Etiological analysis of graft dysfunction following living kidney transplantation: a report of 366 biopsies

Abstract

Aim: The aim of this study is to investigate the clinical features of graft dysfunction following living kidney transplantation and to assess its causes.Methods: We retrospectively analyzed a series of 366 living kidney transplantation indication biopsies with a clear etiology and diagnosis from July 2003 to June 2016 at our center. The classifications and diagnoses were performed based on clinical and pathological characteristics. All biopsies were evaluated according to the Banff 2007 schema.Results: Acute rejection (AR) occurred in 85 cases (22.0%), chronic rejection (CR) in 62 cases (16.1%), borderline rejection (BR) in 12 cases (3.1%), calcineurin inhibitor (CNI) toxicity damage in 41 cases (10.6%), BK virus-associated nephropathy (BKVAN) in 43 cases (11.1%), de novo or recurrent renal diseases in 134 cases (34.7%), and other causes in nine cases (2.3%); additionally, 20 cases had two simultaneous causes. The 80 cases with IgA nephropathy (IgAN) had the highest incidence (59.7%) of de novo or recurrent renal diseases. After a mean ± SD follow up of 3.7 ± 2.3 years, the 5-year graft cumulative survival rates of AR, CR, CNI toxicity, BKVAN, and de novo or recurrent renal diseases were 60.1%, 31.2%, 66.6%, 66.9%, and 67.1%, respectively.Conclusions: A biopsy is helpful for the diagnosis of graft dysfunction. De novo or recurrent renal disease, represented by IgAN, is a major cause of graft dysfunction following living kidney transplantation.

Graft failure of IgA nephropathy in renal allografts following living donor transplantation: predictive factor analysis of 102 biopsies

“…The widespread use of effective immunosuppression has markedly reduced the risk of graft failure due to rejection in recent years [1] . Conversely, de novo or recurrent renal disease has become a major cause of graft dysfunction, which was confirmed in our previous study [2] , and it is the second leading cause of death-censored graft failure and the third leading cause of uncensored graft failure [3,4] .…”

Graft failure of IgA nephropathy in renal allografts following living donor transplantation: predictive factor analysis of 102 biopsies

“…We found that IgAN occurred frequently within 5 years postoperatively and then declined sharply in subsequent years, which was consistent with a previous report [18] . Few patients diagnosed with IgAN in renal allografts showed a remarkable increased sCr level when accepted biopsy [2] , as reported in previous study on IgAN in renal allografts, it had little impact on graft function in the early years after transplantation [19] , but Ortiz et al [20] found that the histopathological injury was not accompanied by abnormalities in the urinalysis in half of early recurrent IgAN patients. Therefore, the disease progression could be concealed, a protocol biopsy was recommended to prevent missed diagnoses, especially in clinically silent patients.…”

Graft failure of IgA nephropathy in renal allografts following living transplantation: predictive factor analysis of 102 biopsies

“…in total series, 27 cases without complete ultrasonic data 2. the baseline level at the time when patients had the lowest sCr level after transplantation, the same…”

“…Predictive factors related to graft failure of IgAN in renal allografts calcineurin inhibitor; BKVAN, BK virus-associated nephropathy 1 the time from onset of initial symptoms to biopsy. 2 the eGFR at the time of the biopsy. The time from transplantation to IgAN in renal allografts.…”

“…We found that it occurred frequently within 5 years postoperatively and then declined sharply in subsequent years, which was consistent with a previous report [18] . Most patients diagnosed with IgAN in renal allografts accepted a biopsy for initial asymptomatic hematuria and/or mild proteinuria, whereas few patients accepted a biopsy for an increased sCr level, which was contrary to the rejection and CNI toxicity [2] . As reported in previous study on IgAN in renal allografts, it had little impact on graft function in the early years after transplantation [19] , but Ortiz et al [20] found that the histopathological injury was not accompanied by abnormalities in the urinalysis in half of early recurrent IgAN patients.…”