Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26617864
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Clinicopathological significance of CD206-positive macrophages in patients with
acute tubulointerstitial disease
#MMPMID26617864
Li J
; Liu CH
; Xu DL
; Gao B
Int J Clin Exp Pathol
2015[]; 8
(9
): 11386-92
PMID26617864
show ga
OBJECTIVE: To investigate the clinicopathological significance of CD206-positive
macrophage expression in patients with acute tubulointerstitial disease,
including acute tubular necrosis (ATN) and acute interstitial nephritis (AIN).
METHODS: Renal tissue samples from patients with ATN (n=10), AIN (n=10), and
minimal change disease (MCD, as disease control, n=8) as well as tissue from
normal control kidneys (negative control, n=3) were included in this study. The
expression of CD206 and CD68 in renal tissues was detected by
immunohistochemistry or immunofluorescence. RESULTS: CD206-positive cells
accumulated in areas around damaged tubular cells and regenerating tubules.
Compared with AIN patients, ATN patients had lower serum albumin, lower
proteinuria, lower urinary osmolality and higher plasma hemoglobin, (P=0.002;
P=0.01; P<0.001; P=0.002, respectively). CD206-positive cells could also be
observed in the tubular basement membrane and tubule lumen. Some CD206-positive
cells infiltrated into the tubular cells in patients with AIN. Compared to
patients with ATN, patients with AIN had more CD206-positive cells (P=0.005). In
the ATN patients, there were more CD206-positive cells in ischemic tissue.
CD206-positive cells were negatively correlated with hemoglobin (r=-0.565,
P=0.009) and positively correlated with serum albumin (r=0.496, P=0.026), urinary
osmolality (r=0.567, P=0.009) and proteinuria (r=0.460, P=0.041). There was no
correlation between CD206-positive cells and eGFR. CONCLUSION: CD206-positive
macrophages are involved in the pathogenesis of acute tubular necrosis and acute
interstitial nephritis.