LCN2 and glomerulonephritis: Several publications demonstrate that podocytes could express NGAL under inflammation, which is another possible source of sNGAL [7]; however, IHC results from the present study suggest most staining of NGAL is still in the tubular area, and not glomeruli, which is consistent with the results from anti-GBM glomerulonephritis in rodents where NGAL is expressed in tubular interstitium.