Abstract Background and Aims Glomerulonephritis is one of the most common causes of chronic kidney disease (CKD). Causes of glomerular diseases include lupus nephritis (LN), focal segmental glomerulonephritis (FSGS) and minimal change disease (MCD). The hallmark of CKD is renal fibrosis characterized by an imbalanced turnover of extracellular matrix (ECM) components and CKD is associated with increased inflammation. The aim for this study was to screen a biomarker panel based on extracellular matrix remodeling biomarkers as well as fibrotic activity and inflammation biomarkers. Additionally, to identify biomarkers that are differentially expressed in glomerular diseases compared to healthy and that are differently expressed between the different etiologies. Method The study included 79 healthy controls (age (median years): 35, sex (%women): 51), 48 patients with LN (age: 39, sex: 63), 13 patients with FSGS (age: 44, sex: 23), and 14 patients with MCD (age: 51, sex: 47). The following biomarkers were measured in serum and/or urine samples from all 154 subjects: • Interstitial matrix remodeling biomarkers; formation of collagen type III (PRO-C3) and VI (PRO-C6), and degradation of collagen type III (C3M). • Basement membrane remodeling biomarkers; MMP-mediated degradation of collagen type IV (C4M, C4G, TUM), laminin (LG1M) and perlecan (LG3). • Two biomarkers of fibrotic activity; acetylated N-terminal of alpha-smooth muscle actin (αSMA) and transforming growth factor β (TGF-β). • An inflammation biomarker of calprotectin (CPa9-HNE) reflecting neutrophil activity. Results Overall, all three diseases showed the same trend of change (either no change, increase or decrease compared to healthy controls) in biomarker levels. There was a significant increase of PRO-C3, PRO-C6, TUM, LG1M, αSMA, and CPa9-HNE in serum, and a significant decrease of C3M and C4M serum in patients compared to heathy controls. Four of the biomarkers were differently expressed between the different etiologies. In serum, C4G levels were significantly higher LN and MCD compared to FSGS, LG1M levels were significantly higher in LN compared to MCD, and CPa9-HNE levels were significantly higher in MCD compared to LN (all, P<0.05). In urine, TUM levels were significantly higher in LN compared to FSGS and MCD (P<0.05). Conclusion The data presented in this study indicate that both biomarkers of interstitial matrix and basement membrane remodeling as well as biomarkers of fibrotic activity and inflammation reflect the changes that take place during development of glomerular diseases. Some of these markers may be able to distinguish etiologies including the hardly differentiated diseases FSGS and MCD. This needs to be tested in larger studies.