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Abstract: FR-OR35

Differentiating Steroid-Sensitive Minimal Change Disease and Primary and Secondary Focal Segmental Glomerulosclerosis: A Proteomics-Based Approach

Session Information

Category: Glomerular Diseases

  • 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix


  • Madhavan, Sethu M., The Ohio State University, Columbus, Ohio, United States
  • Almaani, Salem, The Ohio State University, Columbus, Ohio, United States
  • Shapiro, John P., The Ohio State University, Columbus, Ohio, United States
  • Satoskar, Anjali A., The Ohio State University, Columbus, Ohio, United States
  • Ayoub, Isabelle, The Ohio State University, Columbus, Ohio, United States
  • Rovin, Brad H., The Ohio State University, Columbus, Ohio, United States
  • Parikh, Samir V., The Ohio State University, Columbus, Ohio, United States

Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are common causes of nephrotic syndrome. Whether distinct molecular mechanisms are involved in the pathogenesis of MCD and FSGS remains unclear. We used proteomic studies in human kidney biopsies to characterize the differentiating molecular phenotype of steroid-sensitive MCD and primary and secondary FSGS.


Formalin-fixed paraffin-embedded kidney biopsies from patients with steroid-sensitive MCD (n=9), primary FSGS (pFSGS, n= 3), and secondary FSGS (sFSGS, n=4) were included. Patients with pFSGS had nephrotic syndrome and diffuse foot process effacement (FPE) in kidney biopsy. Patients with sFSGS were obese and had non-nephrotic range proteinuria, normal serum albumin and evidence of hyperfiltration and <80% FPE in kidney biopsy. Glomeruli were isolated using laser capture microdissection and HPLC MS/MS were performed using Orbitrap eclipse mass spectrometer. Paired t-test in the normalized data was used to compare the groups.


733 and 701 significant differentially expressed proteins were detected between MCD, and pFSGS and sFSGS respectively. Proteins regulating cell-cell and cell-matrix adhesion and differentiation (THY1, TRIP6, ACTN3, ACTN1, ITGA7, ITGB2, COL6A1, MMP9, FN1) were significantly upregulated in glomeruli of pFSGS compared to MCD. In the glomeruli of sFSGS, immune regulatory pathways predominantly from the complement system (C3, C5, C6, C8A, C8B, C8G, C9, CFHR1, CFHR5, CFH) were upregulated compared to MCD (Figure 1). FN1, EIF2AK4, MAP2K3, PHKB, INTS12, BET1 were the most significantly overexpressed proteins in pFSGS compared to MCD.


Proteomic signatures of glomeruli from primary and secondary FSGS are distinct from MCD. The differential upregulation of cell-cell, cell-matrix interacting proteins in pFSGS and immune regulatory proteins in sFSGS suggest distinct underlying pathogenic mechanisms. The causal role of novel molecules dysregulated in pFSGS compared to MCD needs to be investigated. A larger cohort of patient samples needs to be interrogated to validate the observation.


  • Clinical Revenue Support