戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
1                                              FSGS as a cause of pediatric end-stage renal disease lea
2                                              FSGS caused by mutations in INF2 is characterized by a p
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 common glomerular disorder that has a high pro
6                                              FSGS is characterized by podocyte injury and depletion a
7                                              FSGS is characterized by segmental scarring of the glome
8                                              FSGS is characterized by the presence of partial scleros
9                                              FSGS is the most common primary glomerular disease under
10                                              FSGS recurrence is highest in young, white children, whe
11                                              FSGS results from podocyte injury, yet the mechanistic d
12                                              FSGS, the most common primary glomerular disorder causin
13                                 In addition, FSGS-linked ACTN4 mutants not only mislocalized to the c
14                              In contrast, an FSGS-linked ACTN4 mutant, K255E, which has increased act
15                          Here, we present an FSGS-like model in zebrafish larvae, an eligible vertebr
16 to a murine embryonic stem cell line with an FSGS-susceptible genetic background that allows shRNA-me
17 second cohort of patients with DN (n=19) and FSGS (n=21).
18 that differed in abundance between cFSGS and FSGS-NOS, 41 were more abundant in cFSGS and 17 in FSGS-
19 n PECs prevents glomerular damage in CGN and FSGS mouse models.
20  markedly in PECs in mouse models of CGN and FSGS, and in kidneys from individuals diagnosed with the
21  switch driving the PEC phenotype in CGN and FSGS, while offering a potential therapeutic avenue to t
22  as the pathological uPAR is circulating and FSGS can recur even after a damaged kidney is replaced w
23 veness, presence of a genetic diagnosis, and FSGS or diffuse mesangial sclerosis on initial biopsy as
24 lopathies such as minimal change disease and FSGS.
25 erulosclerosis (FSGS), a kidney disease, and FSGS+Charcot-Marie-Tooth neuropathy.
26 lasia of the patellae, nails, and elbows and FSGS with specific ultrastructural lesions of the glomer
27 indings of minimal change glomerulopathy and FSGS, respectively.
28  with HIV-associated nephropathy (HIVAN) and FSGS.
29 d in disturbance of podocyte homeostasis and FSGS development.
30 meruli with mesangial expansion, injury, and FSGS at study end.
31 ing of the glomerular basement membrane, and FSGS-like lesions.
32  subgroups (children, adults, MCD/MesGN, and FSGS; P<0.01).
33 sociated with HIV-associated nephropathy and FSGS in African Americans.
34 diseases, such as membranous nephropathy and FSGS, persistent injury often leads to irreversible stru
35 cin aminoglycoside-induced podocytopathy and FSGS in vivo.
36 cess architecture results in proteinuria and FSGS.
37 stant nephrotic syndrome, which manifests as FSGS, is not completely understood.
38 wever, for some genes previously reported as FSGS related, we identified rare variants at similar or
39 lves to progressive glomerulopathies such as FSGS or collapsing glomerulopathy.
40 t diseases affecting the glomerulus, such as FSGS, IgA nephropathy, lupus nephritis, and diabetic nep
41 echanisms underlying ACTN4 mutant-associated FSGS are not completely understood.
42 GS: 70 patients from the North America-based FSGS clinical trial (CT) and 94 patients from PodoNet, t
43      Our data provide the first link between FSGS-linked ACTN4 mutants and transcriptional activation
44                                      In both FSGS patients and PAN-treated rats, miR-30s were downreg
45 rovides a tool to rapidly evaluate candidate FSGS-associated genes.
46                               Nine candidate FSGS susceptibility genes were identified in our patient
47 Abrogation of Coq6 in mouse podocytes caused FSGS and proteinuria (>46-fold increases in albuminuria)
48              Identification of genes causing FSGS has improved our understanding of disease mechanism
49 might be part of the complex process causing FSGS.
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 PA induces severe proteinuria and collapsing FSGS.
53        A single Black patient had collapsing FSGS.
54 hat glomerular ECM composition in collapsing FSGS (cFSGS) differs from that of other variants.
