Collapsing Glomerulopathy (CG) is a histological entity characterized by glomerular capillary collapse, wrinkling and retraction of the glomerular basement membrane, and glomerular epithelial cell hypertrophy and hyperplasia. Podocyte injury with secondary dedifferentiation and hyperplasia is a key pathogenetic event. CG can be idiopathic or can be due to HIV, parvovirus B19, autoimmune diseases and drugs.

CG has been reported in the kidney allograft but its characteristics have not been well described. It is not clear if CG of the allograft is a distinct entity or a disease similar to idiopathic CG of native kidney.

We herein report the largest series to date of 45 kidney transplant recipients with post-transplant CG and describe their demographics, clinical, histological and laboratory data as well as their outcome. We compare these findings to those of 55 patients with idiopathic CG of their native kidneys.

Mean (±SD) age of the 45 transplant recipients was 53±15 years, compared with 35±15 for the idiopathic group (Table). All recipients were on calcineurin inhibitor-based immunosuppression and 4 subjects received sirolimus prior to biopsy. Pathological findings revealed evidence of severe vascular disease in transplant recipients as compared with idiopathic CG (Table). Nearly two-thirds had concomitant rejection on biopsy.

The median follow up after biopsy diagnosis was 28 months. Sixteen (36%) recipients lost their graft within 6 months of the biopsy diagnosis. The median survival was 12 months after the biopsy diagnosis.

Collapsing glomerulopathy of kidney allograft is probably a distinct entity as compared with idiopathic CG of native kidney. The strong association with vascular lesions suggests the possibility of chronic microvascular disease and renal ischemia as a cause of post transplant CG.

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