The assessment of phosphate reabsorption

Bijvoet, O. L. M.; Morgan, D. V.; Fourman, Paul

doi:10.1016/0009-8981(69)90280-0

Cited by 143 publications

(46 citation statements)

References 18 publications

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“…Renal phosphate handling was assessed by calculating the TmP/GFR using serum samples obtained after an overnight fast and urine samples from 24-hour urine collections, using an adaptation of the technique and nomogram of Walton and Bijovet (24,34,35). Patients were considered to have normal excretion of phosphate in the urine (non-phosphate wasters, NPW) or renal phosphate wasting (phosphate wasters, PW) if their value of TmP/GFR was higher or lower, respectively, than the lower limit of the ageand gender-specific normal range (36).…”

Section: Methodsmentioning

confidence: 99%

FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting

Riminucci¹,

Collins²,

Fedarko³

et al. 2003

J. Clin. Invest.

581

319

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FGF-23, a novel member of the FGF family, is the product of the gene mutated in autosomal dominant hypophosphatemic rickets (ADHR). FGF-23 has been proposed as a circulating factor causing renal phosphate wasting not only in ADHR (as a result of inadequate degradation), but also in tumor-induced osteomalacia (as a result of excess synthesis by tumor cells). Renal phosphate wasting occurs in approximately 50% of patients with McCune-Albright syndrome (MAS) and fibrous dysplasia of bone (FD), which result from postzygotic mutations of the GNAS1 gene. We found that FGF-23 is produced by normal and FD osteoprogenitors and bone-forming cells in vivo and in vitro. In situ hybridization analysis of FGF-23 mRNA expression identified "fibrous" cells, osteogenic cells, and cells associated with microvascular walls as specific cellular sources of FGF-23 in FD. Serum levels of FGF-23 were increased in FD/MAS patients compared with normal age-matched controls and significantly higher in FD/MAS patients with renal phosphate wasting compared with those without, and correlated with disease burden bone turnover markers commonly used to assess disease activity. Production of FGF-23 by FD tissue may play an important role in the renal phosphate-wasting syndrome associated with FD/MAS

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Section: Methodsmentioning

confidence: 99%

FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting

Riminucci¹,

Collins²,

Fedarko³

et al. 2003

J. Clin. Invest.

581

319

View full text Add to dashboard Cite

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“…Plasma calcium was adjusted for albumin levels (14). The following parameters were calculated: i) estimated GFR (eGFR), using the Cockroft and Gault formula; ii) fasting urinary calcium-to-creatinine ratio (bone resorption index, BRI); iii) renal tubular reabsorption of phosphate (TmPi/GFR) and calcium (TRCaI), calculated as described elsewhere (15,16). Serum intact PTH (iPTH) and osteocalcin were measured using two-site chemiluminescent immunometric assays (Elecsys R, Roche).…”

Section: Serum and Urinary Measurementsmentioning

confidence: 99%

“…These were significantly higher in patients who developed hypophosphatemia after renal transplantation: 30 (95% CI, 22-37) vs 19 (95% CI, [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29] pmol/l in hypophosphatemic and normophosphatemic patients respectively, P!0.05.…”

Section: Early Post-transplantation Periodmentioning

confidence: 99%

Early post-transplantation hypophosphatemia is associated with elevated FGF-23 levels

Trombetti¹,

Richert²,

Hadaya³

et al. 2011

European Journal of Endocrinology

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Background: We examined the hypothesis that high FGF-23 levels early after transplantation contribute to the onset of hypophosphatemia, independently of parathyroid hormone (PTH) and other factors regulating phosphate metabolism. Methods: We measured serum phosphate levels (sPi), renal tubular reabsorption of Pi (TmPi/GFR), estimated GFR (eGFR), intact PTH (iPTH), calcitriol, intact (int) and C-terminal (Cter) FGF-23, dietary Pi intake and cumulative doses of glucocorticoids in 69 patients 12 days (95% confidence interval, 10-13) after renal transplantation. Results: Hypophosphatemia was observed in 43 (62%) of the patients 12 days after transplantation. Compared with non-hypophosphatemic subjects, their post-transplantation levels of intact and CterFGF-23 were higher (195 (108-288) vs 48 (40-64) ng/l, P!0.002 for intFGF-23; 205 (116-384) vs 81 (55-124) U/ml, P!0.002, for CterFGF-23). In all subjects, Cter and intFGF-23 correlated inversely with sPi (rZK0.35, P!0.003; K0.35, P!0.003, respectively), and TmPi/GFR (rZK0.50, P!0.001; K0.54, P!0.001, respectively). In multivariate models, sPi and TmPi/GFR were independently associated with FGF-23, iPTH and eGFR. Pre-transplant iPTH levels were significantly higher in patients developing hypophosphatemia after renal transplantation. Pretransplant levels of FGF-23 were not associated with sPi at the time of transplantation. Conclusion: In addition to PTH, elevated FGF-23 may contribute to hypophosphatemia during the early post-renal transplant period.

