Excretion of phosphate and calcium. Physiology of their renal handling and relation to clinical medicine

Massry, Shaul G.

doi:10.1001/archinte.131.6.828

Cited by 52 publications

(18 citation statements)

References 263 publications

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“…While fasting could produce varying degrees of volume depletion, and thereby change tubular calcium reabsorption (28), there was no evidence that patients with absorptive hypercalciuria could conserve sodium less perfectly than control subjects. The renal excretion of sodium was not significantly different between the two groups.…”

Section: Discussionmentioning

confidence: 98%

The Hypercalciurias CAUSES, PARATHYROID FUNCTIONS, AND DIAGNOSTIC CRITERIA

Pak¹,

Oata²,

Lawrence³

et al. 1974

J. Clin. Invest.

496

137

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A B S T R A C T The causes for the hypercalciuria and diagnostic criteria for the various forms of hypercalciuria were sought in 56 patients with hypercalcemia or nephrolithiasis (Ca stones), by a careful assessment of parathyroid function and calcium metabolism. A study protocol for the evaluation of hypercalciuria, based on a constant liquid synthetic diet, was developed. In 26 cases of primary hyperparathyroidism, characteristic features were: hypercalcemia, high urinary cyclic AMP (cAMP, 8.58+3.63 SD gmol/g creatinine; normal, 4.02±0.70 umol/g creatinine), high immunoreactive serum parathyroid hormone (PTH), hypercalciuria, the urinary Ca exceeding absorbed Ca from intestinal tract (CaA), high fasting urinary Ca (0.2 mg/mg creatinine or greater), and low bone density by 'I photon absorption. The results suggest that hypercalciuria is partly secondary to an excessive skeletal resorption (resorptive hypercalciuria). The 22 cases with renal stones had normocalcemia, hypercalciuria, intestinal hyperabsorption of calcium, normal or low serum PTH and urinary cAMP, normal fasting urinary Ca, and normal bone density. Since their CaA exceeded urinary Ca, the hypercalciuria probably resulted from an intestinal hyperabsorption of Ca (absorptive hypercalciuria). The primacy of intestinal Ca hyperabsorption was confirmed by responses to Ca load and deprivation under a metabolic dietary regimen. During a Ca load of 1,700 mg/day, there was an exaggerated increase in the renal excretion.of Ca and a suppression of cAMP excretion. The urinary Ca of 453±+154 SD mg/day was significantly higher than the control group's 211+42 mg/ day. The urinary cAMP of 2.26±0.56 umol/g creatinine was significantly lower than in the control group. In contrast, when the intestinal absorption of calcium was limited by cellulose phosphate, the hvpercalciuria was kc'ceiz(l for plblicatifn 9 July 1073 and in rezxsed form 11 September 1973. corrected and the suppressed renal excretion of cAMP returned towards normal. Two cases with renal stones had normocalcemia, hypercalciuria, and high urinary cAMP or serum PTH. Since CaA was less than urinary Ca, the hypercalciuria may have been secondary to an impaired renal tubular reabsorption of Ca (renal hypercalciuria). Six cases with renal stones had normal values of serum Ca, urinary Ca, urinary cAMP, and serum PTH (normocalciuric nephrolithiasis). Their CaA exceeded urinal Ca, and fasting urinary Ca and bone density were normal. The results support the proposed mechanisms for the hypercalciuria and provide reliable diagnostic criteria for the various forms of hypercalciuria.

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Section: Discussionmentioning

confidence: 98%

The Hypercalciurias CAUSES, PARATHYROID FUNCTIONS, AND DIAGNOSTIC CRITERIA

Pak¹,

Oata²,

Lawrence³

et al. 1974

J. Clin. Invest.

496

137

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“…Several as yet contradictory results of studies recently reviewed (15,16,25) have pointed to the possible role of the calcemia per se in the renal handling of Pi. The higher plasma calcium concentration observed in TPTX rats fed the low Pi diet could be directly related to the higher fractional reabsorption displayed by these animals under NaCl infusion.…”

Section: Methodsmentioning

confidence: 99%

“…Thus, as pointed out in two recent reviews (15,16), no conclusive evidence has been presented so far showing that variations in dietary Pi modify the capacity of the renal epithelium to translocate Pi. This uncertainty obviously prevented the drawing of any conclusions as to a possible role of PTH in the renal response to changes in the dietary input of Pi.…”

Section: Introductionmentioning

confidence: 97%

Inorganic phosphate homeostasis. Renal adaptation to the dietary intake in intact and thyroparathyroidectomized rats.

