Kidney Week

Abstract: FR-PO884

Exploring Kidney Function Decline and Proteinuria in IgA Nephropathy: Insights from a Single-Center Study

Session Information

• IgA Nephropathy: Clinical, Outcomes, and Therapeutics
  October 25, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Glomerular Diseases

• 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

• Dias, Joana Pereira, Unidade Local de Saude de Vila Nova de Gaia/Espinho, Vila Nova de Gaia, Portugal

Joana Pereira Dias, MD

• Paes de Faria, Vitória Vaz da Rocha, Unidade Local de Saude de Vila Nova de Gaia/Espinho, Vila Nova de Gaia, Portugal

Vitória Vaz da Rocha Paes de Faria, MD

• Bessa, Maria Beatriz, Unidade Local de Saude de Vila Nova de Gaia/Espinho, Vila Nova de Gaia, Portugal

Maria Beatriz Bessa, MD

• Carmo, Rute, Unidade Local de Saude de Vila Nova de Gaia/Espinho, Vila Nova de Gaia, Portugal

Rute Carmo, MD

• Almeida, Clara, Unidade Local de Saude de Vila Nova de Gaia/Espinho, Vila Nova de Gaia, Portugal

Clara Almeida, MD

• Gomes, Ana Marta, Unidade Local de Saude de Vila Nova de Gaia/Espinho, Vila Nova de Gaia, Portugal

Ana Marta Gomes, MD

Background

IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis and a major cause of CKD worldwide. Reduction in proteinuria is a surrogate end point for IgAN. We aimed to assess demographic, clinical, histologic and analytic characteristics of our population and determine if there was any association with renal function decline.

Methods

Disease progression was classified as the need for dialysis initiation or doubling of creatinine by the end of follow-up. Patients with secondary IgA were excluded. Data were analyzed using parametric and non-parametric tests.

Results

Data on 26 patients were included. Results are shown in image 1. Progressors exhibited significantly lower hemoglobin, albumin and eGFR at diagnosis, and higher mean proteinuria during follow-up. At the last visit, they continued to show significantly lower hemoglobin and eGFR, and higher proteinuria. Non-progressors had higher usage of ACEi and iSGLT2. The linear regression revealed a significant association between mean proteinuria and eGFR (r = -,673, p<0,001).

Conclusion

In our study, progressors had significantly lower renal function at baseline, which could have limited the extent of our intervention. The lower levels of hemoglobin and albumin in progressors align with the expected findings given their reduced eGFR. Additionally, our study shows that progressors experienced higher proteinuria during follow-up, emphasizing the association between poorer kidney function, higher proteinuria and disease progression. Our findings underscore the significance of proteinuria as a predictor of renal function decline in IgAN, aligning with existing literature. Given the retrospective nature of our study and its inherent limitations, such as small sample size and lack of comprehensive exploration of biomarkers, determining the ideal threshold for proteinuria reduction was beyond the scope of this investigation.