutants failed to potentiate transcrip

57 g revealed two distinct clusters delineating FSGS and COLL from Normal and MCD.

58 with DAF-sufficient T cells did not develop FSGS.

59 econstituted with Daf(-/-) T cells developed FSGS.

60 ew cases aged 35 (15-66) years who developed FSGS recurrence at 12 (1.5-27) days posttransplantation.

61 an estimated 4% lifetime risk for developing FSGS, and untreated HIV-infected individuals have a 50%

62 rom patients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membranoproliferative GN (

63 Compared with control glomeruli, DN, FSGS, IgAN, and MPGN glomeruli exhibited differential ex

64 Compared with control proximal tubules, DN, FSGS, IgAN, and MPGN proximal tubules had differential e

65 ree of five patients with autosomal dominant FSGS but without either extrarenal features or ultrastru

66 he cause of nonsyndromic, autosomal dominant FSGS in two Northern European kindreds from the United S

67 we identified a locus for autosomal-dominant FSGS susceptibility on a region of chromosome 14q.

68 in members of an index family with dominant FSGS revealed a nonconservative, disease-segregating var

69 ections and in biopsies demonstrating either FSGS (n = 8) or HIVAN (n = 2).

70 ng the proposal that genetic factors enhance FSGS susceptibility.

71 We then induced experimental FSGS, typified by abrupt podocyte depletion, with a cyto

72 Sequencing in probands of a familial FSGS cohort revealed seven rare and private heterozygous

73 e data support a new gene locus for familial FSGS on chromosome 2p15.

74 hannel 6 (TRPC6) were identified in familial FSGS, and increased expression of wild-type TRPC6 in glo

75 Studies of familial FSGS have been instrumental in identifying podocytes as

76 formin 2 INF2 are a common cause of familial FSGS.

77 ein alpha-actinin-4, are a cause of familial FSGS.

78 -exome sequencing in a kindred with familial FSGS, we identified a missense mutation R431C in anillin

79 2 gene (INF2) in the mutational hotspot for FSGS.

80 ecent histologic classification proposed for FSGS has provided additional insights into the prognosis

81 x 10(-10) and 3 x 10(-22), respectively, for FSGS, HIVAN and H-ESKD; OR 5.7; P = 9 x 10(-27) for comb

82 ults indicate that patients at high risk for FSGS recurrence can be identified and may benefit from c

83 d G2) explain much of the increased risk for FSGS, HIV-associated nephropathy, and hypertension-attri

84 rend analysis of kidney transplantations for FSGS in children (n=2157) showed an increase in cases of

85 who had focal segmental glomerulosclerosis (FSGS) (four with recurrent FSGS after transplantation an

86 ericans, focal segmental glomerulosclerosis (FSGS) and hypertension-attributed end-stage kidney disea

87 CD), focal and segmental glomerulosclerosis (FSGS) and membranous nephropathy.

88 ation of focal segmental glomerulosclerosis (FSGS) and proteinuria in a cohort of 10 bodybuilders (si

89 disease focal segmental glomerulosclerosis (FSGS) and the neurological disorder Charcot-Marie Tooth

90 26) for focal segmental glomerulosclerosis (FSGS) and twenty-nine-fold higher odds (95% CI 13 to 68)

91 forms of focal segmental glomerulosclerosis (FSGS) have been linked to gain-of-function mutations in

92 Focal segmental glomerulosclerosis (FSGS) is a cause of proteinuric kidney disease, compromi

93 Focal segmental glomerulosclerosis (FSGS) is a common form of idiopathic nephrotic syndrome

94 Focal segmental glomerulosclerosis (FSGS) is a leading cause of nephrotic syndrome and end-s

95 Focal segmental glomerulosclerosis (FSGS) is a pattern of kidney injury observed either as a

96 Focal segmental glomerulosclerosis (FSGS) is a relatively prevalent glomerular disorder that

97 Focal segmental glomerulosclerosis (FSGS) is a syndrome that involves kidney podocyte dysfun

98 ation of focal segmental glomerulosclerosis (FSGS) lesions.

99 Primary focal segmental glomerulosclerosis (FSGS) often causes nephrotic proteinuria and frequently

100 els, and focal segmental glomerulosclerosis (FSGS) patients, whose TNF levels resembled those of heal

101 nts with focal segmental glomerulosclerosis (FSGS) recurrence.