55                                Consequently, FSGS-linked ACTN4 mutants failed to potentiate transcrip
56  a new therapeutic strategy to cure or delay FSGS and potentially other glomerulopathies.
57 ew cases aged 35 (15-66) years who developed FSGS recurrence at 12 (1.5-27) days posttransplantation.
58 rom patients with diabetic nephropathy (DN), FSGS, IgA nephropathy (IgAN), membranoproliferative GN (
59         Compared with control glomeruli, DN, FSGS, IgAN, and MPGN glomeruli exhibited differential ex
60  Compared with control proximal tubules, DN, FSGS, IgAN, and MPGN proximal tubules had differential e
61 ree of five patients with autosomal dominant FSGS but without either extrarenal features or ultrastru
62 he cause of nonsyndromic, autosomal dominant FSGS in two Northern European kindreds from the United S
63 the most common causes of autosomal dominant FSGS.
64  in members of an index family with dominant FSGS revealed a nonconservative, disease-segregating var
65 PEC proliferation and the formation of early FSGS lesions in experimental FSGS and reduced human PEC
66 ants that have been reported to cause either FSGS alone or with Charcot-Marie-Tooth disease.
67 ng the proposal that genetic factors enhance FSGS susceptibility.
68 mation of early FSGS lesions in experimental FSGS and reduced human PEC proliferation in vitro.
69                 We then induced experimental FSGS, typified by abrupt podocyte depletion, with a cyto
70         Sequencing in probands of a familial FSGS cohort revealed seven rare and private heterozygous
71 hannel 6 (TRPC6) were identified in familial FSGS, and increased expression of wild-type TRPC6 in glo
72                          Studies of familial FSGS have been instrumental in identifying podocytes as
73 formin 2 INF2 are a common cause of familial FSGS.
74 lated family units with sporadic or familial FSGS and compared this to data from 363 ancestry-matched
75 s from individuals with sporadic or familial FSGS.
76 -exome sequencing in a kindred with familial FSGS, we identified a missense mutation R431C in anillin
77 unidentified role within the target cell for FSGS, the kidney podocyte.
78  2 gene (INF2) in the mutational hotspot for FSGS.
79 ecent histologic classification proposed for FSGS has provided additional insights into the prognosis
80 d G2) explain much of the increased risk for FSGS, HIV-associated nephropathy, and hypertension-attri
81 rend analysis of kidney transplantations for FSGS in children (n=2157) showed an increase in cases of
82 analysis of purified podocyte fractions from FSGS mouse models showed an early stress response that i
83 sitive proteome analysis of human glomerular FSGS tissue and purified native mouse podocytes during e
84 disease focal segemental glomerulosclerosis (FSGS), as well as to cases of the neurologic disorder Ch
85  who had focal segmental glomerulosclerosis (FSGS) (four with recurrent FSGS after transplantation an
86 sions in focal segmental glomerulosclerosis (FSGS) and crescentic glomerulonephritis (CGN) remain poo
87 rized by focal segmental glomerulosclerosis (FSGS) and proteinuria.
88 uced focal and segmental glomerulosclerosis (FSGS) and streptozotocin (STZ)-induced diabetic glomerul
89  disease focal segmental glomerulosclerosis (FSGS) and the neurological disorder Charcot-Marie Tooth
90 uPAR) in focal segmental glomerulosclerosis (FSGS) as the circulating factor or as a predictor of rec
91 forms of focal segmental glomerulosclerosis (FSGS) have been linked to gain-of-function mutations in
92  form of focal segmental glomerulosclerosis (FSGS) in affected humans.
93 llapsing focal segmental glomerulosclerosis (FSGS) in humans with collapse of the glomerular tuft and
94      Focal and segmental glomerulosclerosis (FSGS) is a histological pattern frequently found in pati
95          Focal segmental glomerulosclerosis (FSGS) is a relatively prevalent glomerular disorder that
96          Focal segmental glomerulosclerosis (FSGS) is a syndrome that involves kidney podocyte dysfun
97 ation of focal segmental glomerulosclerosis (FSGS) lesions.
