Table 3.
A table comparing the clinical and pre-clinical biomarkers, their AUC values and their advantages and disadvantages
| Biomarker | AUC values | Region of kidney predominantly released from | Advantages | Disadvantages | |
|---|---|---|---|---|---|
| Urinary protein concentration | Urinary albumin concentration | 0.81–0.98 | Glomerulus |
• Established marker of disease • Available in clinical laboratories • Associated with prediction of severity of nephritis |
• Only present when damage has already occurred as it is a sign of kidney damage • Albuminuria superior to proteinuria • 24-UPRO rarely performed in practice |
| 24-h urinary protein (24h-UPRO) or protein:creatinine ratio (PCR) | 0.73–0.77 | Glomerulus | |||
| Kidney injury molecule-1 (KIM-1) | 0.93 | Tubulointerstitial |
• Not expressed in other organs so very specific • Outstanding AUC • Has been suggested to correlate with IgAV-N and IgA nephropathy in the adult population where correlation with the degree of tubulointerstitial injury was also reported [31, 32] |
• May only be released due to downstream result of glomerular damage • One paper found no clear relationship • Not yet an established marker of disease • Not reported to correlate with histology |
|
| Monocyte chemoattractant protein-1 (MCP-1) | 0.83 | Glomerular |
• Reported to provide early identification of nephritis and predict histology in two papers • Associated with histology • Previously found to be associated with IgA nephropathy and lupus nephritis in adult populations |
• Not yet an established marker of disease | |
| N-Acetyl-beta-glucosaminidase (NAG) | 0.82 | Tubular | • Early identification of nephritis and predictive potential, able to correlate with histology |
• Few previous studies on IgA-mediated diseases • Not yet an established marker of disease • May only be released due to downstream result of glomerular damage |
|
| Urinary angiotensinogen (UAGT) | n/a | Glomerular and/or tubular | • May imply novel pathophysiology not previously studied |
• No AUC value to compare • Not yet an established marker of disease • If tubular involvement, may only be released due to downstream result of glomerular damage |
|