102 Focal segmental glomerulosclerosis (FSGS) recurs after kidney transplantation in more than 3

103 inked to focal segmental glomerulosclerosis (FSGS), a chronic kidney disease characterized by protein

104 forms of focal segmental glomerulosclerosis (FSGS), a kidney disease characterized by proteinuria due

105 ns cause focal segmental glomerulosclerosis (FSGS), a kidney disease, and FSGS+Charcot-Marie-Tooth ne

106 of human focal segmental glomerulosclerosis (FSGS), evidence supporting mechanisms involving loss-of-

107 iopathic focal segmental glomerulosclerosis (FSGS), HIV-1-associated nephropathy (HIVAN), and hyperte

108 iopathic focal segmental glomerulosclerosis (FSGS), HIV-associated nephropathy (HIVAN) and end-stage

109 iseases, focal segmental glomerulosclerosis (FSGS), HIV-associated nephropathy (HIVAN), and hypertens

110 primary focal segmental glomerulosclerosis (FSGS), proteinuria and renal dysfunction recur after kid

111 Focal segmental glomerulosclerosis (FSGS), the second leading cause of end stage renal disea

112 n called focal segmental glomerulosclerosis (FSGS).

113 cases of focal segmental glomerulosclerosis (FSGS).

114 dominant focal segmental glomerulosclerosis (FSGS).

115 e called focal segmental glomerulosclerosis (FSGS).

116 thic focal and segmental glomerulosclerosis (FSGS).

117 lt onset focal segmental glomerulosclerosis (FSGS).

118 such as focal segmental glomerulosclerosis (FSGS).

119 t in focal and segmental glomerulosclerosis (FSGS).

120 y-proven focal segmental glomerulosclerosis (FSGS).

121 familial focal segmental glomerulosclerosis (FSGS).

122 induced) focal segmental glomerulosclerosis (FSGS).

123 nts with focal segmental glomerulosclerosis (FSGS).

124 tly with focal segmental glomerulosclerosis (FSGS).

125 llele, 40% had immune-complex GN and 12% had FSGS.

126 N as the predominant lesion and only 23% had FSGS.

127 se patients, 67% were pediatric, and 44% had FSGS on biopsy.

128 o APOL1 risk alleles, the majority (76%) had FSGS and 10% had hypertensive nephrosclerosis.

129 ction as an additional concept of hereditary FSGS and provides molecular insights into the mechanism

130 ere, we present six kindreds with hereditary FSGS that did not associate with mutations in known caus

131 tions were found in families with hereditary FSGS, and TRPC5 and TRPC6 channels are now known as the

132 statistics of 0.80, 0.73 and 0.65 for HIVAN, FSGS and H-ESKD, respectively, allowing prediction of ge

133 We then characterized 19 human FSGS-related TRPC6 mutations, the majority of which caus

134 ith Adriamycin nephropathy, a model of human FSGS, blocking endogenous retinoic acid synthesis increa

135 C3 deposits frequently accompany idiopathic FSGS and secondary glomerulosclerosis, but it is unknown

136 cans, with odds ratios of 10.5 in idiopathic FSGS and 7.3 in hypertension-attributed ESRD.

137 ith the largest increases in children and in FSGS subgroups.

138 glomeruli, fewer cells stained for APOL1 in FSGS and HIVAN glomeruli, even when expression of the po

139 r losartan (angiotensin-receptor blocker) in FSGS mice stimulated the proliferation of CoRL, increasi

140 erular injury and structural degeneration in FSGS.

141 that in the context of podocyte depletion in FSGS, RAAS inhibition augments CoRL proliferation and pl

142 PEC markers were detected in FSGS lesions from the earliest stages of disease.

143 docytes is an important pathogenic factor in FSGS and that the mechanism involves disruption of the a

144 suPAR) as a circulating factor implicated in FSGS.

145 Moreover, RAAS inhibition in FSGS mice increased RFP(+)CoRL transdifferentiation in t

146 pportunities for therapeutic intervention in FSGS.

147 idly progressive GN and sclerotic lesions in FSGS.

148 ous nephropathy to the role of a microRNA in FSGS.

149 minant effects exerted by ACTN4 mutations in FSGS.

