Objective      To investigate the relationship between peritubular capillary (PTC) loss and tubule injury

proliferation and repair in aristolochic acid-induced nephropathy mice.       Methods      Forty male C57BL/6J mice were randomly divided into two groups

a control group and an AA group (

n

=10). The AA group was intraperitoneally injected with aristolochic acid (AA) dissolved in phosphate-buffered saline at a

dose of 5 mg/kg per day for up to 7  or 9 d

while the control group received saline injection only. Blood

urine and kidneys of ten mice in each group were collected for tubular injury evaluation using a semi-quantitative scale

quantification of peritubular capillary loss (CD34 immunohistochemistry staining) and proliferation (PCNA immunohistochemistry staining) of tubule principally. Furthermore

the correlations between PTC loss and both of tubular injury and proliferation in the cortex

cortex-medulla junction and medulla of kidney were analyzed.       Results      The tubule injury score [2.02±0.81 (7 d)

2.82±1.31 (9 d)

]

PTC loss [22.47±20.62 (7 d)

40.00±23.50 (9 d)

]

and positive expression of PCNA [3.31±2.14 (7 d)

1.30±1.07 (9 d)

]

of the AA group were significantly higher than those of the control group. Moreover

the tubule injury score and PTC loss were maximum in the cortex

less higher in the cortex-medulla junction and minimum in the medulla. The positive expression of PCNA of day 9 group was significantly less than that of day 7 group. The PCNA-positive cells in the cortex of day 7 group and day 9 group were both less than those in the cortex-medulla junction. PTC loss was correlated with the lesion of tubule (positively) and the expression level of PCNA (negatively) in the cortex and cortex-medulla junction

with a more predominant correlation in the cortex than in the cortex-medulla junction.       Conclusion      The damage of PTC is significantly correlated with progressive lesion of tubule and inhibition of remodeling in aristolochic acid nephropathy. The PTC loss may be the key reason for the progression of aristolochic acid nephropathy.