Aminoaciduria of phosphate depletion manifests at the renal brush border membrane.

Vitamin-D deficiency is associated with secondary hyperparathyroidism, hypophosphatemia, generalized aminoaciduria, phosphaturia and, late in its course, hypocalcemia. The tubulopathy has been attributed to the elevated levels of circulating parathyroid hormone. To further delineate the mechanisms responsible for aminoaciduria, vitamin-D deficiency and/or phosphate depletion were induced by placing weanling Sprague-Dawley rats on one of the following diets for 5 weeks: (1) control = 0.7% P, 5.5 micrograms % vitamin D; (2) D-P- = 0.1% P, 0 microgram % vitamin D; (3) D+P- = 0.1% P, 5.5 micrograms % vitamin D; (4) D-P+ = 0.3% P, 0 microgram % vitamin D, and (5) D-P++ = 0.7% P, 0 microgram % vitamin D. Short-term P depletion was produced in a group of animals fed D-P++ for 4 weeks, then fed D-P- for another week. To study the effects of acute supplementation with a pharmacological dose of calcitriol on the transport of amino acids by renal brush border membrane vesicles, the latter experimental group received 500 pmol of calcitriol (and is known as the SUPP group), or an equal amount of the vehicle (and is referred to as the ETH group). The uptake of taurine and proline by renal brush border membrane vesicles was blunted by 50 +/- 3 and 40 +/- 5%, respectively, at the peak of the overshoot, in all diets except D-P++. No changes were observed in vesicle size or Vmax.(ABSTRACT TRUNCATED AT 250 WORDS)