In individuals with proteinuric kidney disease, the relative content of albumin to other lower-molecular-weight (LMW) proteins may provide information on the pathologic process responsible for proteinuria. Tubular lesions or excessive systemic production could account for a relative predominance of LMW proteins that normally pass across the glomerular filtration barrier and then undergo catabolism.1 By contrast, lesions in the glomerular filtration barrier may allow passage of albumin in addition to LMW proteins, with albumin predominating owing to the much higher concentration of albumin in plasma.