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.

Keywords: IgA nephropathy; Living kidney transplantation; biopsy; graft dysfunction; rejection.

Figure 1.

To investigate the causes of graft dysfunction, this series included patients with repeated indication biopsies, but excluded protocol biopsies and repeated indication biopsies with the same diagnosis. Additionally, biopsy results without a clear etiology and clinical diagnosis were excluded, such as chronic changes without evidence of any specific etiology (category 5 or 6 in Banff 2007).

Figure 2.

The incidence of various causes in different clinical settings. AR was established within the first year after transplantation and then declined sharply in the following years. The peak incidence of BKVAN occurred within 1–2 years postoperatively. FSGS occurred more frequently within the first year and nearly 10 years postoperatively. IgAN, CR, and CNI toxicity damage occurred similarly in each year.