150 ck-1 (sdk-1) is up-regulated in podocytes in FSGS both in rodent models and in human kidney biopsy sa

151 d increases in suPAR concentration result in FSGS-like glomerular lesions and proteinuria.

152 In conclusion, B7-1 blockade did not induce FSGS remission after transplant in our study.

153 tal transgenic ablation of podocytes induces FSGS but the effect of specific ablation of PECs is unkn

154 tified that, when mutated, lead to inherited FSGS and/or the related nephrotic syndrome.

155 ive nephropathy provided novel insights into FSGS pathogenesis in the absence of a primary podocyte a

156 r whether they should be considered isolated FSGS or simply a misdiagnosed type of the Alport spectru

157 summary, these results suggest that isolated FSGS could result from mutations in genes that are also

158 roximal tubular epithelia in normal kidneys, FSGS, and HIVAN.

159 in the pathogenesis of mutant TRPC6-mediated FSGS and that suppression of NFAT activity may contribut

160 Whether TRPC5 activity mediates FSGS onset and progression is unknown.

161 We modeled FSGS by passively transferring mouse podocyte-specific s

162 high salt; severe albuminuria, nephrinuria, FSGS, and podocyte foot effacement in Ang II-induced hyp

163 podocyte homeostasis and causes nonsyndromic FSGS.

164 rying two APOL1 risk alleles explains 18% of FSGS and 35% of HIVAN; alternatively, eliminating this e

165 Class comparison analysis of FSGS + COLL combined versus Normal + MCD revealed 316 si

166 ility of both sporadic and familial cases of FSGS and provides a tool to rapidly evaluate candidate F

167 inary suPAR appears to be higher in cases of FSGS destined for recurrence and merits further evaluati

168 ion (R458Q) in WT1 isoform D as the cause of FSGS in this family.

169 actin binding cell cycle gene, as a cause of FSGS.

170 hts into the molecular and genetic causes of FSGS have enhanced our understanding of disease pathogen

171 Histologically, features characteristic of FSGS, including mesangial sclerosis, podocyte foot proce

172 these findings, which are characteristic of FSGS, were substantially reduced by depleting CD4+ T cel

173 n that may play a role in the development of FSGS.

174 n lead to cellular injury and development of FSGS.

175 plant recipients with a primary diagnosis of FSGS in children 1 to 20 years of age.

176 Although 5.0% carried some diagnosis of FSGS, only 1.9% (n=30) met strict diagnostic criteria fo

177 d robust albuminuria, structural features of FSGS, and reduced numbers of glomerular podocytes.

178 histological and ultrastructural features of FSGS, marked albuminuria, periglomerular monocytic and T

179 Inherited forms of FSGS are caused by Rac1-activating mutations, and Rac1 i

180 Hereditary forms of FSGS have been linked to mutations in the transient rece

181 Although idiopathic forms of FSGS predominate, recent insights into the molecular and

182 that are also involved in syndromic forms of FSGS.

183 retinoic acid and promotes the generation of FSGS lesions.

184 Progressive sclerosis is a hallmark of FSGS, and genetic tracing studies have shown that pariet

185 raction of patients with a family history of FSGS.

186 hree biopsies revealed collapsing lesions of FSGS, four had perihilar lesions, and seven showed > or

187 her genetics plays a role in the majority of FSGS cases that are identified as primary or sporadic FS

188 ent is the first pathologic manifestation of FSGS after transplantation.

189 rther insight into the disease mechanisms of FSGS.

190 what we believe to be a novel mouse model of FSGS attributable to DAF-deficient T cell immune respons

191 emic insults, a humanized xenograft model of FSGS resulted in an expansion of Gr-1(lo) cells in the B

192 d podocyte loss in a transgenic rat model of FSGS.

193 , per se, contributes to the pathogenesis of FSGS in humans remains controversial.

194 ort the role of suPAR in the pathogenesis of FSGS.

195 evelopmental programs in the pathogenesis of FSGS.

196 The pathophysiology of FSGS is unknown, but podocytes seem to be the target of

197 Progression of FSGS is associated with TGF-beta activation in podocytes

198 nderlies an increased risk for recurrence of FSGS after transplantation.

199 Early recurrence of FSGS was defined as development of nephrotic range prote

200 ct the development of clinical recurrence of FSGS.

201 b was required for 4 patients as a result of FSGS relapse, with good results.

