ライフサイエンスコーパス: minimal change disease

1 en diagnosed as early primary FSGS and 57 as minimal change disease.

2 duced the gene expression profile of in vivo minimal change disease.

3 and membranous nephropathy than for presumed minimal change disease.

4 rchitecture, underlies nephrotic syndrome in minimal change disease.

5 ocal segmental glomerulosclerosis (FSGS) and minimal change disease.

6 ubstantial in FSGS, and less but not zero in minimal change disease.

7 atment response in a subset of patients with minimal change disease.

8 teroid therapy prescribed for a suspicion of minimal change disease.

9 n with genetic nephrotic syndrome, FSGS, and minimal change disease.

10 toantibodies may be present in patients with minimal change disease.

11 proteinuria from disease onset for FSGS and minimal change disease.

12 the histologically unremarkable glomeruli in minimal change disease.

13 ients with idiopathic FSGS, classic FSGS, or minimal-change disease.

14 In FSGS and minimal change disease, 10-year eGFR slope was strongly

15 lapsing glomerulopathy, 1 was diagnosed with minimal change disease, 2 were diagnosed with membranous

16 SGS [40%], membranous nephropathy [40%], and minimal change disease [20%]).

17 (40.4% and 46.7%, respectively), followed by minimal change disease (28.1% and 21.7%, respectively);

18 e found in 46 of the 105 patients (44%) with minimal change disease, 7 of 74 (9%) with primary focal

19 d with adults (FSGS 61 ml/min per 1.73 m(2); minimal change disease 76 ml/min per 1.73 m(2)).

20 genetic 29% (20 to 38), FSGS 58% (55 to 61), minimal change disease 87% (85 to 89) with mean (SD) rat

21 e use ExPath for optical diagnosis of kidney minimal-change disease, a process that previously requir

22 dies in a subset of adults and children with minimal change disease aligns with published animal stud

23 s identified in 136/71 and 1875/746 genes in minimal change disease and FSGS models, respectively.

24 lly associated with glomerulopathies such as minimal change disease and FSGS.

25 In minimal change disease and membranous glomerulopathy, al

26 ts with FSGS and 4 (20%) of 20 patients with minimal change disease and membranous nephropathy (P < 0

27 ted Crk-dependent signaling - was induced in minimal change disease and membranous nephropathy, but n

28 Minimal change disease and primary focal segmental glome

29 taining improves the differentiation between minimal change disease and primary FSGS and may serve to

30 g event in primary glomerulopathies, such as minimal change disease and primary FSGS, and glucocortic

31 rome in children is commonly associated with minimal change disease and response to steroid therapy.

32 omerular disease type: a high correlation in minimal-change disease and a low correlation in membrano

33 lopathy, autoimmune (membranous nephropathy, minimal change disease) and paraneoplastic manifestation

34 In total, 1303 patients had FSGS, 1153 had minimal change disease, and 105 had monogenic nephrotic

35 ry disease, 15 with type 2 diabetes, 10 with minimal change disease, and 17 normal individuals.

36 ry glomerulopathies including sporadic FSGS, minimal change disease, and IgA nephropathy.

37 sion noted in vivo in the podocytes in human minimal change disease biopsies.

38 ing nephrin have been found in patients with minimal change disease, but their clinical and pathophys

39 or development, we examined 125 biopsies for Minimal Change Disease collected across 29 NEPTUNE enrol

40 We evaluated sera from patients with minimal change disease, enrolled in the Nephrotic Syndro

41 phrotic syndrome encompasses the spectrum of minimal change disease, focal segmental glomeruloscleros

42 n adults with glomerular diseases, including minimal change disease, focal segmental glomeruloscleros

43 ns in podocytes differentiated children with minimal change disease from children with FSGS and corre

44 Patients with minimal change disease had better proteinuria control th

45 ropathy, focal segmental glomerulosclerosis, minimal change disease, idiopathic membranous GN, and an

46 ulosclerosis, membranous glomerulonephritis, minimal change disease, IgA nephropathy, and diabetic ne

47 Pre-CsA histology showed minimal change disease in three patients, immunoglobulin

48 the hypothyroid, low T3, and low T3T4 groups minimal change disease is now the leading type (48.8%, 3

49 immunization induced a nephrotic syndrome, a minimal change disease-like phenotype, IgG localization

50 Minimal change disease (MCD) and focal segmental glomeru

51 t presence of anti-nephrin autoantibodies in minimal change disease (MCD) and focal segmental glomeru

52 focal segmental glomerulosclerosis (FSGS) or minimal change disease (MCD) cases in the 130,000 member

53 Minimal change disease (MCD) is the etiology of 10%-25%

54 shared by subgroups of patients with either minimal change disease (MCD) or focal segmental glomerul

55 While most children with minimal change disease (MCD) show favorable responses to

56 l glomerulosclerosis (FSGS) and 119/113 with minimal change disease (MCD)) to segment cortex, tubular

57 g focal segmental glomerulosclerosis (FSGS), minimal change disease (MCD), and membranous nephropathy

58 rimary classic FSGS, collapsing FSGS (COLL), minimal change disease (MCD), and normal controls (Norma

59 nephrotic syndrome are diabetic nephropathy, minimal change disease (MCD), focal and segmental glomer

60 omerulopathy (ORG), while the frequencies of minimal change disease (MCD), focal segmental glomerulos

61 membranous nephropathy, nephrotic syndrome, minimal change disease (MCD), focal segmental glomerulos

62 r frequently relapsing nephrotic syndrome of minimal change disease (MCD), mesangial proliferative GN

63 he appearance of proteinuria are features of minimal-change disease (MCD).

64 inary soluble CD80 increased with idiopathic minimal-change disease (MCD).

65 (focal segmental glomerulosclerosis [FSGS], minimal-change disease [MCD], membranous nephropathy [MN

66 and HIV-associated nephropathy compared with minimal change disease, membranous glomerulopathy, as we

67 om 1%-2% in ANCA-related glomerulonephritis, minimal change disease, membranous nephropathy, or FSGS

68 In minimal change disease, no PEC activation was observed b

69 adult patients with podocytopathies (either minimal change disease or FSGS) are largely unknown.

70 mino-nucleoside or adriamycin to mimic human minimal change disease or FSGS, respectively, and RNA-se

71 EPTUNE renal biopsies from 242 patients with minimal change disease or FSGS, with duplicate readings

72 In the subgroup of patients with active minimal change disease or idiopathic nephrotic syndrome

73 autoantibodies were common in patients with minimal change disease or idiopathic nephrotic syndrome

74 corticoid responsiveness in 35 patients with minimal change disease or primary FSGS.

75 ntly greater than in other FSGS variants, in minimal change disease, or in membranous nephropathy.

76 ne care of subjects with a diagnosis of AKI, minimal change disease, or on nephrectomy tissue with no

77 For minimal change disease, patients' 10-year kidney surviva

78 llapsing glomerulopathy and the patient with minimal change disease revealed that all four patients h

79 r to that of AKI which was not identified in minimal change disease samples.

80 o irreversible structural damage, whereas in minimal change disease, structural alterations are mostl

81 d a patient with steroid-dependent childhood minimal change disease that progressed to end stage kidn

82 , in 25% of biopsies originally diagnosed as minimal change disease the presence of small lesions ind

83 cular classification of nephrin autoantibody minimal change disease to serve as a framework for insti

84 ous studies in a rat model that mimics human minimal change disease, we observed localized secretion

85 dult patients (n=64 with FSGS and n=119 with minimal change disease) with difficult-to-treat nephroti

86 In experimental minimal change disease, ZHX3 was transiently down-regula