Renal tubular reabsorption of calcium in familial hypocalciuric hypercalcaemia

1986 ◽  
Vol 112 (4) ◽  
pp. 541-546 ◽  
Author(s):  
J. H. Kristiansen ◽  
J. Brøchner-Mortensen ◽  
K. O. Pedersen

Abstract. To investigate the nephron site of the enhanced tubular calcium reabsorption in familial hypocalciuric hypercalcaemia (FHH), the renal plasma clearance of lithium and calcium and the glomerular filtration rate were determined simultanously after an overnight fast in nine FHH patients and ten healthy controls. As the renal plasma clearance of lithium equals the rate of the proximal tubular fluid delivered into the thin descending loop of Henle's loop, the reabsorption of calcium in the proximal and distal tubule, respectively, could be calculated. We found that the FHH patients had a significantly higher fractional calcium reabsorption in the proximal tubule (77.6 ± 4.7 (%) vs 73.3 ± 3.1, P < 0.05). The same held true for the absolute proximal calcium reabsorption (1.49 ± 0.12 (mmol/l) vs 1.07 ± 0.05, P < 0.001). There was a significant linear correlation between the increased tubular capacity for calcium reabsorption and the absolute proximal calcium reabsorption (r = 0.70, P < 0.05). The distal tubular calcium reabsorption did not differ in the two groups. Our results therefore suggest that the enhanced tubular calcium reabsorption in FHH takes place exclusively in the proximal renal tubule.

1990 ◽  
Vol 123 (2) ◽  
pp. 194-202 ◽  
Author(s):  
Jan H. Kristiansen ◽  
Jens Brøchner-Mortensen ◽  
Kaj O. Pedersen ◽  
Søren Jensen ◽  
Torben Glud

Abstract. Nine patients with primary hyperparathyroidism were studied to investigate the renal tubular reabsorption of calcium and sodium. Fasting serum and urine samples were analysed, and the glomerular filtration rate and the renal plasma clearance of lithium were determined simultaneously. Comparison was made with 9 ageand sex-matched normocalcemic controls. In the proximal tubule, there was a significantly higher absolute reabsorption of calcium in patients than in controls, whereas the fractional reabsorption rate of calcium did not differ between the two groups. In the distal tubule, the absolute calcium reabsorption rate was significantly higher in the patients, whereas the fractional reabsorption rate of calcium was significantly lower than in controls. In the patient group there was a significantly positive linear correlation between the increased tubular capacity for calsium reabsorption and the absolute proximal calcium reabsorption rate, but not between the increased capacity and the absolute distal calcium reabsorption rate. No significant differences were found in the renal tubular handling of sodium between patients and controls. Our results suggest that the increased capacity for tubular calcium reabsorption in primary hyperparathyroidism mainly is localized in the proximal tubule, and that the renal tubular handling of calcium and sodium in this disease differs from that in familial hypocalciuric hypercalcemia.


1976 ◽  
Vol 51 (4) ◽  
pp. 345-351 ◽  
Author(s):  
R. A. L. Sutton ◽  
N. L. M. Wong ◽  
J. H. Dirks

1. The effect of purified bovine parathyroid hormone on renal tubular reabsorption of sodium and calcium has been studied by micropuncture in intact and recently thyroparathyroidectomized dogs. 2. Parathyroid hormone increased the rejection of sodium and calcium proportionately at the late proximal tubule in both intact and operated dogs. 3. In both groups of dogs, there was increased delivery of sodium and calcium to the distal tubule after the hormone. However, the Ca/Na ratio decreased, suggesting some selective enhancement of calcium reabsorption before the superficial distal puncture site. 4. In the final urine, the Ca/Na ratio decreased highly significantly in both groups of dogs, indicating a further selective effect of parathyroid hormone on calcium reabsorption in or beyond the distal convoluted tubule.


1963 ◽  
Vol 204 (5) ◽  
pp. 771-775 ◽  
Author(s):  
William E. Lassiter ◽  
Carl W. Gottschalk ◽  
Margaret Mylle

Anesthetized rats and hamsters were given Ca45 intravenously, and fluid was subsequently collected by micropuncture from glomeruli and surface tubules in the rats, and from loops of Henle in the hamsters. In nondiuretic animals, fluid:plasma calcium ratios averaged 0.71 in the glomerulus; 0.76 in the proximal tubule; 2.0 in the loop of Henle; 0.47 in the distal convolution; and 0.9 in ureteral urine. In mannitol diuresis, the calcium ratio of glomerular fluid was unchanged, but ratios as low as 0.21 were noted in the proximal tubule. In this circumstance, the average proximal ratio was 0.61, and the distal ratio 0.07. These results indicate active transport of calcium out of all major parts of the nephron, with the bulk of calcium reabsorption occurring in the convoluted portion of the proximal tubule. Furthermore, the pattern of tubular reabsorption of calcium is similar to that of sodium, suggesting that the two are related.


