ライフサイエンスコーパス: tubulitis

1 rstitial inflammation (i > 0 with or without tubulitis).

2 1 (0-10% interstitial inflammation with mild tubulitis).

3 e Banff-scored interstitial inflammation and tubulitis.

4 in cases with moderate as opposed to severe tubulitis.

5 2 had similar levels of molecular injury and tubulitis.

6 xception and showed active inflammation with tubulitis.

7 nt (hazard ratio 1.1, CI: 1.0-1.2 per year), tubulitis (1.5, 1.3-1.8) and microvasculature injury (2.

8 s interstitial/perivascular infiltration and tubulitis 3 and 5 days after Tx, and a lower level of IL

9 and tubular atrophy, n = 52), and borderline tubulitis (3.3, [1.3, 4.9], n = 36).

10 ic glomerulitis, 55% versus 4%; neutrophilic tubulitis, 55% versus 9%; severe ATI, 75% versus 9%; and

11 s were frequent: acute tubular injury (94%), tubulitis (82%), tubular rupture (62%), giant cell react

12 Neutrophilic tubulitis accompanied by intratubular neutrophil cluster

13 Neutrophilic tubulitis accompanied by neutrophil clusters in the tubu

14 with AR and also associated with severity of tubulitis, among the top 15 SNPs.

15 rred with a threshold of > or =1 tubule with tubulitis and > or =5% cortex with interstitial infiltra

16 onship with histologic lesions (particularly tubulitis and atrophy-fibrosis) and time posttransplant.

17 showed reduced interstitial inflammation and tubulitis and fMRI analysis revealed improved allograft

18 reased graft function, and a higher grade of tubulitis and inflammation in AMR are negative predictor

19 BKN with molecular TCMR had more tubulitis and inflammation than BKN without molecular TC

20 ch as IFNG fell progressively with time, but tubulitis and molecular injury were sustained.

21 UTI in biopsies with concurrent neutrophilic tubulitis and PTC C4d staining.

22 a, the thresholds for number of tubules with tubulitis and the percent infiltrate were varied, and th

23 linear regression model, both CD3(+) T cell tubulitis and tubular atrophy independently associated w

24 days showed significantly reduced scores for tubulitis and vasculitis in the grafts of these recipien

25 d CD8 interstitial mononuclear inflammation, tubulitis, and endarteritis.

26 group showed more interstitial inflammation, tubulitis, and glomerulitis.

27 the extent of the interstitial infiltrate or tubulitis, are correlated with response to antirejection

28 It correlated with tubulitis, arteritis, and antibody markers within concur

29 expression of CD103 was examined in situ in tubulitis associated with acute rejection.

30 ular infiltrates without overt vasculitis or tubulitis, but these infiltrates disappeared without tre

31 Isolated VR (n = 34, Banff i < 1 without tubulitis) comprised 24 T cell-mediated VR and 10 antibo

32 The v-lesions with minimal or high-grade tubulitis displayed similar graft survival (72.7% vs. 72

33 racterized by a T cell (CD25(+)) infiltrate, tubulitis, endothelialitis and glomerulitis, and anti-do

34 rtex, a total of at least three tubules with tubulitis in 10 consecutive high-power fields from the m

35 grafts showed interstitial inflammation with tubulitis in 7 of 10 (70%) patients; in 3 of 10 (30%) pa

36 We examined the impact of i-IFTA and t-IFTA (tubulitis in areas of atrophy) in the first biopsy for c

37 ion in the absence of tubulitis nor isolated tubulitis in the absence of interstitial inflammation re

38 sfying Banff thresholds for inflammation and tubulitis in the presence of viruria but negative for BK

39 The SNPs associated with AR and severity of tubulitis in this study will need to be validated in ind

40 ma cell infiltration, as well as scoring for tubulitis, interstitial inflammation, and glomerulitis.

41 al fibrosis scores in early AMR patients and tubulitis, interstitial inflammation, g, ptc, and C4d in

42 roved mean scores for acute Banff components tubulitis, interstitial inflammation, g, ptc, g + ptc, C

43 Tubulitis is a defining feature for the diagnosis and ma

44 Tubulitis is a defining feature of renal allograft rejec

45 ormally show no lymphocyte infiltration, but tubulitis is a feature of renal allograft rejection with

46 carring, graft interstitial inflammation and tubulitis, microcirculation inflammation, and circulatin

47 interstitial inflammation in the absence of tubulitis nor isolated tubulitis in the absence of inter

48 The extent of tubulitis or of the interstitial infiltrate did not corr

49 i-INT was followed by delayed resolution of tubulitis (P < 0.001).

50 rs independently associated with severity of tubulitis (P<0.05).

51 group was significantly associated with less tubulitis (P=0.0021), and more chronic allograft arterio

52 ion score (2.6+/-0.1 to 1.3+/-0.1, P<0.001), tubulitis score (2.6+/-0.1 to 1.1+/-0.1, P<0.001), and s

53 + to CD8+ cells increased significantly with tubulitis score (P values 0.005, 0.009, and 0.02, respec

54 n tubules also increasing significantly with tubulitis score (P=0.034).

55 bles at the time of index TCMR, although the tubulitis scores tended to be higher (P = 0.079).

56 ed 15 novel SNPs associated with severity of tubulitis scores, after adjusting for transplant center

57 ance treatment with immunosuppressive drugs, tubulitis still occurs and can lead to structural kidney

58 (10-25% interstitial inflammation with mild tubulitis) to i0t1 (0-10% interstitial inflammation with

59 imes exaggerating Banff i in the presence of tubulitis, to reach a diagnosis of Borderline.

60 ing related-rejection i-INT was dependent on tubulitis using multivariable analysis.

61 CD8+ T cell tubulitis was especially associated with progressive cha

62 Mononuclear cell tubulitis was more common in the C4d(-) group (70% versu

63 f simultaneous C4d staining and neutrophilic tubulitis were correlated with urine culture (U/C) resul

64 nt Inflammation) and 304 with SCI-T (SCI and Tubulitis) which was further subdivided into 182 with SC

65 Given the strong association of tubulitis with clinical rejection, these data are consis