98  Primary focal segmental glomerulosclerosis (FSGS) often causes nephrotic proteinuria and frequently
99 els, and focal segmental glomerulosclerosis (FSGS) patients, whose TNF levels resembled those of heal
100 rats and focal segmental glomerulosclerosis (FSGS) patients.
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  for focal and segmental glomerulosclerosis (FSGS), a common cause of kidney failure.
105 forms of focal segmental glomerulosclerosis (FSGS), a kidney disease characterized by proteinuria due
106 ns cause focal segmental glomerulosclerosis (FSGS), a kidney disease, and FSGS+Charcot-Marie-Tooth ne
107 ncluding focal segmental glomerulosclerosis (FSGS), as a primary podocytopathy.
108 e (MCD), focal segmental glomerulosclerosis (FSGS), LN and hepatitis B associated glomerulonephritis
109          Focal segmental glomerulosclerosis (FSGS), the second leading cause of end stage renal disea
110 y-proven focal segmental glomerulosclerosis (FSGS).
111 n called focal segmental glomerulosclerosis (FSGS).
112  such as focal segmental glomerulosclerosis (FSGS).
113 familial focal segmental glomerulosclerosis (FSGS).
114 induced) focal segmental glomerulosclerosis (FSGS).
115 nts with focal segmental glomerulosclerosis (FSGS).
116 tly with focal segmental glomerulosclerosis (FSGS).
117 cases of focal segmental glomerulosclerosis (FSGS).
118 dominant focal segmental glomerulosclerosis (FSGS).
119 ria, and focal segmental glomerulosclerosis (FSGS).
120 ften focal and segmental glomerulosclerosis (FSGS).
121  such as focal segmental glomerulosclerosis (FSGS).
122 N as the predominant lesion and only 23% had FSGS.
123 se patients, 67% were pediatric, and 44% had FSGS on biopsy.
124 ction as an additional concept of hereditary FSGS and provides molecular insights into the mechanism
125               We then characterized 19 human FSGS-related TRPC6 mutations, the majority of which caus
126  and c-Src in msuPAR2 signaling and in human FSGS kidney biopsies.
127 ith Adriamycin nephropathy, a model of human FSGS, blocking endogenous retinoic acid synthesis increa
128 epletion in larval zebrafish resembles human FSGS in several important characteristics.
129  C3 deposits frequently accompany idiopathic FSGS and secondary glomerulosclerosis, but it is unknown
130 OS, 41 were more abundant in cFSGS and 17 in FSGS-NOS.
131 ith the largest increases in children and in FSGS subgroups.
132 r losartan (angiotensin-receptor blocker) in FSGS mice stimulated the proliferation of CoRL, increasi
133 that in the context of podocyte depletion in FSGS, RAAS inhibition augments CoRL proliferation and pl
134                 PEC markers were detected in FSGS lesions from the earliest stages of disease.
135 ted with migration defects commonly found in FSGS.
136 suPAR) as a circulating factor implicated in FSGS.
137 pts for cathepsins B and C were increased in FSGS glomeruli compared with normal controls, and urinar
138                 Moreover, RAAS inhibition in FSGS mice increased RFP(+)CoRL transdifferentiation in t
139 pportunities for therapeutic intervention in FSGS.
140 idly progressive GN and sclerotic lesions in FSGS.
141 findings suggest a novel injury mechanism in FSGS, with possible implications for new treatment strat
142 ous nephropathy to the role of a microRNA in FSGS.
143 minant effects exerted by ACTN4 mutations in FSGS.
144 ch the actin-cytoskeleton can be released in FSGS.
145 d increases in suPAR concentration result in FSGS-like glomerular lesions and proteinuria.
146 examine podocytes in early disease states in FSGS mouse models, we used podocyte fractions isolated f
147 and still poorly understood role of suPAR in FSGS.
