Renal tubular reabsorption of phosphate, often reported as TmP/GFR (the tubular maximum reabsorption rate of phosphate relative to the glomerular filtration rate), was originally devised to help distinguish the cause of hypercalcemia (particularly differentiating hyperparathyroidism from other causes). Although it has largely been superseded for that purpose by intact parathyroid hormone (PTH) measurements, TmP/GFR remains clinically useful. It represents the maximum amount of phosphate the renal tubules can reabsorb per unit of filtrate, independent of the rate of phosphate entering the extracellular space or the glomerular filtration rate. This makes it superior to older indices of phosphate handling, such as the phosphate excretion index, which lack a direct physiological basis.

Serum phosphate (PO4, S)Urine phosphate (PO4, U)Serum creatinine (Cr, S)Urine creatinine (Cr, U)

Measuring TmP/GFR typically involves collecting a fasting urine sample alongside a blood sample for both phosphate and creatinine. The fractional tubular reabsorption of phosphate (TRP) can be calculated from the ratio of phosphate clearance to creatinine clearance.

Clinically, TmP/GFR can be valuable in conditions that affect phosphate regulation or renal tubular function. For instance, it helps confirm hypophosphatemic disorders such as oncogenic osteomalacia or X-linked hypophosphatemic rickets, both of which involve a reduced TmP/GFR and diminished 1,25-dihydroxycholecalciferol levels. Conversely, TmP/GFR can be elevated when phosphate influx into the extracellular compartment is low (e.g., during repletion after malnutrition). In general, a persistently low TmP/GFR indicates significant renal phosphate wasting, highlighting the need for phosphate replacement therapy. Furthermore, monitoring TmP/GFR during recovery from metabolic or toxin-induced tubular damage (as seen in Fanconi syndrome) can guide whether tubular function and intracellular phosphate stores have truly normalized.

Though TmP/GFR is no longer central in investigating calcium imbalances, it remains crucial for diagnosing and managing certain renal phosphate-handling disorders, monitoring hypophosphatemia of various causes, and distinguishing conditions that involve abnormal phosphate metabolism.

Emmens JE, de Borst MH, Boorsma EM, Damman K, Navis G, van Veldhuisen DJ, Dickstein K, Anker SD, Lang CC, Filippatos G, Metra M, Samani NJ, Ponikowski P, Ng LL, Voors AA, Ter Maaten JM. Assessment of Proximal Tubular Function by Tubular Maximum Phosphate Reabsorption Capacity in Heart Failure. Clin J Am Soc Nephrol. 2022 Feb;17(2):228-239.