ライフサイエンスコーパス: MPGN

1 Although MPGN has been reported in other conditions in which unco

2 herapeutic approach for cryoglobulinemia and MPGN in humans.

3 with control glomeruli, DN, FSGS, IgAN, and MPGN glomeruli exhibited differential expression of 18,

4 ontrol proximal tubules, DN, FSGS, IgAN, and MPGN proximal tubules had differential expression of 13,

5 tates are at greater risk of developing CKD, MPGN, and cryoglobulinemia.

6 eficient in factor H (Cfh(-/-) mice) develop MPGN spontaneously and are hypersensitive to developing

7 LPtg and TSLPtg/FcRgamma(-/-) mice developed MPGN with massive glomerular immune deposits, mesangial

8 mphopoietin transgenic mice with established MPGN also diminished cryoglobulin production and reverse

9 c level may lead to effective treatments for MPGN II.

10 of membranoproliferative glomerulonephritis (MPGN) and cryoglobulinemia in chronic HCV patients.

11 Membranoproliferative glomerulonephritis (MPGN) is seen in patients infected with hepatitis C viru

12 Membranoproliferative glomerulonephritis (MPGN) occurs in factor H-deficient humans and pigs.

13 Membranoproliferative glomerulonephritis (MPGN) recently was reclassified to reflect the underlyin

14 nd membranoproliferative glomerulonephritis (MPGN) remains poorly studied and, given the risk of neph

15 Membranoproliferative glomerulonephritis (MPGN) type II (dense deposit disease) is an inflammatory

16 ed membranoproliferative glomerulonephritis (MPGN), in which some glomerular manifestations likely re

17 ic membranoproliferative glomerulonephritis (MPGN).

18 nd membranoproliferative glomerulonephritis (MPGN).

19 ephropathy (IgAN), membranoproliferative GN (MPGN) (n=19-23 for each disease), and a control group (n

20 roangiopathies and membranoproliferative GN (MPGN) can manifest similar clinical presentations and hi

21 Membranoproliferative GN (MPGN) was recently reclassified as alternative pathway c

22 eristic finding in membranoproliferative GN (MPGN).

23 inhibition therapy might be useful in human MPGN type II.

24 ple algorithm to assign patients with C3G/IC-MPGN to specific clusters.

25 ent parameters from 173 patients with C3G/IC-MPGN.

26 omplex-mediated membranoproliferative GN (IC-MPGN).

27 athway abnormalities are also observed in IC-MPGN.

28 d Ig-associated membranoproliferative GN (Ig-MPGN) for anti-FB and anti-C3b autoantibodies using ELIS

29 ernative pathway activation is similar in Ig-MPGN and C3G, suggesting similar pathogenic mechanisms.

30 dentification of the underlying defect in Ig-MPGN could lead to improved treatment.

31 ients with C3G and one [10%] patient with Ig-MPGN).

32 hese 15 patients, ten were diagnosed with Ig-MPGN.

33 anoproliferative glomerulonephritis type II (MPGN II) is a rare disease characterized by the depositi

34 anoproliferative glomerulonephritis type II (MPGN II) is an uncommon form of complement-dependent acq

35 of the alternative pathway of complement in MPGN.

36 re were 23 patients with complement-mediated MPGN and available eye examination results.

37 m, and all patients with complement-mediated MPGN require screening eye examinations.

38 nent among patients with complement-mediated MPGN when compared with patients with immune complex-med

39 ere 23 patients with immune complex-mediated MPGN and available eye examination results.

40 rmed complement- and immune complex-mediated MPGN who had available ophthalmology records from 1997 t

41 d with patients with immune complex-mediated MPGN.

42 ion in this model of immune complex-mediated MPGN.

43 The pathophysiologic basis of MPGN II is associated with the uncontrolled systemic act

44 ants have been reported in sporadic cases of MPGN, although their functional significance has not bee

45 in vivo is essential for the development of MPGN associated with deficiency of factor H.

46 ated the role of C5 activation in a model of MPGN that develops spontaneously in complement factor H-

47 reased risk of proteinuria and occurrence of MPGN that was only partially responsive to interferon.

48 e of C3 dysregulation in the pathogenesis of MPGN is not understood.

49 twofold and a nearly 17-fold higher risk of MPGN (HR, 2.23; 95% CI, 1.84-2.71) and cryoglobulinemia

50 Antiviral therapies reduce the severity of MPGN due to hepatitis C virus.

51 These data indicate that recurrent MPGN II has a significant negative impact on renal allog

52 Treatment of HCV-related MPGN with interferon-alpha2b appeared to stabilize prote

53 tion (P=0.05) and had renal biopsies showing MPGN than did HCV- recipients (4/10 HCV+ patients vs. 0/

54 an important role for C5 in both spontaneous MPGN and experimentally induced nephritis in factor H-de

55 it has been recognized since the 1970s that MPGN II recurs almost universally in renal transplants,

56 or ophthalmologists to recognize the updated MPGN classification system, and all patients with comple

57 were studied at 30 and 50 days of age, when MPGN is in early and fully developed stages, respectivel

58 ement factor H has long been associated with MPGN.

59 mber of patients and the number of eyes with MPGN-related pathologic features were examined.

60 We describe a family with MPGN and acquired partial lipodystrophy.

61 sk polymorphisms carried by individuals with MPGN.

62 ical and pathologic records of patients with MPGN and eye examination results were reviewed from year

63 scribe related eye findings in patients with MPGN based on the new classification.

64 il numbers, frequently seen in patients with MPGN during disease flares, were also observed in Cfh(-/

65 Patients with MPGN had normal levels of factor H, and structural analy

66 Many patients with MPGN have chronic hepatitis C infection.

67 ive comparative analysis of 75 patients with MPGN II contained in the North American Pediatric Renal

68 Five-year graft survival for patients with MPGN II was significantly worse (50.0 +/- 7.5%) compared