148 s as plausible therapeutic targets: TRPC6 in FSGS, PKD2 in polycystic kidney disease, and TRPM6 in fa
149  In conclusion, B7-1 blockade did not induce FSGS remission after transplant in our study.
150 tal transgenic ablation of podocytes induces FSGS but the effect of specific ablation of PECs is unkn
151 ive nephropathy provided novel insights into FSGS pathogenesis in the absence of a primary podocyte a
152 ation between podocyte loss and irreversible FSGS and global glomerulosclerosis, this study points to
153 r whether they should be considered isolated FSGS or simply a misdiagnosed type of the Alport spectru
154 summary, these results suggest that isolated FSGS could result from mutations in genes that are also
155  by the nontrivial rate of variants in known FSGS genes among people without kidney disease.
156   Although our analysis validated many known FSGS-causing genes, we detected a nontrivial number of p
157 d closer than a random set of genes to known FSGS genes.
158 eveloping targeted therapy for INF2-mediated FSGS.
159              Whether TRPC5 activity mediates FSGS onset and progression is unknown.
160  that are accompanied by nephropathy, mostly FSGS.
161  high salt; severe albuminuria, nephrinuria, FSGS, and podocyte foot effacement in Ang II-induced hyp
162  or biopsy-based minimal change nephropathy, FSGS, or membranous nephropathy, with 94% sensitivity an
163 podocyte homeostasis and causes nonsyndromic FSGS.
164 ases of posttransplant recurrent and de novo FSGS resistant to conventional therapy with TPE and ritu
165 nterquartile range) of recurrent and de novo FSGS was 3 (0.75-7.5) months posttransplant.
166  our monogenic podocyte ER stress-induced NS/FSGS mouse model, the podocyte type 2 ryanodine receptor
167 e treatment of podocyte ER stress-induced NS/FSGS.
168 ether the elevated actin binding activity of FSGS mutants can be downregulated by EGF-mediated phosph
169 , albuminuria, podocyte loss, and aspects of FSGS during aging.
170 ility of both sporadic and familial cases of FSGS and provides a tool to rapidly evaluate candidate F
171 inary suPAR appears to be higher in cases of FSGS destined for recurrence and merits further evaluati
172 ion (R458Q) in WT1 isoform D as the cause of FSGS in this family.
173 actin binding cell cycle gene, as a cause of FSGS.
174 hts into the molecular and genetic causes of FSGS have enhanced our understanding of disease pathogen
175 ever, despite many known monogenic causes of FSGS, single gene defects explain only 30% of cases.
176 ns of severe renal disease characteristic of FSGS with proteinuria, loss of kidney function, and glom
177   Histologically, features characteristic of FSGS, including mesangial sclerosis, podocyte foot proce
178 endently and helps explain the clustering of FSGS-associated mutations.
179 FSGS from those that caused a combination of FSGS and Charcot-Marie-Tooth disease.
180 nce of genetic factors in the development of FSGS has become increasingly clear.
181 n that may play a role in the development of FSGS.
182 plant recipients with a primary diagnosis of FSGS in children 1 to 20 years of age.
183 d robust albuminuria, structural features of FSGS, and reduced numbers of glomerular podocytes.
184 ene are associated with an inherited form of FSGS.
185                           Inherited forms of FSGS are caused by Rac1-activating mutations, and Rac1 i
186                          Hereditary forms of FSGS have been linked to mutations in the transient rece
187                 Although idiopathic forms of FSGS predominate, recent insights into the molecular and
188 that are also involved in syndromic forms of FSGS.
189 retinoic acid and promotes the generation of FSGS lesions.
190       Progressive sclerosis is a hallmark of FSGS, and genetic tracing studies have shown that pariet
191 e glomerular tuft which are all hallmarks of FSGS.
192 raction of patients with a family history of FSGS.
193 her genetics plays a role in the majority of FSGS cases that are identified as primary or sporadic FS
194 ent is the first pathologic manifestation of FSGS after transplantation.
195 emic insults, a humanized xenograft model of FSGS resulted in an expansion of Gr-1(lo) cells in the B
196 d podocyte loss in a transgenic rat model of FSGS.
