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Abstract: PO1894

Differentiating Focal and Segmental Glomerulosclerosis

Session Information

Category: Glomerular Diseases

  • 1203 Glomerular Diseases: Clinical, Outcomes, and Trials

Authors

  • Santos, Afonso, Nephrology Department, Hospital Professor Doutor Fernando Fonseca EPE, Lisboa, Portugal
  • Lima, Anna, Nephrology Department, Hospital Professor Doutor Fernando Fonseca EPE, Lisboa, Portugal
  • Gaspar, Ana, Nephrology Department, Hospital Professor Doutor Fernando Fonseca EPE, Lisboa, Portugal
  • Brás, Ana Catarina, Nephrology Department, Hospital Professor Doutor Fernando Fonseca EPE, Lisboa, Portugal
  • Pereira Campos, Pedro, Nephrology Department, Hospital Professor Doutor Fernando Fonseca EPE, Lisboa, Portugal
  • Theias Manso, Rita, Pathology Department, Hospital Professor Doutor Fernando Fonseca EPE, Lisboa, Portugal
  • Soto, Karina, Nephrology Department, Hospital Professor Doutor Fernando Fonseca EPE, Lisboa, Portugal
Background

FSGS is a histological pattern of kidney injury associated to broad causes and pathogenesis. FSGS can be primary, genetic or secondary to other conditions. Differentiating these subclasses is crucial for management and prognosis, but there is no biomarker for it and genetic testing is not suitable for all patients. Herein, we present a series of patients with FSGS classification based on clinical and histological criteria comparing outcomes.

Methods

In a retrospective analysis of 359 kidney biopsies were identified patients with FSGS histological diagnosis.Primary and secondary FSGS were identified based on clinical and histological data.Genetic FSGS was considered if they present at least one of the following:a)nephrotic syndrome (NS) resistant to corticosteroids;b)NS with normal serum albumin;c)NS with focal foot process effacement or d)non-nephrotic proteinuria with diffuse foot process effacement.Each group was divided in immunosuppression treatment (IST) or only supportive treatment (ST) groups.Renal and survival outcomes were assessed.

Results

Among 66 FSGS patients, 65% were males, 71% non-black, 74% had HTN, 26% diabetes; median eGFR 26.5mL/min/1.73m2 (IQR 15.3-48.8), 24h-UProt 4.4g (IQR 2.5-7.6). Globally, 38% (n=25) progressed to ESKD and mean time to RRT was longer in IST group (p=0.37).According to the applied criteria 52% (n=34) were classified as having secondary FSGS, 23% (n=15) primary and 25% (n=17) as genetic FSGS.Among primary FSGS patients 40% received IST.In ST group 25% progressed to ESKD in a median time to RRT of 24 months (SD±31.7) vs 13% in 66mo (SD±93.3) in IST group.Among secondary FSGS, 17.6% received IST.Of them, 50% developed ESKD in 31.7mo (IQR SD±28.6) vs ST group with 46% progression to ESKD in 12mo (SD±28.7).From the genetic group 59% were in IST group and 30% progressed to ESKD in 12mo (SD±27.1) vs ST group with 29% ESKD in 42mo (SD±27.1).

Conclusion

FSGS etiology is not straightforward in most patients. Since IST can be inappropriate and potentially harmful in some FSGS subclasses, it is crucial to identify patients who are likely to benefit from such therapies, in order to obtain better outcomes. Most of genetic forms of FSGS do not respond to IST and have a rapid progression to ESKD. Therefore, in a suspicion of a genetic cause a genetic screening should be performed for appropriate management.