Table 1.
Biomarker | Species | Activity | Reference |
---|---|---|---|
Soluble urokinase-type plasminogen
activator receptor (SuPAR) |
Human | Elevated levels in the plasma of primary FSGS patients and in plasma and urine of transplanted patients with recurrent FSGS | [23–25] |
Still inconclusive for primary FSGS diagnosis in children | [26] | ||
Mice | Causes foot process effacement, proteinuria, and FSGS-like glomerulopathy by direct activation of podocyte integrins | [16, 27] | |
| |||
Cardiotrophin-like cytokine
factor 1 (CLC-1 ) |
Human | Elevated plasma levels in patients with recurrent FSGS, mimicking the effects of FSGS plasma on Palb. Anti-CLC-1- specific monoclonal antibody blocks the Palb effect of active FSGS sera | [4, 13] |
| |||
Transforming growth factor-beta
(TGF-β) |
Human | Circulating plasma levels correlated with other biomarkers in patients with diverse glomerulopathies | [28] |
Increased renal expression in children with FSGS | [29] | ||
Increased expression of the protein, its receptor, and associated signalling proteins in podocytes of FSGS patients | [30] | ||
In situ expression is associated with changes in extracellular matrix and podocyte apoptosis | [31] | ||
Mice | Induces podocyte apoptosis | [32] | |
| |||
Malondialdehyde | Human | Potent marker of oxidative stress-induced lipid peroxidation used in several acute and chronic kidney diseases in adults and children | [33–35] |
Elevated urine and serum levels associated with glomerular overexpression in patients with FSGS | [36, 37] | ||
Mice | Associated with reactive oxygen species overproduction in animal glomeruli mimicking human FSGS | [38] | |
| |||
Dystroglycan | Human | Differential expression between MCD and FSGS patients | [39] |
Increased expression in FSGS compared to MDC renal biopsies | [40] | ||
Rat | Serves as matrix anchor to the glomerular filtration membrane | [41] | |
| |||
Transient receptor potential cation
channel 6 (TRP6) |
Human | Fundamental component of the glomerular basement membrane. Gene mutations cause inherited glomerular diseases such as FSGS | [42, 43] |
| |||
MicroRNAs (miR-192 and miR-205) |
Human | Higher serum levels in primary FSGS than MCD patients. They correlate with the degree of interstitial fibrosis in FSGS | [44] |
Rat | They are mainly expressed in the renal cortex | [45] | |
| |||
Metalloproteinases (MMP-2 and MMP-9) and Tissue inhibitors of metalloproteinases
(TIMPs) |
Human | Elevated plasma levels associated with kidney allograft survival | [46] |
Circulating plasma levels correlated with other biomarkers in patients with diverse glomerulopathies | [28] | ||
Mice | Decreased expression in the kidneys of mice presenting glomerulonephritis | [47] | |
Rat | Reduced expression was associated with fibronectin deposition in FSGS injured glomeruli | [48] | |
| |||
Human neutrophil gelatinase-associated lipocalin (NGAL) |
Human | Increase in urine and kidney cortical tubules of patients with acute renal failure | [49–51] |
Elevated levels in the urine from children with FSGS, presenting positive correlation with urinary protein excretion but negative correlation with estimated creatinine clearance at disease diagnosis | [52] |