Tubular calcium reabsorption and other aspects of calcium homeostasis in primary and secondary hyperparathyroidism

2014 ◽  
Vol 82 (08) ◽  
pp. 83-91 ◽  
Author(s):  
Kenneth R. Phelps ◽  
Kim S. Stote ◽  
Darius Mason
Keyword(s):  
Secondary Hyperparathyroidism ◽  
Calcium Homeostasis ◽  
Calcium Reabsorption ◽  
Tubular Calcium Reabsorption

Pathophysiology of hypercalciuria

1984 ◽  
Vol 247 (1) ◽  
pp. F1-F13 ◽  
Author(s):  
F. L. Coe ◽  
D. A. Bushinsky
Keyword(s):  
Parathyroid Hormone ◽  
Bone Mineral Content ◽  
Bone Mineral ◽  
Calcium Homeostasis ◽  
Calcium Transport ◽  
Mineral Content ◽  
Renal Tubule ◽  
Urine Calcium ◽  
Dihydroxyvitamin D3 ◽  
Calcium Reabsorption

The mechanisms responsible for hypercalciuria may involve intestinal calcium transport, renal tubule calcium reabsorption, and the regulation of bone mineral content. Both parathyroid hormone and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) may alter urine calcium. For these reasons, understanding the pathogenesis of hypercalciuria in patients has proven to be difficult. We present here an analysis of pathways that regulate systemic calcium homeostasis and of the various mechanisms that have been proposed to explain normocalcemic hypercalciuria in humans. Available evidence seems to implicate disordered regulation of 1,25(OH)2D3 as a basis for at least one common form of hypercalciuria.

scholarly journals 1,25(OH)2D3-enhanced hypercalciuria in genetic hypercalciuric stone-forming rats fed a low-calcium diet

2013 ◽  
Vol 305 (8) ◽  
pp. F1132-F1138 ◽  
Author(s):  
Kevin K. Frick ◽  
John R. Asplin ◽  
Nancy S. Krieger ◽  
Christopher D. Culbertson ◽  
Daniel M. Asplin ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Cells ◽  
Idiopathic Hypercalciuria ◽  
Sprague Dawley ◽  
Vitamin D Receptors ◽  
Low Calcium Diet ◽  
Calcium Reabsorption ◽  
Renal Tubular ◽  
Intestinal Ca Absorption ◽  
Tubular Calcium Reabsorption

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.

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
Keyword(s):  
Plasma Clearance ◽  
Renal Tubule ◽  
Distal Tubule ◽  
Significant Linear Correlation ◽  
Calcium Reabsorption ◽  
Renal Tubular Reabsorption ◽  
Proximal Tubular ◽  
The Absolute ◽  
Renal Tubular ◽  
Tubular Calcium Reabsorption

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.

The Parathyroids

2017 ◽  
Author(s):  
Courtney J. Balentine ◽  
C Taylor Geraldson
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Secondary Hyperparathyroidism ◽  
Calcium Homeostasis ◽  
Multiple Endocrine Neoplasia ◽  
Laryngeal Nerve ◽  
Parathyroid Glands ◽  
Tertiary Hyperparathyroidism ◽  
Endocrine Neoplasia ◽  
And Function

Successful surgery of the parathyroid glands depends on a thorough knowledge of their anatomic and developmental relations. This knowledge is crucial for locating ectopic parathyroids or preventing injury to the recurrent laryngeal nerve. In addition, the surgeon should understand the physiology and function of these glands. Unlike other conditions a surgeon might treat, physiology, and not anatomy alone, often dictates the timing and course of parathyroid procedures. This surgeon-oriented, focused review covers the development, histology, anatomy, physiology, and pathophysiology of the parathyroid. Figures show the location and frequencies of ectopic upper and lower parathyroid glands, and regulation of calcium homeostasis. This review contains 2 highly rendered figures, and 16 references Key words: calcitonin; hypercalcemia; hyperparathyroidism; multiple endocrine neoplasia; parathyroid; parathyroid hormone; primary hyperparathyroidism; secondary hyperparathyroidism; tertiary hyperparathyroidism

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