Regulation of Phosphate Excretion

  • Because phosphate is not secreted by the tubule, the rate of renal phosphate excretion is ultimately determined by the balance between its rate of glomerular filtration and tubular resorption. Because the rate of glomerular filtration is maintained at a fairly constant level, specific regulation of phosphate excretion is principally achieved by modulation of its tubular resorption rate. Below we summarize the mechanisms by which the tubule resorbs phosphate and how these processes are regulated.
  • Phosphate resorption only occurs in the proximal tubule and any phosphate remaining in the tubular fluid after this segment is excreted in the urine. Luminal resorption of phosphate occurs via Sodium-Phosphate symporters and is powered by secondary active transport through the inward electrochemical gradient for sodium generated by the basolateral NaK ATPase.
  • An important feature of these sodium-phosphate symporters is their limited transport capacity which can become overwhelmed at high concentrations of tubular phosphate. Once the symporter's transport capacity is exceeded, any remaining unresorbed phosphate passes through the proximal tubule and is excreted. This "Transport Maximum" phenomenon can be thought of as an effective autoregulatory mechanism that allows for increased urinary phosphate excretion when ECF phosphate levels become excessive.
  • In addition, the transport capacity of the sodium-phosphate symporter is subject to hormonal regulation. Parathyroid Hormone (PTH) appears to reduce the symporter's transport capacity, thus decreasing the transport maximum threshold, and in turn resulting in phosphate excretion at lower tubular concentrations. By modulating the concentration at which the tubule begins to excrete phosphate, PTH can act as an important regulator of ECF phosphate concentration.