Abstract: TH-PO1012
Primary IgA and Membranous Nephropathies with Collapsing Glomerular Pattern: A Case Series
Session Information
- Glomerular Diseases: Minimal Change Disease, FSGS, IgAN
November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1203 Glomerular Diseases: Clinical, Outcomes, and Trials
Authors
- Souza, Rafael A. S., University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Torres, Fabio M., University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Reis, Fábio A., University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Santa Catharina, Guilherme P., University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Smolentzov, Igor, University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Cavalcante, Livia Barreira, University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Neves, Precil D., University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Dias, Cristiane B., University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Yu, Luis, University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Woronik, Viktoria, University of São Paulo (USP), São Paulo, São Paulo, Brazil
- Jorge, Lectícia, University of São Paulo (USP), São Paulo, São Paulo, Brazil
Background
The presence of collapsing pattern is often associated with severe clinical manifestations and renal impairment. These findings and its outcomes in primary Membranous (MN) and IgA (IgAN) Glomerulopathies is poorly studied. The aim of this study is to analyse the impact of collapse lesions on renal survival.
Methods
Clinical data was obtained through the analysis of medical records of patients with IgAN and MN confirmed by kidney biopsies between 2009 and 2018 at a tertiary academic center. Patients presenting collapsing glomerular pattern were investigated for APOL1 risk alleles by direct gene test (sequencing by SANGER). Increase in SCr and progression to ESRD were assessed as primary outcomes.
Results
IgAN and MN were diagnosed in 280 patients and collapsing lesions were identified in 13 samples (9 IgAN and 4 MN). The cohort included 12 patients (one patient was excluded for presenting IgAN associated with HIV infection), 9 men, mean age of 35.5 ± 11 years, 92% caucasian, 50% hypertensive, 42% required dialysis at the time of biopsy. Laboratory findings included: mean SCr 5.3 ± 4.2 mg/dL, eGFR 29.7 ± 32.6 mL/min/1.73 m2, Serum Albumin 3.1 ± 1 mg/dL, 24h proteinuria 5.2 ± 3.2 g, 83% presence of hematuria, hemoglobin 10.3 ± 2.3 g/dL and platelets 214 ± 80 x 103/mm3. The direct gene test for allele APOL1 was performed in 9 patients resulting only 1 variant of risk (APOL1 G2/G2) in a patient with IgAN. During 1 year of follow-up the mean SCr increased to 5.7 ± 4.1 mg/dL and 50% progressed to ESRD. These findings are greater than our previous IgAN cohort with 111 patients, in which a decline of eGFR of 2.3 mL/min/1,73m2/year was found.
Conclusion
We observed the presence of collapse lesions in 4.3% of the biopsies with Primary IgAN and MN and it was associated with worse renal outcomes. Although the APOL1 variant is a known factor for Collapsing Glomerulopathy, only 1 patient was found with variant of risk. Unknown predisposing factors may be involved in the collapsing pathogenesis.