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1 and the hamsters that survived showed severe tubulointerstitial nephritis.
2 some forms of immunologically mediated human tubulointerstitial nephritis.
3 nt of the changes characteristically seen in tubulointerstitial nephritis.
4 k accuracy for diagnosing histological acute tubulointerstitial nephritis.
5 et to attenuate fibrosis after toxin-induced tubulointerstitial nephritis.
8 polyendocrine syndrome type 1 who developed tubulointerstitial nephritis and ESRD in association wit
9 ains, develop ESRD associated with prominent tubulointerstitial nephritis and fibrosis within 3 month
10 ic interstitial nephropathy characterized by tubulointerstitial nephritis and formation of enlarged n
11 ed glomerular filtration rate (GFR), chronic tubulointerstitial nephritis and ultrastructural changes
16 80%) carried the diagnosis of FSGS, 2 (6.7%) tubulointerstitial nephritis, and 1 (3.3%) nephrolithias
19 467 aa was 46% identical with that of human tubulointerstitial nephritis antigen (TIN-ag), and there
21 therapeutic delivery of the secreted protein Tubulointerstitial nephritis antigen-like 1 (Tinagl1) su
22 he pathogenesis of leukocyte infiltration in tubulointerstitial nephritis associated with glomerular
23 s of monocyte/macrophage infiltration in the tubulointerstitial nephritis associated with PAN nephros
25 h worse renal prognosis, whereas concomitant tubulointerstitial nephritis-causing medications and tre
26 athy is characterized by rapidly progressive tubulointerstitial nephritis culminating in end-stage re
29 from infantile polycystic kidneys to chronic tubulointerstitial nephritis, fibrosis, and cortical mic
31 s affected with isolated kidney failure (and tubulointerstitial nephritis in individuals with availab
32 ficant histological changes corresponding to tubulointerstitial nephritis including interstitial infl
33 trogen levels, more severe histologic GN and tubulointerstitial nephritis, increased glomerular cresc
35 phronophthisis (NPH), an autosomal-recessive tubulointerstitial nephritis, is the most common cause o
37 ur clinical tests accurately predicted acute tubulointerstitial nephritis on biopsy in two separate p
38 y injury (AKI), glomerulonephritis (GN), and tubulointerstitial nephritis (TIN) and assessed dispropo
41 nterior chamber inflammation and evidence of tubulointerstitial nephritis with either (1) a positive
42 a 36-year-old man with AIDS showed a severe tubulointerstitial nephritis with intranuclear inclusion
43 for immune and genetic causes of microcystic tubulointerstitial nephritis with little attention to it
44 ted animals showed renal dysfunction and had tubulointerstitial nephritis with nuclear inclusions, ap
45 2, 21.1%), infectious uveitis (6/52, 11.5%), tubulointerstitial nephritis with uveitis (6/52, 11.5%),