2013 ◽  
Vol 305 (8) ◽  
pp. F1132-F1138 ◽  
Author(s):  
Kevin K. Frick ◽  
John R. Asplin ◽  
Nancy S. Krieger ◽  
Christopher D. Culbertson ◽  
Daniel M. Asplin ◽  
...  

The inbred genetic hypercalciuric stone-forming (GHS) rats exhibit many features of human idiopathic hypercalciuria and have elevated levels of vitamin D receptors (VDR) in calcium (Ca)-transporting organs. On a normal-Ca diet, 1,25(OH)2D3 (1,25D) increases urine (U) Ca to a greater extent in GHS than in controls [Sprague-Dawley (SD)]. The additional UCa may result from an increase in intestinal Ca absorption and/or bone resorption. To determine the source, we asked whether 1,25D would increase UCa in GHS fed a low-Ca (0.02%) diet (LCD). With 1,25D, UCa in SD increased from 1.2 ± 0.1 to 9.3 ± 0.9 mg/day and increased more in GHS from 4.7 ± 0.3 to 21.5 ± 0.9 mg/day ( P < 0.001). In GHS rats on LCD with or without 1,25D, UCa far exceeded daily Ca intake (2.6 mg/day). While the greater excess in UCa in GHS rats must be derived from bone mineral, there may also be a 1,25D-mediated decrease in renal tubular Ca reabsorption. RNA expression of the components of renal Ca transport indicated that 1,25D administration results in a suppression of klotho, an activator of the renal Ca reabsorption channel TRPV5, in both SD and GHS rats. This fall in klotho would decrease tubular reabsorption of the 1,25D-induced bone Ca release. Thus, the greater increase in UCa with 1,25D in GHS fed LCD strongly suggests that the additional UCa results from an increase in bone resorption, likely due to the increased number of VDR in the GHS rat bone cells, with a possible component of decreased renal tubular calcium reabsorption.


1985 ◽  
Vol 69 (5) ◽  
pp. 625-630 ◽  
Author(s):  
Norman L. M. Wong ◽  
Roger A. L. Sutton ◽  
Viroon Mavichak ◽  
Gary A. Quamme ◽  
John H. Dirks

1. The effect of acute potassium infusion on renal tubular reabsorption of potassium by magnesium-deficient and pair-fed control rats has been studied by the recollection micropuncture method. 2. During potassium chloride infusion, the amount of potassium remaining in the distal tubule is lower in magnesium-deficient than in pair-fed rats. This could be due to a reduction in potassium secretion or to an enhancement of potassium reabsorption. 3. The present study demonstrates enhanced renal potassium retention in the magnesium-deficient rat, and is in contrast to previous reports of renal potassium wasting in this circumstance.


1975 ◽  
Vol 229 (1) ◽  
pp. 200-205 ◽  
Author(s):  
GA Quamme ◽  
NL Wong ◽  
RA Sutton ◽  
JH Dirks

Sodium and calcium are normally reabsorbed in parallel in the renal tubule. Both parathyroid hormone (PTH) and thiazide diuretics may influence this relationship. This study was designed to show whether the dissociation of Na from Ca transport produced by thiazides is dependent upon the presence of PTH. Hydropenic thyroparathyroidectomized (TPTX) dogs were given chlorothiazide alone and together with PTH. Chlorothiazide alone significantly increased fractional excretion of sodium (0.5 +/- 0.3-5.6 +/- 0.3%) and calcium (0.74 +/- 0.18-1.4 +/- 0.24%). However, the Ca/Na excretion ratio fell markedly from 1.57 to 0.24%. Micropuncture revealed this dissociation to occur at the distal tubule. Proximal reabsorption of water, sodium, and calcium were inhibited to an equal extent. However, distal fractional sodium reabsorption fell 10% whereas calcium reabsorption remained unchanged following chlorothiazide administration in TPTX animals. When phosphaturic doses of PTH were administered with chlorothiazide, no significant changes were observed in calcium or sodium reabsorption. It is concluded that PTH plays no role in the dissociation of sodium from calcium reabsorption resulting from acute chlorothiazide administration.


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