2020
DOI: 10.5414/cn110059
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Resolution of IgA and C3 immune deposits in Staphylococcus infection-associated glomerulonephritis in a kidney transplant recipient

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Cited by 4 publications
(5 citation statements)
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“…In addition, only 11 cases of IRGN in allograft kidneys were reported in 2014 [4]. Except for streptococcal organisms, the etiology of these infections has been diverse in most cases [5][6][7][8][9][10][11]. The etiology of the infection in this case was unclear despite frequent culture tests; however, the presence of infection in his right lower leg was definitely evident.…”
Section: Discussionmentioning
confidence: 82%
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“…In addition, only 11 cases of IRGN in allograft kidneys were reported in 2014 [4]. Except for streptococcal organisms, the etiology of these infections has been diverse in most cases [5][6][7][8][9][10][11]. The etiology of the infection in this case was unclear despite frequent culture tests; however, the presence of infection in his right lower leg was definitely evident.…”
Section: Discussionmentioning
confidence: 82%
“…In contrast, the tubulointerstitial changes, such as the infiltration of T cells and macrophages, the positive staining for α-SMA (myofibroblast infiltration), and the interstitial fibrosis, were observed with persistence or exacerbation, which may have led to the development of the severe IFTA and the clinical progression to ESKD. Similarly, Nguyen et al pointed out the importance of interstitial changes in allograft IRGN in ESKD progression [11]. The prognostic relevance of the tubulointerstitial infiltration of T cells and macrophages has also been reported in other forms of glomerulonephritis in native kidneys, such as IgA nephropathy [15].…”
Section: Discussionmentioning
confidence: 92%
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“…The key to differentiate from C3G is that complement C3 in C3G often decreases continuously, while the decrease of C3 level in patients with staphylococcal infection associated glomerulonephritis is often temporary. With the control of infection and the improvement of disease condition, C3 level can return to normal [18,22] . In this case, there is no direct evidence that C3GN is caused by infection, despite an interesting phenomenon that with the remission of urinary tract infection symptoms, complement C3 increased, but whether there is a direct relationship between chronic infection of Gram-negative bacteria and C3GN with a CD46 variation is still uncertain.…”
Section: Discussionmentioning
confidence: 99%