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1 od pressure did correlate with the degree of focal segmental glomerulosclerosis.
2 icularly in podocytes, in human kidneys with focal segmental glomerulosclerosis.
3 ents with renal failure caused by idiopathic focal segmental glomerulosclerosis.
4 racterized by skeletal changes, glaucoma and focal segmental glomerulosclerosis.
5 damage, but chronic overactivation leads to focal segmental glomerulosclerosis.
6 -function mutations cause autosomal dominant focal segmental glomerulosclerosis.
7 th HIV-associated nephropathy and idiopathic focal segmental glomerulosclerosis.
8 teinuric kidney disease that resembles human focal segmental glomerulosclerosis.
9 disease and membranous nephropathy, but not focal segmental glomerulosclerosis.
10 progressed to renal failure associated with focal segmental glomerulosclerosis.
11 he underlying disease mechanism in inherited focal segmental glomerulosclerosis.
12 risk for hypertension-attributable ESRD and focal segmental glomerulosclerosis.
13 njury in sclerosing glomerulopathies such as focal segmental glomerulosclerosis.
14 thelial cells in diabetic nephropathy and in focal segmental glomerulosclerosis.
15 ic domain showed histology characteristic of focal segmental glomerulosclerosis.
16 resulting in progressive kidney failure and focal segmental glomerulosclerosis.
17 odocyte numbers decrease in association with focal segmental glomerulosclerosis.
18 13.1, a region with genes linked to familial focal segmental glomerulosclerosis.
19 in assembly assay identified alpha-actinin-4/focal segmental glomerulosclerosis 1 (FSGS1) as an essen
20 a cross-linking approach, we have identified focal segmental glomerulosclerosis 3/CD2-associated prot
21 There was a surprisingly high prevalence of focal segmental glomerulosclerosis (50%) and global glom
22 e models of both obstructive nephropathy and focal segmental glomerulosclerosis (adriamycin nephropat
24 -associated nephropathy with collapsing-type focal segmental glomerulosclerosis and characteristic tu
25 ed normal at birth but developed progressive focal segmental glomerulosclerosis and died in terminal
26 tients with congenital (onset 0 to 3 months) focal segmental glomerulosclerosis and five patients wit
27 ium channel TRPC6 lead to autosomal dominant focal segmental glomerulosclerosis and podocyte expressi
28 r receptor (suPAR) have been associated with focal segmental glomerulosclerosis and poor clinical out
29 kidney abnormalities, including albuminuria, focal segmental glomerulosclerosis and progressive kidne
30 duction, we briefly review new insights into focal segmental glomerulosclerosis and the role of podoc
31 table syndrome in evaluation of females with focal segmental glomerulosclerosis and to consider their
32 sses the spectrum of minimal change disease, focal segmental glomerulosclerosis, and related disorder
33 s of nephrosis and why some patients develop focal segmental glomerulosclerosis are less striking, bu
34 females with normal genital development and focal segmental glomerulosclerosis associated with a WT1
35 s an early pathomechanism in mice developing focal-segmental glomerulosclerosis associated with funct
36 e associated with kidney diseases, including focal segmental glomerulosclerosis, characterized by pro
37 Obesity has been associated with a secondary focal segmental glomerulosclerosis coined obesity-relate
39 and lies near the K255E mutation that causes focal segmental glomerulosclerosis) demonstrated increas
41 polycystic kidney disease (ADPKD), familial focal segmental glomerulosclerosis (FSG), hypomagnesemia
42 esent report describes five patients who had focal segmental glomerulosclerosis (FSGS) (four with rec
43 A) administration to patients with recurrent focal segmental glomerulosclerosis (FSGS) after transpla
44 Here, we show that, in African Americans, focal segmental glomerulosclerosis (FSGS) and hypertensi
46 Mutations in INF2 lead to the kidney disease focal segmental glomerulosclerosis (FSGS) and the neurol
47 enteenfold higher odds (95% CI 11 to 26) for focal segmental glomerulosclerosis (FSGS) and twenty-nin
51 The histopathologic diagnosis of primary focal segmental glomerulosclerosis (FSGS) has come to in
53 ulin M nephropathy (IgM) in 14 patients, and focal segmental glomerulosclerosis (FSGS) in five patien
54 both familial and sporadic steroid-resistant focal segmental glomerulosclerosis (FSGS) in the pediatr
68 ents, who displayed elevated TNF levels, and focal segmental glomerulosclerosis (FSGS) patients, whos
69 nt of kidney transplantation recipients with focal segmental glomerulosclerosis (FSGS) recurrence.