Tröhler¹,

Bonjour²,

Fleisch³

1976

J. Clin. Invest.

182

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A B S T R A C T The possibility of renal tubular adaptation to variations in dietary inorganic phosphate (Pi) was investigated in intact and thyroparathyroidectomized (TPTX) rats pair-fed diets containing low, normal, and high amounts of Pi for periods up to 10 days. Clearances were measured before and during acute i.v. infusions with Pi in conscious animals. Thus tubular reabsorption of phosphate (TRPi) could be assessed over a wide range of plasma phosphate concentrations ([Pt]Pi). It was found that the renal tubule could adapt its capacity to transport Pi according to the dietary Pi: TRPt was always higher, for a given [Pt]P1, in the animals fed low than in those fed higher Pi diets. This diet-induced modification also occurred in the absence of thyroparathyroid glands, in the presence of the same calcemia and urinary pH, and during marked extracellular volume expansion. A time-course study in rats TPTX both before and during the administration of the experimental diets showed that a difference in the tubular handling of Pi was detectable as early as 3 days after switching the animals from a normal to low-or high-Pi diets. These results indicate that factors other than parathyroid hormone are implicated in the tubular response to variations in the dietary intake of inorganic phosphate.

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“…The association of urinary calcium excretion with vitamin D was mainly explained by 25(OH)D 3 and not 25(OH)D 2 . These results suggest important sex differences in the relationships of urinary calcium excretion with serum calcium and vitamin D levels in the population.…”

Section: Discussionmentioning

confidence: 86%

“…Tight control of plasma calcium is achieved by complex regulatory mechanisms, including calcium-sensing receptor, and calcitropic hormones, such as vitamin D (1) and parathyroid hormone (PTH) (2,3). Two distinct sources of vitamin D are known: vitamin D 2 is mainly provided by food, and vitamin D 3 is synthesized de novo in the skin (4) and constitutes the major and more potent isoform (5,6).…”

Section: Introductionmentioning

confidence: 99%

Association of Urinary Calcium Excretion with Serum Calcium and Vitamin D Levels

Rathod

Bonny

Guessous

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objectives Population-based data on urinary calcium excretion are scarce. The association of serum calcium and circulating levels of vitamin D [25(OH)D 2 or D 3 ] with urinary calcium excretion in men and women from a population-based study was explored.Design, settings, participants, & measurements Multivariable linear regression was used to explore factors associated with square root-transformed 24-hour urinary calcium excretion (milligrams per 24 hours) taken as the dependent variable with a focus on month-specific vitamin D tertiles and serum calcium in the Swiss Survey on Salt Study.Results In total, 624 men and 669 women were studied with mean ages of 49.2 and 47.0 years, respectively (age range=15-95 years). Mean urinary calcium excretion was higher in men than in women (183.05 versus 144.60 mg/24 h; P,0.001). In adjusted models, the association (95% confidence interval) of square root urinary calcium excretion with protein-corrected serum calcium was 1.78 (95% confidence interval, 1.21 to 2.34) mg/24 h per milligram per deciliter in women and 0.59 (95% confidence interval, 20.11 to 1.29) mg/24 h per milligram per deciliter in men. Men in the third 25(OH)D 3 tertile had higher square root urinary calcium excretion than men in the first tertile (0.99; 95% confidence interval, 0.36 to 1.63 mg/24 h per nanogram per milliliter), and the corresponding association was 0.32 (95% confidence interval, 20.22 to 0.85) mg/24 h per nanogram per milliliter in women. These sex differences were more marked under conditions of high urinary sodium or urea excretions.Conclusions There was a positive association of serum calcium with urinary calcium excretion in women but not men. Vitamin 25(OH)D 3 was associated with urinary calcium excretion in men but not women. These results suggest important sex differences in the hormonal and dietary control of urinary calcium excretion.

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Excretion of phosphate and calcium. Physiology of their renal handling and relation to clinical medicine

Cited by 52 publications

References 263 publications

The Hypercalciurias CAUSES, PARATHYROID FUNCTIONS, AND DIAGNOSTIC CRITERIA

The Hypercalciurias CAUSES, PARATHYROID FUNCTIONS, AND DIAGNOSTIC CRITERIA

Inorganic phosphate homeostasis. Renal adaptation to the dietary intake in intact and thyroparathyroidectomized rats.

Association of Urinary Calcium Excretion with Serum Calcium and Vitamin D Levels

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