202 At advanced stages of FSGS, fawn-hooded hypertensive rat kidneys exhibited dis

203 or cell-specific therapy in the treatment of FSGS and other proteinuric kidney diseases.

204 served with light microscopy were typical of FSGS and were morphologically heterogeneous, similar to

205 ations in PAX2 may contribute to adult-onset FSGS in the absence of overt extrarenal manifestations.

206 ldren and 20 adults with MCD/MesGN (n=22) or FSGS who had suffered >/=2 recurrences over the previous

207 Specifically, compared with control or FSGS glomeruli, IgAN glomeruli exhibited downregulated e

208 results of resequencing MYH9 in 40 HIVAN or FSGS cases and controls revealed non-synonymous changes

209 MCD), mesangial proliferative GN (MesGN), or FSGS may be poor and with major treatment toxicity.

210 Overexpression of wild-type or FSGS-inducing mutant TRPC6 in synaptopodin-depleted podo

211 Moreover, posttransplantation FSGS recurrence is a major problem, and there is concern

212 study of 25 adults with posttransplantation FSGS.

213 of TRPC6 in GqQ>L-expressing mice prevented FSGS development and inhibited both tubular damage and p

214 Primary FSGS was once considered an entity nonresponsive to pred

215 n between minimal change disease and primary FSGS and may serve to guide clinical decision making.

216 , such as minimal change disease and primary FSGS, and glucocorticoids remain the initial and often,

217 he biopsies of patients diagnosed as primary FSGS.

218 rix); 38 had been diagnosed as early primary FSGS and 57 as minimal change disease.

219 ) met strict diagnostic criteria for primary FSGS including biopsy-proven FSGS, lack of secondary fac

220 In human primary FSGS, we noted reduced glomerular expression of YAP.

221 to be uniquely elevated in cases of primary FSGS, with higher levels noted in cases that recurred af

222 been implicated in familial forms of primary FSGS.

223 ients with minimal change disease or primary FSGS.

224 patients with histologically proven primary FSGS (n = 2) or recurrent FSGS after transplantation (n

225 ildren and adults with biopsy-proven primary FSGS: 70 patients from the North America-based FSGS clin

226 athology in animal models similar to primary FSGS, and one recent study demonstrated elevated levels

227 Causes of native kidney disease were primary FSGS, diabetic nephropathy, membranous nephropathy, immu

228 on in African-American subjects with primary FSGS and may also be present in individuals who do not s

229 rvival was lower for recipients with primary FSGS compared with all others and inferior graft surviva

230 ial portion of nephrotic adults with primary FSGS do respond to treatment with a significantly improv

231 S after transplantation and one with primary FSGS) and proteinuria with B7-1 immunostaining of podocy

232 vated in two-thirds of subjects with primary FSGS, but not in people with other glomerular diseases.

233 therapeutic approach in adults with primary FSGS.

234 Over the last 20 years, primary FSGS has emerged as one of the leading causes of idiopat

235 ria for primary FSGS including biopsy-proven FSGS, lack of secondary factors, negative family history

236 Recurrent FSGS cases had substantially higher proteinuria compared

237 in the pathogenesis of native and recurrent FSGS.

238 FSGS that will ultimately develop recurrent FSGS.

239 Of these, 47% had recurrent FSGS compared with 8% of those not meeting strict criter

240 s associated with stabilization of recurrent FSGS and a temporary lowering of plasma suPAR as well as

241 cyte injury in the pathogenesis of recurrent FSGS and further supports the presence of circulating fa

242 proteinuria in the small cohort of recurrent FSGS cases.

243 ine suPAR was elevated in cases of recurrent FSGS compared with all other causes of end-stage renal d

244 lly proven primary FSGS (n = 2) or recurrent FSGS after transplantation (n = 10).

245 graft survival was attributable to recurrent FSGS.

246 cacy of abatacept in patients with recurrent FSGS after renal transplantation, we investigated B7-1 e

247 ctively treated nine patients with recurrent FSGS after transplant using either abatacept or belatace

248 Indeed, in four patients with recurrent FSGS after transplant, treatment with the B7-1 blocker a

249 omerulosclerosis (FSGS) (four with recurrent FSGS after transplantation and one with primary FSGS) an

250 ey transplantation recipients with recurrent FSGS, rituximab therapy may be a recommended treatment f

251 tively, eliminating this effect would reduce FSGS and HIVAN by 67%.