197 , per se, contributes to the pathogenesis of FSGS in humans remains controversial.
198                       The pathophysiology of FSGS is unknown, but podocytes seem to be the target of
199 cesses, it does not do so in the presence of FSGS-associated INF2 mutations.
200                               Progression of FSGS is associated with TGF-beta activation in podocytes
201                          Early recurrence of FSGS was defined as development of nephrotic range prote
202 ct the development of clinical recurrence of FSGS.
203       That the tyrosine kinase regulation of FSGS mutation binding to actin filaments can occur in ce
204 b was required for 4 patients as a result of FSGS relapse, with good results.
205                        At advanced stages of FSGS, fawn-hooded hypertensive rat kidneys exhibited dis
206 vide evidence for targeting the N-termini of FSGS ACTN4 mutants to downregulate their actin binding a
207 or cell-specific therapy in the treatment of FSGS and other proteinuric kidney diseases.
208 erular capillaries in histologic variants of FSGS are unknown.
209 ations in PAX2 may contribute to adult-onset FSGS in the absence of overt extrarenal manifestations.
210 ldren and 20 adults with MCD/MesGN (n=22) or FSGS who had suffered >/=2 recurrences over the previous
211       Specifically, compared with control or FSGS glomeruli, IgAN glomeruli exhibited downregulated e
212  242 patients with minimal change disease or FSGS, with duplicate readings to evaluate reproducibilit
213 MCD), mesangial proliferative GN (MesGN), or FSGS may be poor and with major treatment toxicity.
214               Overexpression of wild-type or FSGS-inducing mutant TRPC6 in synaptopodin-depleted podo
215 FSGS was significantly greater than in other FSGS variants, in minimal change disease, or in membrano
216 clerosis in cFSGS differs from that in other FSGS variants.
217  to actin filaments than K255E and the other FSGS mutants.
218                Moreover, posttransplantation FSGS recurrence is a major problem, and there is concern
219  study of 25 adults with posttransplantation FSGS.
220  of TRPC6 in GqQ>L-expressing mice prevented FSGS development and inhibited both tubular damage and p
221                                      Primary FSGS was once considered an entity nonresponsive to pred
222 n between minimal change disease and primary FSGS and may serve to guide clinical decision making.
223 , such as minimal change disease and primary FSGS, and glucocorticoids remain the initial and often,
224 he biopsies of patients diagnosed as primary FSGS.
225 rix); 38 had been diagnosed as early primary FSGS and 57 as minimal change disease.
226                             In human primary FSGS, we noted reduced glomerular expression of YAP.
227  to be uniquely elevated in cases of primary FSGS, with higher levels noted in cases that recurred af
228 been implicated in familial forms of primary FSGS.
229 ients with minimal change disease or primary FSGS.
230  patients with histologically proven primary FSGS (n = 2) or recurrent FSGS after transplantation (n
231 ildren and adults with biopsy-proven primary FSGS: 70 patients from the North America-based FSGS clin
232 athology in animal models similar to primary FSGS, and one recent study demonstrated elevated levels
233 Causes of native kidney disease were primary FSGS, diabetic nephropathy, membranous nephropathy, immu
234 on in African-American subjects with primary FSGS and may also be present in individuals who do not s
235 ial portion of nephrotic adults with primary FSGS do respond to treatment with a significantly improv
236 S after transplantation and one with primary FSGS) and proteinuria with B7-1 immunostaining of podocy
237  therapeutic approach in adults with primary FSGS.
238                                    Recurrent FSGS cases had substantially higher proteinuria compared
239  in the pathogenesis of native and recurrent FSGS.
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 nsplant recipients with de novo or recurrent FSGS resistant to therapeutic plasma exchange (TPE) and/
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         Kidneys from patients with recurrent FSGS had negative immunostaining for uPAR.
251 ey transplantation recipients with recurrent FSGS, rituximab therapy may be a recommended treatment f
252 ated factors, compared with IgAN (referent), FSGS, membranous nephropathy, membranoproliferative GN,
253  may mediate the development of INF2-related FSGS.
