IgA nephropathy in renal allograft: report of 10 cases
E.Theodoropoulou 1, E.Chaviaras 1, G.Vlachopanos 1, J.Boletis1, G.Zavvos 1,E. Patsouris 2,
H.Gakiopoulou2
1
Transplantation Unit, Laiko Hospital, Athens, Greece
2
First Department of Pathology, School of Medicine, University of Athens, Greece
Objectives IgA nephropathy in renal transplants represents in most cases recurrence of the
primary disease and less commonly de novo disease. IgA nephropathy recurrence is
reported with a frequency of 37% to 60% increasing over time. We present 10 cases of renal
transplant IgA nephropathy in relation to clinicopathological parameters.
Methods Ten renal transplant biopsies were investigated by means of light microscopy
using conventional histochemical and immunohistochemical stains and under
immunofluorescence microscopy by which a diagnosis of IgA nephropathy was made.
Results Patients’ mean age was 42.5 years and the male /female ratio was 8/2. Mean time
from renal transplantation to recurrence was 47.33 months (13 – 78months). The primary
disease was unknown in 7 patients while 2 patients had a history of IgA nephropathy and 1
patient had a history of Henoch-Shonlein purpura. All patients developed glomerular
hematuria which was the main indication for biopsy in 6 patients. In one , the main
indication was the sudden onset of proteinuria while in two, it was the deterioration of renal
function. The latter demonstrated focal segmental glomerular necroses reminiscent - in one
of them – of the lesions described in the native renal biopsy. In two cases with stable renal
function the presence of interstitial inflammation and mild tubulitis created a differential
diagnostic problem with subclinical borderline acute rejection.
Conclusions Performance of immunofluorescence in renal transplant biopsies reveals cases
of IgA nephropathy in several patients with unknown primary disease. Although in most
cases, the presence of IgA deposits does not seem to influence renal function, a proportion
of patients does exhibit renal dysfunction related to IgA nephropathy and possibly to the
severity of the disease in the native kidneys.