252 ated factors, compared with IgAN (referent), FSGS, membranous nephropathy, membranoproliferative GN,

253 may mediate the development of INF2-related FSGS.

254 d glomerulosclerosis postnatally, resembling FSGS.

255 Renal biopsy revealed FSGS in nine patients, four of whom also had glomerulome

256 Focal segmental glomerular sclerosis (FSGS) is a primary kidney disease that is commonly assoc

257 ndothelial transcription factor in secondary FSGS.

258 We hypothesize that secondary FSGS results from a combination of postadaptive glomerul

259 lly progressive heavy proteinuria and severe FSGS.

260 Renal biopsy specimens uniformly showed FSGS.

261 primary glomerulopathies including sporadic FSGS, minimal change disease, and IgA nephropathy.

262 s that are identified as primary or sporadic FSGS and have no known cause.

263 ferential diagnosis in adolescents with SRNS/FSGS and/or CKD of unknown origin.

264 The FSGS Clinical Trial involved 138 children and young adul

265 ional studies documented that several of the FSGS-associated PAX2 mutations perturb protein function

266 these genes in all diagnostic approaches to FSGS that involve next-generation sequencing.

267 One patient suffered allograft loss due to FSGS recurrence.

268 anging from a minimal-change-type lesions to FSGS or collapsing glomerulopathy.

269 polipoprotein L1 (APOL1) have been linked to FSGS in African Americans with HIV or hypertension, supp

270 tic variants in APOL1 with susceptibility to FSGS and HIVAN among African Americans.

271 sease, elevated serum suPAR is not unique to FSGS cases.

272 at endothelial-derived signaling can trigger FSGS and illustrate the potential importance of the EPAS

273 Additionally, two FSGS-associated alpha-actinin-4 mutations (R310Q and Q34

274 xicity, inflammation, and infection underlie FSGS; however, highly penetrant disease genes have been

275 We therefore examined whether FSGS-associated mutations in TRPC6 result in activation

276 mericans with various nephropathies (44 with FSGS, 21 with HIVAN, 32 with IgA nephropathy, and 74 hea

277 evated in sera from children and adults with FSGS compared with levels in healthy persons or those wi

278 All six variants associated with FSGS and HIVAN (additive ORs, 1.8 to 3.0; P values 3 x 1

279 n of alpha-actinin-4 (K255E) associated with FSGS failed to support actin assembly and acted as a dom

280 ular filtration barrier were associated with FSGS in endothelial Epas1-deficient mice only.

281 ed for virtually all of the association with FSGS and HIVAN on chromosome 22q13 (haplotype P value =

282 th minimal change disease from children with FSGS and correlated with poor clinical outcome.

283 We screened 250 additional families with FSGS and found another variant, G618C, that segregates w

284 reened 73 additional unrelated families with FSGS and found mutations involving the same amino acid (

285 L) in the TTC21B gene in seven families with FSGS.

286 regates with disease in a second family with FSGS.

287 was associated with disease in a family with FSGS.

288 idney biopsy specimens from individuals with FSGS and kidney samples from a murine model of HIV-1-ass

289 hically and ethnically diverse patients with FSGS and do not reflect a nonspecific proinflammatory mi

290 ephronophthisis was present in patients with FSGS and the p.P209L mutation.

291 Biopsies from patients with FSGS exhibited increased mitochondrial DNA damage, consi

292 encing of the ARHGAP24 gene in patients with FSGS identified a mutation that impaired its Rac1-GAP ac

293 elevated in 84.3% and 55.3% of patients with FSGS patients in the CT and PodoNet cohorts, respectivel

294 es, and treatment responses of patients with FSGS were determined among 1573 KTx recipients.

295 were detectable in a subset of patients with FSGS; C3 was present as an activation fragment and coloc

296 dy using 79 MYH9 SNPs in AA populations with FSGS, HIVAN and H-ESKD (typed for a subset of 46 SNPs),

297 in renal transplantation of recipients with FSGS that will ultimately develop recurrent FSGS.

298 0% of kidney transplant (KT) recipients with FSGS will experience recurrence characterized by protein

299 us inhibitory domain of INF2, segregate with FSGS in 11 unrelated families and alter highly conserved

300 ients with proteinuria, including those with FSGS and type 2 diabetic nephropathy (DN).