254 fective therapy for posttransplant resistant FSGS cases that fail to respond to TPE and rituximab.
255 w of cases of de novo or recurrent resistant FSGS at 2 large US transplant centers between April 2012
256 ent of focal segmental glomerular sclerosis (FSGS) after kidney transplantation is challenging with u
257        Focal segmental glomerular sclerosis (FSGS) is a primary kidney disease that is commonly assoc
258 ndothelial transcription factor in secondary FSGS.
259                         We validated several FSGS-associated genes that show a marked enrichment of d
260      Renal biopsy specimens uniformly showed FSGS.
261  patients with FSGS not otherwise specified (FSGS-NOS) or cFSGS and from normal controls were disting
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 ) revealed high mTOR activity in PECs of the FSGS lesions of these mice.
266 ional studies documented that several of the FSGS-associated PAX2 mutations perturb protein function
267 agment in podocytes and assessed whether the FSGS-associated R218Q mutation impairs INF2 cleavage or
268  these genes in all diagnostic approaches to FSGS that involve next-generation sequencing.
269   One patient suffered allograft loss due to FSGS recurrence.
270 F2 mutations that were linked exclusively to FSGS from those that caused a combination of FSGS and Ch
271 anging from a minimal-change-type lesions to FSGS or collapsing glomerulopathy.
272 polipoprotein L1 (APOL1) have been linked to FSGS in African Americans with HIV or hypertension, supp
273 sease, elevated serum suPAR is not unique to FSGS cases.
274 at endothelial-derived signaling can trigger FSGS and illustrate the potential importance of the EPAS
275 xicity, inflammation, and infection underlie FSGS; however, highly penetrant disease genes have been
276          To investigate mutations underlying FSGS, we sequenced 662 whole exomes from individuals wit
277                We therefore examined whether FSGS-associated mutations in TRPC6 result in activation
278 evated in sera from children and adults with FSGS compared with levels in healthy persons or those wi
279 ular filtration barrier were associated with FSGS in endothelial Epas1-deficient mice only.
280 th minimal change disease from children with FSGS and correlated with poor clinical outcome.
281 significantly greater in cFSGS compared with FSGS-NOS.
282     We screened 250 additional families with FSGS and found another variant, G618C, that segregates w
283 reened 73 additional unrelated families with FSGS and found mutations involving the same amino acid (
284 L) in the TTC21B gene in seven families with FSGS.
285 regates with disease in a second family with FSGS.
286 idney biopsy specimens from individuals with FSGS and kidney samples from a murine model of HIV-1-ass
287 hically and ethnically diverse patients with FSGS and do not reflect a nonspecific proinflammatory mi
288 ephronophthisis was present in patients with FSGS and the p.P209L mutation.
289                  Biopsies from patients with FSGS exhibited increased mitochondrial DNA damage, consi
290           Genetic diagnosis in patients with FSGS is complicated by the nontrivial rate of variants i
291                   Glomeruli of patients with FSGS lack DAF and stain positive for C3d, and urinary C3
292 eruli from biopsy specimens of patients with FSGS not otherwise specified (FSGS-NOS) or cFSGS and fro
293 elevated in 84.3% and 55.3% of patients with FSGS patients in the CT and PodoNet cohorts, respectivel
294 ome analysis of glomeruli from patients with FSGS revealed an underrepresentation of podocyte-specifi
295 docytes in biopsy samples from patients with FSGS, in single glomeruli from proteinuric rats, and in
296 oteome analysis to tissue from patients with FSGS.
297 were detectable in a subset of patients with FSGS; C3 was present as an activation fragment and coloc
298 0% of kidney transplant (KT) recipients with FSGS will experience recurrence characterized by protein
299 ilies with an X-linked early-onset SRNS with FSGS.
300            Renal biopsies from subjects with FSGS, but not those with other glomerular diseases, mani
301 ients with proteinuria, including those with FSGS and type 2 diabetic nephropathy (DN).

 
Page Top