ライフサイエンスコーパス: glomerular lesion

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1 itial nephritis with little attention to its glomerular lesion.

2 layed type hypersensitivity-like necrotizing glomerular lesions.

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

4 at aged female B6 mice developed progressive glomerular lesions.

5 with reduced GFR had more advanced diabetic glomerular lesions.

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

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

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

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

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

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

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

13 Glomerular lesions are considered one of the more detrim

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

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

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

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

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

19 Patients with glomerular lesions had higher urinary albumin than those

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

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

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

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

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

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

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

27 Glomerular lesions may therefore be perpetuated or aggra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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