Renal proximal tubule: phosphate handling
Target organ · NaPi-IIa / NaPi-IIc Phosphaturia
Some 80-90% of filtered phosphate is reclaimed by the sodium-phosphate cotransporters NaPi-IIa and NaPi-IIc on the proximal brush border. PTH and FGF23 both cause these transporters to be internalised and degraded, so both hormones waste phosphate in the urine.
Traced from the start
Detail
- Transporters
- Apical, sodium-driven NaPi-IIa (SLC34A1) and NaPi-IIc (SLC34A3)
- Inhibited by
- PTH and FGF23, which both internalise the transporters; also dopamine and glucocorticoids
- Measure
- The renal phosphate threshold TmP/GFR separates renal phosphate wasting from redistribution or poor intake
- Side effect of PTH here
- PTH also inhibits proximal NHE3 and bicarbonate reabsorption, which is why marked PTH excess gives a mild hyperchloraemic metabolic acidosis
When it goes wrong
Primary hyperparathyroidism
Hypophosphataemia with inappropriate phosphaturia alongside the hypercalcaemia; the low phosphate is what separates it from most other causes of hypercalcaemia
Proximal tubular injury in Fanconi syndrome (myeloma, tenofovir, ifosfamide, Wilson disease)
Phosphaturia with glycosuria, aminoaciduria and a proximal renal tubular acidosis, producing hypophosphataemic osteomalacia
Practise this structure
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