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1 and UBD in glomerulus; SNOR14B and MUC13 in tubulointerstitium).
2 HIF-target genes with eGFR in glomeruli and tubulointerstitium.
3 ssion of CSE, localized to glomeruli and the tubulointerstitium.
4 lammation, and scarring in glomeruli and the tubulointerstitium.
5 c abnormalities of the kidney glomerulus and tubulointerstitium.
6 ls from apoptotic death in the glomeruli and tubulointerstitium.
7 membrane of the glomerulus and in the renal tubulointerstitium.
8 scents and in infiltrating leukocytes in the tubulointerstitium.
9 as well as by infiltrating leukocytes in the tubulointerstitium.
10 t a dose of 5 mg/kg did not affect the renal tubulointerstitium.
11 rythropoietin-producing cells located in the tubulointerstitium.
12 f complement is rapidly activated within the tubulointerstitium after renal ischemia/reperfusion (I/R
13 an ameliorated inflammatory infiltration in tubulointerstitium and a favored M2-skewed macrophage po
14 h high dose CsA showed increased Nox2 in the tubulointerstitium and greater Nox2, alpha-SMA, phosphor
15 appaB pathway were evaluated in the cortical tubulointerstitium and in cellular infiltrates using dig
16 Upon SNx, extracellular TG2 deposited in the tubulointerstitium and peri-glomerulus via binding to he
17 the loss of nephron function by damaging the tubulointerstitium and that prevention of C5b-9 formatio
19 Matrix deposition was present mostly in the tubulointerstitium and vessels in accordance with the FK
20 gen matrix deposition within the glomerulus, tubulointerstitium, and arterial walls (all with P < 0.0
21 deposition within the glomerulus, the renal tubulointerstitium, and the posterior pole of the eye.
26 zed the expression of genes in glomeruli and tubulointerstitium in kidney biopsies from diabetic neph
28 expression was dramatically decreased in the tubulointerstitium in obstructive and aristolochic acid
32 nce Nox2 and alpha-SMA were increased in the tubulointerstitium of kidneys from 15 liver transplant r
34 ophages) were found in glomeruli but not the tubulointerstitium of the macaques inoculated with SIVma
35 , apoptotic cells were identified within the tubulointerstitium on day 3 and progressively increased
36 and Col4a3;Tsp1 DKO mice exhibited a widened tubulointerstitium, predominant lesions in Col4a3 KO kid
37 contributes to the fibrotic response in the tubulointerstitium (TI) after unilateral ureteral obstru
39 ntrast to the severe glomerular lesions, the tubulointerstitium was not involved in the disease proce
40 Renal inflammation in both glomeruli and tubulointerstitium was significantly attenuated, associa
41 1(+) T cells were localized primarily to the tubulointerstitium, whereas TGF-beta1(-)FoxP3(+)CD25(+)
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