Progressive albuminuria and glomerulosclerosis in a rat model of chronic renal allograft rejection.

摘要: A significant proportion of renal allografts fail within several months or years after transplantation, primarily because chronic rejection. The etiology and pathophysiology this condition remain unclear. We studied the function, morphology, immunohistology, in parallel, among F344-to-Lewis (n = 23) isografts 13) over course 24 weeks. Only an initial 10-day CsA (5 mg/kg/day) was given to both groups prevent acute Hypertension did not develop, although awake systolic blood pressure significantly higher at end study. Significant differences urine albumin excretion (UalbV) between were evident as early 4 weeks engraftment but rose dramatically by 20 (3.3 +/- 0.7 vs. 21.2 3.7 mg/day, respectively, P < .001). This pattern continued until conclusion study (5.0 1.1 53.5 7.6 Serum creatinine values only elevated 16 weeks, which temporally corresponded dramatic increase UalbV. However, flow glomerular filtration rate, measured paraaminohippurate inulin clearances, lower allografted organs, frequency glomerulosclerosis lesions increased kidneys correlated with UalbV values. Glomerular localization mononuclear leukocyte subsets equivalent isografts; however, numbers interstitial macrophages, CD8+, pan-T-cells all greater infiltration macrophages lymphocytes into tubulointerstitium allograft group suggests a effector cell mediation progressive abnormalities model rejection rat.