ライフサイエンスコーパス: minimal change disease

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

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

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

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

5 In minimal change disease and membranous glomerulopathy, al

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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