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“…The patients with months, 1 patient with chronic idiopathic hypoparathyroidism, 4 D-deficiency rickets and the children with PDR had radiologic children with terminal stage chronic renal failure, and 2 children examinations of the wrist and knee bones at the initiation and at with cystinosis. In these different diagnostic groups the effects of the end of 1,25-(0H),-D3 la-OH-D3 short term administration of 1 , 2 5 -( 0~) , -~, were with During the short term and the long term studies the following some patients whereas I~-O H -D , was given to the others, ~h~ two biochemical data were collected: serum calcium, phosphorus, with cystinosis had severe impairment of their glomerular creatinine, citrate, alkaline phosphatase; urine calcium, phosfunctions, i.e,, creatinine clearances, were, respectively, 6 and 30 phorus creatinine, and cyclic AMP; endogenous creatinine clearml/min/1.73 m2; both received 1 , 2 5 -( 0~) , -~, , ~h~ effects of "=, tubular reabsorption of phosphorus (TRP), and phosphorus I ,~~-( o H ) , -D , and of la-0H-D, were analyzed in the same maximum tubular reabsorption rate per 100 ml glomerular patient with chronic idiopathic hypoparathyroidism, All children filtration rate (Tm/GFR) calculated according to the nomogram with VDRR or with PDR, the adolescent with late acquired of Bijvoet et al (7). The laboratory techniques used were the D-resistant rickets, and the patient with chronic idiopathic hypo-following: phosphorus, Fiske and SubbaRow (~u t o~n a l y z e r ) : parathyroidism had been previously treated with D or creatinine (AutoAnalyzer); calcium, automated complexometric 2 5 -0~-~, .…”

Section: Speculationmentioning

confidence: 99%

1,25-Dihydroxyvitamin D3 and 1,α-Hydroxyvitamin D3 in Children: Biologic and Therapeutic Effects in Nutritional Rickets and Different Types of Vitamin D Resistance

et al. 1975

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ExtractDuring the past few years the metabolism of vitamin D has This investigation confirms the high level of biologic activity and the similarity of the effects of small doses of 1,25-dihydroxyvitamin D, (1,,-D,) and of its analog la-hydroxyvitamin D , (la-OH-D,) on children with nutritional rickets, "pseudodeficiency" rickets (PDR), hereditary hypophosphatemia, chronic idiopathic hypoparathyroidism, and chronic renal failure. It also shows that cystinotic patients may develop, at the end stage of the disease, a certain degree of resistance to 1,25-(OH),D,. The comparison of the therapeutic effects of long term oral administration of 1,25-(OH),-D, or la-OH-D, to two D-deficient children and two sibs with PDR demonstrates differences in sensitivity. In the patients with nutritional rickets, 0.5 pg/24 hr of either drug corrects the biochemical abnormalities, initiates healing of skeletal lesions in 28 days, and cures the metaphyseal lesions in 60 days of therapy. In contrast, it appears that doses of either drug that are curative in D deficiency rickets are only partly active in PDR. These observations indicate that the hypothesis of a deficit in 25-hydroxycholecalciferol la-hydroxylase in patients with PDR must await for confirmation more direct evidences, and that such a deficit, even if proven, may not account for all of the biochemical and skeletal alterations seen in patients with this inherited disorder. SpeculationThe similarity of action of 1,25-(OH),-D, and la-OH-D, observed in the present study presents additional evidence that la-OH-D, can be considered a valuable substitute for the hormonal form of cholecalciferol, especially for the management of children with chronic renal failure, hypoparathyroidism, or pseudodeficiency rickets. In this latter disease, the active therapeutic doses of either drug appear to be greater than the amount required for the treatment of simple nutritional rickets. This observation indicates that investigations on the pathogenesis of pseudodeficiency rickets must be continued in order to confirm or invalidate the hypothesis suggested by us and others that this inherited disorder might be related to a deficit in 25-hydroxycholecalciferol la-hydroxylase. Preliminary results obtained during this investigation established that children with P D R were sensitive to quite small doses of 1,25-(OH),-D,. These observations led us to suggest that this inherited disorder might be caused by a deficit in 25-hydroxycholecalciferol la-hydroxylase (4); a hypothesis also suggested by Fraser et al. (14), and more recently by Prader (29), Fanconi (l3), and Scriver et a/. (32). According to this hypothesis the biochemical and skeletal lesions in PDR, just as they are in simple D deficiency rickets, may be related to a deficit in 1,25-(OH),-D,. Hence, one would expect children with P D R and patients with D deficiency rickets to respond similarly to 1,25-(OH),-D, or la-OH-D, therapy. In an attempt to test the validity of this assumption our study was completed by a cornparisin of the therapeuti...

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The assessment of phosphate reabsorption

Cited by 143 publications

References 18 publications

FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting

FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting

Early post-transplantation hypophosphatemia is associated with elevated FGF-23 levels

1,25-Dihydroxyvitamin D3 and 1,α-Hydroxyvitamin D3 in Children: Biologic and Therapeutic Effects in Nutritional Rickets and Different Types of Vitamin D Resistance

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