71 y potential markers of steroid-resistance in focal segmental glomerulosclerosis (FSGS) we evaluated i
72 nary cells from 15 (41%) of 36 patients with focal segmental glomerulosclerosis (FSGS), 2 (10%) of 20
73 Common forms of glomerulonephritis seen were focal segmental glomerulosclerosis (FSGS), 57; immunoglo
74 tein, alpha-actinin 4 (ACTN4), are linked to focal segmental glomerulosclerosis (FSGS), a chronic kid
75 alpha-actinin-4 have been linked to familial focal segmental glomerulosclerosis (FSGS), a common rena
77 in 4 (ACTN4) are linked to familial forms of focal segmental glomerulosclerosis (FSGS), a kidney dise
78 n (CELL), seen in some patients with primary focal segmental glomerulosclerosis (FSGS), comprises pro
79 ble for a dominantly inherited form of human focal segmental glomerulosclerosis (FSGS), evidence supp
80 ssociates with increased risk for idiopathic focal segmental glomerulosclerosis (FSGS), HIV-1-associa
81 ociate with the nondiabetic kidney diseases, focal segmental glomerulosclerosis (FSGS), HIV-associate
82 MYH9 as a susceptibility gene for idiopathic focal segmental glomerulosclerosis (FSGS), HIV-associate
84 of idiopathic nephrotic syndrome, including focal segmental glomerulosclerosis (FSGS), minimal chang
85 a subset of adults and children with primary focal segmental glomerulosclerosis (FSGS), proteinuria a
88 disposing to idiopathic and HIV-1-associated focal segmental glomerulosclerosis (FSGS), we carried ou
105 docytes in all examined glomerular diseases (focal segmental glomerulosclerosis [FSGS], minimal-chang
108 se individuals without such variants to have focal segmental glomerulosclerosis, HIV-associated nephr
109 ) (referent) and lower for all other groups: focal segmental glomerulosclerosis (HR, 0.80; 95% CI, 0.
110 hropathy (HRa, 0.47; 95% CI, 0.29-0.75), and focal segmental glomerulosclerosis (HRa, 0.69; 95% CI, 0
111 arteriosclerosis in idiopathic and secondary focal segmental glomerulosclerosis, hypertensive nephros
112 tified five families with autosomal dominant focal segmental glomerulosclerosis in which disease segr
113 ion of podocytes associated with progressive focal-segmental glomerulosclerosis in CD2AP-/- mice.
116 rculating factor found in some patients with focal segmental glomerulosclerosis is associated with re
118 responsive nephrotic syndrome, in particular focal segmental glomerulosclerosis, its pathogenesis and
119 icient to induce spontaneous proteinuria and focal segmental glomerulosclerosis-like glomerular damag
121 en healthy control samples and patients with focal-segmental glomerulosclerosis, membranous glomerulo
122 l expansion, capsular adhesions (synechiae), focal segmental glomerulosclerosis, mild persistent prot
123 obtained from patients with IgA nephropathy, focal segmental glomerulosclerosis, minimal change disea
124 rtensive nephrosclerosis (n = 7), idiopathic focal segmental glomerulosclerosis (n = 11), focal scler
125 athy, diffuse proliferative lupus nephritis, focal segmental glomerulosclerosis (not collapsing glome
126 pathologic entity that includes proteinuria, focal segmental glomerulosclerosis often of the collapsi
127 Podocytes in glomeruli from humans with focal segmental glomerulosclerosis or diabetic nephropat
128 ht recent progress in the physiopathology of focal segmental glomerulosclerosis recurrence after tran
129 ) and a form of autosomal recessive familial focal segmental glomerulosclerosis (SRN1), respectively.
130 basement membrane glomerulonephritis, and a focal segmental glomerulosclerosis that is characteristi
131 were associated with morphologic changes of focal segmental glomerulosclerosis together with interst
132 ey diseases such as diabetic nephropathy and focal segmental glomerulosclerosis, we observed upregula
133 used by idiopathic membranous nephropathy or focal segmental glomerulosclerosis were confirmed by gen
134 sis in the 5/6 nephrectomy (Nx) rat model of focal segmental glomerulosclerosis were investigated.
137 ophy and a renal biopsy specimen that showed focal segmental glomerulosclerosis with abnormal podocyt
138 (HIVAN), is an aggressive form of collapsing focal segmental glomerulosclerosis with accompanying tub
140 This review discusses the development of focal segmental glomerulosclerosis, with particular atte
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