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Recent progress in the pathophysiology and treatment of FSGS recurrence
Abstract:
Focal segmental glomerulosclerosis (FSGS) is a glomerular disease characterized by proteinuria, frequent progression to end-stage renal disease, and recurrence after kidney transplantation in ∼25% of patients, which negatively impacts long-term allograft survival. Experimental studies suggest that abnormalities in T and, possibly, B cells may represent one initial pathogenic trigger, leading to podocyte injury and progressive loss. New data also support the existence of circulating permeability factors able to damage the podocytes, but no single molecule has been consistently identified as the causal pathogenic element in FSGS recurrence. Unfortunately, major progress from mechanistic studies has not translated into substantial advancements in patient treatment, with plasmapheresis (PP) and high doses of cyclosporine (CsA) remaining the mainstays of therapy. Despite consistent experimental and clinical evidence that treatment of proteinuria slows renal function decline in proteinuric nephropathies, maximal use of antiproteinuric agents such as renin angiotensin system antagonists is not routine in the management of FSGS recurrence. More recently, encouraging results have been reported with anti-CD20 depleting antibody rituximab, but further studies are needed to establish its safety/efficacy profile.
Insights
Focal segmental glomerulosclerosis (FSGS) is a kidney disease causing proteinuria and often progressing to kidney failure. Current treatments for FSGS recurrence after transplant are limited, highlighting the need for new therapeutic strategies.
Area of Science:
- Nephrology
- Immunology
- Transplantation
Background:
- Focal segmental glomerulosclerosis (FSGS) is a leading cause of nephrotic syndrome and end-stage renal disease.
- FSGS recurrence post-kidney transplantation affects approximately 25% of patients, jeopardizing graft survival.
- Pathogenesis may involve T and B cell abnormalities or circulating permeability factors damaging podocytes.
Purpose of the Study:
- To review the current understanding of FSGS pathogenesis and recurrence.
- To evaluate existing and emerging treatment strategies for FSGS recurrence.
- To highlight the unmet need for effective therapies in FSGS.
Main Methods:
- Literature review of experimental and clinical studies on FSGS.
- Analysis of data on T and B cell roles in FSGS pathogenesis.
- Evaluation of treatment outcomes for plasmapheresis, cyclosporine, antiproteinuric agents, and rituximab.
Main Results:
- Current treatments like plasmapheresis and cyclosporine have limitations for FSGS recurrence.
- Antiproteinuric agents are underutilized despite evidence of slowing renal decline.
- Rituximab shows promise but requires further investigation for safety and efficacy.
Conclusions:
- FSGS recurrence remains a significant challenge in kidney transplantation.
- Novel therapeutic approaches are urgently needed to improve long-term allograft survival.
- Targeting immune pathways and optimizing proteinuria management are key areas for future research.
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