ライフサイエンスコーパス: glomerular lesion

1 itial nephritis with little attention to its glomerular lesion.

2 layed type hypersensitivity-like necrotizing glomerular lesions.

3 at aged female B6 mice developed progressive glomerular lesions.

4 with reduced GFR had more advanced diabetic glomerular lesions.

5 ine ratio and development of focal segmental glomerular lesions.

6 yte injury is a classic hallmark of diabetic glomerular lesions.

7 the kidney revealed a membranoproliferative glomerular lesion, a lesion usually associated with lymp

8 verities of renal failure, hypertension, and glomerular lesions, according to their genetic backgroun

9 An awareness of other glomerular lesion and tubulointerstitial lesions has bro

10 nt with sirolimus reduced the development of glomerular lesions and glomerular cell proliferation at

11 t alpelisib, a PI3Kalpha inhibitor, improves glomerular lesions and kidney function in different mous

12 tes, despite excessive AER in Cluster 2, DKD glomerular lesions and podocyte structural parameters we

13 s in suPAR concentration result in FSGS-like glomerular lesions and proteinuria.

14 nd is associated with more advanced diabetic glomerular lesions and, probably, with increased risk of

15 s may not correlate well with the underlying glomerular lesion, and therefore, the renal biopsy is an

16 Glomerular lesions are also described, but they are of v

17 Glomerular lesions are considered one of the more detrim

18 persons with type 1 diabetes, where diabetic glomerular lesions are strongly associated with albumin

19 In contrast, each stage of the developing glomerular lesion associated with chronic rejection demo

20 owed greater AER than predicted by their DKD glomerular lesions based on the model.

21 yridoxamine, and BMP-7 significantly inhibit glomerular lesions, BMP-7 is most effective in the inhib

22 mediator of growth responses associated with glomerular lesion development during chronic rejection.

23 inuria, in association with a characteristic glomerular lesion, endotheliosis.

24 Glomerular lesions, first recognized in 18-month-old mic

25 Patients with glomerular lesions had higher urinary albumin than those

26 ly, are the most widely known, several other glomerular lesions have been described in patients with

27 Mesangial expansion, the principal glomerular lesion in diabetic nephropathy, is preceded b

28 nvolved in the pathogenesis of the sclerotic glomerular lesion in HIVAN, representational difference

29 as key processes in the development of these glomerular lesions in patients with ORG, but their impac

30 First delineated from other proteinuric glomerular lesions in the 1980s, CG is now recognized as

31 staining was markedly increased in sclerotic glomerular lesions in the transgenic HIVAN model.

32 Dcn(-/-) diabetic mice exhibited advanced glomerular lesions, including diffuse mesangial matrix a

33 Recent evidence suggests that this unusual glomerular lesion is mediated by a soluble vascular endo

34 Glomerular lesions may therefore be perpetuated or aggra

35 s; however, they did develop albuminuria and glomerular lesions mirroring those in the donors (i.e.,

36 Transplant glomerulopathy, a common glomerular lesion observed after kidney transplant that

37 The glomerular lesions of HIV-associated nephropathy (HIVAN)

38 stologic changes and the pathogenesis of the glomerular lesions of preeclampsia.

39 mice revealed that the development of these glomerular lesions required the formation of IgA-IgG2a i

40 monstrate that PECs can be activated to form glomerular lesions resembling a noninflammatory glomerul

41 ated protein 1 light chain 3 associated with glomerular lesion severity.

42 ic of early DN, were present by 8 weeks, and glomerular lesions similar to those of advanced human DN

43 ion and retinopathy, and, as expected, worse glomerular lesions than slow-track patients.

44 usly unrecognized component of the sclerotic glomerular lesion that develops in the course of experim

45 hase knockout (eNOSKO) mice develop advanced glomerular lesions that include mesangiolysis and nodula

46 Anti-Thy1.1 transgenic mice develop glomerular lesions that mimic collapsing focal segmental

47 In contrast to the severe glomerular lesions, the tubulointerstitium was not invol

48 Pathologists use visual classification of glomerular lesions to assess samples from patients with

49 illary GN, divided according to the grade of glomerular lesions, we found that the accumulation of ma

50 lysis, the proliferative cell populations in glomerular lesions were exclusively composed of activate

51 Morphometric measures of DKD glomerular lesions were more advanced and showed stronge

52 flects the progression of earlier structural glomerular lesions, whereas early GFR decline may not ac

53 Focal and segmental necrotizing glomerular lesions with crescents, mimicking a small ves

54 lomerular neutrophil recruitment, thrombotic glomerular lesions with endothelial cell injury, and ren

55 All had typical glomerular lesions with focal segmental tuft collapse an

56 and interstitial fibrosis in the absence of glomerular lesions, with inescapable progression to end-