Introduction:
Collapsing glomerulopathy (CG) is the segmental or global collapse of the glomerular capillary walls with prominent hypertrophy and hyperplasia of overlying visceral epithelial cells, often accompanied by intracytoplasmic protein resorption droplets. The cardinal manifestations are proteinuria and renal failure. It has multiple etiologies, like drugs, infections, auto-immune diseases, and malignancies. Overall, the prognosis of CG is poor, but there is scarce data on the risk factors, outcomes, and treatment. Our aim is to analyze the clinical profile, outcomes, risk factors, and survival analysis of collapsing glomerulopathy in renal allograft recipients.
Methods:
It is a single-center observational ambi-spective study done at the Institute of Nephrology, Madras Medical College, between January 2011 and October 2022. A retrospective analysis of renal allograft recipients whose biopsies revealed collapsing glomerulopathy between 2011 and 2022 was done.
Patients were divided into two groups according to their allograft status as
1.Patients with functioning allografts
2.Patients who had allograft loss
Demographic data, clinical profile, transplant-related data, immunosuppressive regimen, graft function, viral markers, renal allograft biopsy data, and their 1-year post-CG survival were analyzed between these two groups.
Results:
Of all the renal transplant recipient biopsies, 13 were identified with collapsing glomerulopathy. All patients were males. The mean age was 31.5 ± 5.17 years, with a median presentation after 992 days of transplantation (IQR 137–1538 days). 70% (n = 9) were Live Related Renal Transplantations (LRRT), and 54% (n = 7) had no induction agent, whereas 30% (n = 4) had basiliximab and 16% (n = 2) had ATG as their induction agent. 54% (n = 7) of patients were taking tacrolimus as their choice of CNI. The median presentation creatinine was 3.8mg/dl with an IQR of 2.3 mg/dl–6 mg/dl, and 54% (n = 7) had associated rejections in their allograft biopsies. Only 2 (15%) patients had positive viral markers (1 Parvo virus and 1 CMV). All 13 patients had sustained allograft dysfunction. Among them, 70% (n = 9) had functioning allografts and 33% (n = 4) had allograft loss. On risk factor analyses among the two groups, there was no significant association of graft loss between induction agents (p = 0.472), type of transplant (p = 0.157), associated rejection (p = 0.408), and chronicity of IFTA >20% (p = 0.098). On patient survival analysis using the Kaplan-Meyer, there was no significant difference at 12 months post-collapse glomerulopathy diagnosis between the two groups.
Conclusions:
Collapsing glomerulopathy in renal allograft recipients had uniformly poor outcomes in all our patients. In most cases, the exact etiology could not be ascertained. Further research regarding the cause, risk factors, and treatment to prevent the poor outcome is essential.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.