Renal Tubular Sites of Altered Calcium Transport in Phosphate-depleted Rats

Kai Lau; Zalman S. Agus; Martin Goldberg; Stanley Goldfarb

doi:10.1172/JCI109630

Renal Tubular Sites of Altered Calcium Transport in Phosphate-depleted Rats

Kai Lau, Zalman S. Agus, Martin Goldberg, and Stanley Goldfarb

Published December 1, 1979 - More info

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Abstract

Increased calcium (Ca) excretion is characteristic of chronic phosphate (PO₄) depletion (PD). To study the changes in tubular transport and the site of the hypocalciuric effect of PO₄ administration, clearance and micropuncture experiments were performed in intact rats pair fed either a control diet (0.5% PO₄) or a PO₄-depleted (PD) diet (0.01% PO₄) plus Al(OH₃) and in parathyroidectomized (PTX) PD rats, infused either with saline or with neutral sodium PO₄.

Intact PD rats, compared with intact rats on a control diet, exhibited a lower plasma ultrafiltrable (UF) PO₄ (5.8±0.5 vs. 7.8±0.3 mg/dl), higher fractional excretion (FE) of Ca (4.1±1.2 vs. 0.6±0.1%), and reduced FE PO₄ (0.1±0.01 vs. 10.2±1.8%). Tubular fluid/plasma inulin was lower in the late proximal tubule of PD rats, associated with increases in fractional delivery (FD) from the proximal tubule of Na and Ca.

The%FD of Ca to the early distal tubule of PD rats was increased (20±3 vs. 11±2%), but this difference was abolished by the late distal tubule (5.1±1.2 vs. 3.3±0.9%). In PTX-PD rats, PO₄ infusion increased plasma UF PO₄ (13.8±0.7 vs. 7.8±0.7 mg/dl). FE of Ca was reduced (1.08±0.35 vs. 4.59±1.57%) without correcting the increased Ca delivery to the late distal tubule.

These data indicate that PD impairs Ca reabsorption in tubular segments before but not within the distal convoluted tubule, so that hypercalciuria is ultimately a result of decreased Ca transport either in the terminal nephron or in deeper nephrons where PO₄ infusion stimulates Ca transport independent of parathyroid hormone or changes in the filtered load of Ca.