Collapsing and non-collapsing focal segmental glomerulosclerosis in kidney transplants

The aetiological and clinical associations of collapsing focal segmental glomerulosclerosis (cFSGS) following kidney transplantation (KTx) are poorly described. In this study, post-transplant cFSGS and non-collapsing FSGS (ncFSGS) were compared in recent KTx recipients. Evidence for intragraft viral infection was sought.

Twenty-nine cases of post-KTx FSGS were identified and classified as cFSGS (n = 10) or ncFSGS (n = 19). Biopsies were scored using Banff '97 criteria and subjected to in situ hybridization (ISH) for parvovirus B19 (pvB19), simian virus 40 (SV40) and BK virus (BKV).

cFSGS and ncFSGS patients were comparable for age, gender, weight, delayed function, human leucocyte antigen (HLA) matching, acute rejection and median time to diagnosis. Deceased donor source was more common among cFSGS cases (70 vs 32%, P = 0.05). FSGS was recurrent in 2/10 cFSGS cases compared with 8/19 ncFSGS (P = NS). cFSGS was associated with more proteinuria (11.9 vs 7.2 g/day, P = 0.05) and higher serum creatinine (4.2 vs 1.9 mg/dl, P = 0.0001) at diagnosis. Plasmapheresis was used in two out of 10 cFSGS and seven out of 19 ncFSGS cases with treatment response in 0 of two and three of seven, respectively. Graft loss was more rapid with cFSGS compared with ncFSGS (P = 0.02). Histologically, cFSGS was associated with more severe chronic vascular abnormalities. All biopsies were negative for pvB19, SV40 and BKV by ISH.

cFSGS following KTx presents with higher proteinuria, diminished renal function, more severe vascular disease and higher rate of graft loss compared with the non-collapsing form. There was no evidence for infection by pvB19 or polyomaviruses.