Abstract
Interstitial fibrosis and tubular atrophy (IF/TA) are the most common cause of renal graft failure. Chronic transplant glomerulopathy (CTG) is present in approximately 1.5-3.0% of all renal grafts. We retrospectively studied the contribution of CTG and recurrent post-transplant glomerulopathies (RGN) to graft loss. We analyzed 123 patients with chronic renal allograft dysfunction and divided them into three groups: CTG (N = 37), RGN (N = 21), and IF/TA (N = 65). Demographic data were analyzed and the variables related to graft function identified by statistical methods. CTG had a significantly lower allograft survival than IF/TA. In a multivariate analysis, protective factors for allograft outcomes were: use of angiotensin-converting enzyme inhibitor (ACEI; hazard ratio (HR) = 0.12, P = 0.001), mycophenolate mofetil (MMF; HR = 0.17, P = 0.026), hepatitis C virus (HR = 7.29, P = 0.003), delayed graft function (HR = 5.32, P = 0.016), serum creatinine > or =1.5 mg/dL at the 1st year post-transplant (HR = 0.20, P = 0.011), and proteinuria > or =0.5 g/24 h at the 1st year post-transplant (HR = 0.14, P = 0.004). The presence of glomerular damage is a risk factor for allograft loss (HR = 4.55, P = 0.015). The presence of some degree of chronic glomerular damage in addition to the diagnosis of IF/TA was the most important risk factor associated with allograft loss since it could indicate chronic active antibody-mediated rejection. ACEI and MMF were associated with better outcomes, indicating that they might improve graft survival.
Highlights
The terminology “interstitial fibrosis and tubular atrophy (IF/TA) with no evidence of any specific etiology” recently replaced “chronic allograft nephropathy”, and is used to describe biopsies with fibrosis and atrophy and with no obvious underlying pathogenesis [1]
Even though serum creatinine levels did not differ among groups at the time of the biopsy, the chronic transplant glomerulopathy (CTG) group had higher serum creatinine levels (2.3 ± 1.7 mg/dL) compared to the recurrent post-transplant glomerulonephritis (RGN) (1.6 ± 0.5 mg/dL) and Interstitial fibrosis and tubular atrophy (IF/TA) groups (1.9 ± 0.6 mg/dL)
There is extensive evidence that incipient histological changes characteristic of IF/TA can be visualized in the allograft before the transplant function deteriorates and the serum creatinine level is not the best predictor for renal allograft dysfunction in the early stages [13,14,15,16]
Summary
The terminology “interstitial fibrosis and tubular atrophy (IF/TA) with no evidence of any specific etiology” recently replaced “chronic allograft nephropathy”, and is used to describe biopsies with fibrosis and atrophy and with no obvious underlying pathogenesis [1]. The incidence of chronic transplant glomerulopathy (CTG) is about 1.5-3% of all renal grafts [3,4,5]. According to Banff 09 criteria [6], CTG, called in this classification “chronic active antibody-mediated rejection” is characterized by C4d positive staining, the presence of circulating antidonor antibodies, morphologic evidence of chronic tissue injury, such as glomerular double contours and/or peritubular capillary basement membrane multilayering and/ or interstitial fibrosis/tubular atrophy and/or fibrous intimal thickening in arteries. The pathogenesis of CTG is not clear [3] It has been associated with circulating anti-donor human leukocyte antigen (HLA) antibodies and the deposition of the complement split product C4d in the peritubular capillaries suggesting antibody-mediated injury [7,8,9]. It has been suggested that the same immune process that causes
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