Emerging affinity-based proteomic approaches have been applied to kidney disease research, with the goal to identify markers and mediators of disease.1 However, to what extent perturbations in blood protein levels are attributable to the underlying estimated glomerular filtration rate (eGFR) is unclear. In a prior study, we measured 1,305 proteins in paired arterial and renal venous human plasma samples obtained via invasive cathterization.2 In this proof-of-concept analysis, proteins known to be cleared by the kidney, such as cystatin C, demonstrated a significant reduction from artery (A) to renal vein (V), with a V/A ratio1, consistent with net release by the kidney.