The regulation of RBF and GFR is essential to understanding renal physiology during mammalian development. Without this knowledge, clinical judgment regarding overall renal function in human neonates, especially those considered high risk, is reduced to guesswork. The plethora of reports in which assessment of RBF and GFR were attempted have provided a legacy purporting the neonatal kidney as immature, inadequate and dysfunctional--nothing could be farther from the truth. Our failure to understand kidney function in the neonate does not justify shifting the blame for unwanted disturbances in fluid and electrolyte balance, metabolic acidosis, and azotemia to a small kidney. After a critical stage of renal development has been reached, subsequent changes in RBF and GFR are only quantitatively different from the adult kidney.