Kidney Week

Abstract: PUB318

Urine Proteomics of Primary vs. Secondary Focal Segmental Glomerulosclerosis: Is There a Potential Noninvasive Urine Biomarker?

Session Information

• Publication Only

Category: Glomerular Diseases

• 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology

Authors

• Russo, Ilario, Mayo Clinic Division of Nephrology and Hypertension, Rochester, United States

Ilario Russo, MD

• Bobart, Shane A., Houston Methodist, Houston, Texas, United States

Shane A. Bobart, MD, FASN

• Mekraksakit, Poemlarp, Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States

Poemlarp Mekraksakit, MD

• Vargas-Brochero, Maria Jose, Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States

Maria Jose Vargas-Brochero, MD, MS, MSc

• Krisanapan, Pajaree, Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States

Pajaree Krisanapan, MD

• Nava Chavez, Coraima Claudia, Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States

Coraima Claudia Nava Chavez, DrMed, MSc

• Charlesworth, Cristine, Mayo Clinic Minnesota, Rochester, Minnesota, United States

Cristine Charlesworth, PhD

• Madden, Benjamin J., Mayo Clinic Minnesota, Rochester, Minnesota, United States

Benjamin J. Madden

• Sethi, Sanjeev, Mayo Clinic Department of Laboratory Medicine and Pathology, Rochester, Minnesota, United States

Sanjeev Sethi, MD, PhD

• Fervenza, Fernando C., Mayo Clinic Division of Nephrology and Hypertension, Rochester, Minnesota, United States

Fernando C. Fervenza, MD, PhD, FASN

Background

Focal Segmental Glomerulosclerosis (FSGS) is a histological pattern of glomerular injury. It is classified into primary, secondary and genetic, each requiring distinct management. No reliable biomarkers can distinguish among them. We evaluated urine protein profile among a cohort of patients phenotyped as presumed primary, genetic or secondary FSGS to see if this could further differentiate these patients.

Methods

21 patients with an FSGS lesion were classified as primary, secondary, or genetic FSGS using a clinico-pathological approach (De Vriese 2017). Primary was defined as serum albumin (SA) <3.5 g/dL, proteinuria >3.5g/24h, and diffuse foot process effacement (FPE; >80%). Secondary FSGS was defined as SA >3.5 g/dL, and segmental FPE, regardless of proteinuria. Genetic was defined by the presence of a disease-causing mutation (NPHS2, n= 3, COL4A, n=3, both MYO1E and ITGB4 mutation, n=1). Each group included 7 patients. Total protein concentration for each sample was determined by bicinchoninic acid assay, and 9 ug of protein from each sample was separated by SDS- PAGE. Baseline characteristics are shown in Table 1.

Results

SDS page gel urinary proteomics showed proteins with MW from 250 to 10 (kDa) with the majority of protein running as a 66.5 kDa band compatible with albumin. However, there were no observable differences in any molecular fraction that could help to differentiate patients with primary, secondary or genetic forms of FSGS.

Conclusion

Our analysis indicates that the urine proteomic profile does not provide additional information regarding the underlying cause of the FSGS lesion nor has the ability to differentiate different forms of FSGS.

Table 1.

Figure 1.