Renal threshold phosphate concentration (TmPO4/GFR).

Kruse, K.; Kracht, Ute; Göpfert, Gisela

doi:10.1136/adc.57.3.217

Cited by 101 publications

(36 citation statements)

References 11 publications

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“…Table I demonstrates the marked similarity between our findings in children and those of Brodehl et al [4], who calculated TP/GFR using classical clearance techniques. In contrast, values for TmP/GFR published by Kruse et al [5], using the Walton-Bijvoet nomogram, were considerably higher. Our findings in subjects over 16 (3.2 ±0.3 mg/dl or 1.03 ±0.10 mmol/1) parallel exactly the normal range of TmP/GFR for adults (2.2-4.2 mg/dl or 0.71-1.36 mmol/1), as published by Bijvoet and Morgan [6].…”

Section: Discussioncontrasting

confidence: 47%

Direct Measurement of TP/GFR: A Simple and Reliable Parameter of Renal Phosphate Handling

Stark

Eisenstein

Tieder

et al. 1986

Nephron

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As the Walton-Bijvoet nomogram for estimating renal phosphate (P) threshold (TmP/GFR) is not applicable to children of all ages, we sought an alternative method for measuring renal handling of P. Recognizing that the nomogram represents an indirect correlation between TmP/GFR and TP/GFR under fasting conditions, we examined this directly in 26 children. An excellent correlation was found, expressed as TmP/GFR = (fasting TP/GFR × 1.1) -0.3 (r = 0.95). The regression line in adults, expressed as TmP/GFR = (fasting TP/GFR × 1.4) – 0.9 (calculated from published studies) is markedly different at the higher values typical for children. Since no advantage could be seen in the use of a mathematically derived TmP, we investigated the direct use of measured TP/GFR (tubular P reabsorption per 100 ml glomerular filtrate) as a measure of renal P handling in clinical practice. No differences were found between morning fasting and nonfasting values. Measurements in 151 healthy subjects aged 3 days to 53 years established normal values in relation to age. The use of this parameter in patients is shown to accurately reflect defects and changes in renal P handling. We believe it to be the preferred parameter because it represents a directly measured physiologic function applicable to all age-groups.

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Section: Discussioncontrasting

confidence: 47%

Direct Measurement of TP/GFR: A Simple and Reliable Parameter of Renal Phosphate Handling

Stark

Eisenstein

Tieder

et al. 1986

Nephron

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“…Figure 2 summarizes the relevant biochemical data in all immediate family members, including the patients, before treatment. Since TmP/GFR, serum phosphorus levels and alkaline phosphatase activity vary with age, these data are presented as means denoted by zero ± S D of the normal range for age [16]. As can be seen, the two patients present ed significant hypophosphatemia, decreased Tm P/G FR , elevated serum alkaline phosphatase activity of bone origin and hypercalciuria.…”

Section: Biochemical Methodsmentioning

confidence: 99%

A New Kindred with Hereditary Hypophosphatemic Rickets with Hypercalciuria: Implications for Correct Diagnosis and Treatment

Tieder¹,

Arie²,

Bab³

et al. 1992

Nephron

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Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a new autosomal form of hypophosphatemic rickets, recently described. This disease is characterized, and differs from other forms of hereditary hypophosphatemic rickets and/or osteomalacia by increased serum levels of 1,25-dihydroxyvitamin D, hypercalciuria and complete remission of the disease on phosphate therapy alone. However, only another probable Israeli kindred, and seemingly a few sporadic cases from Europe, North America and Japan have been reported in the literature. We describe here a new kindred of Jewish Yemenite origin (unrelated to other Israeli families) with typical HHRH. Two additional members of this family suffer from a milder asymptomatic form of the disease, which presents as absorptive hypercalciuria without signs or symptoms of bone disease. It seems to us that HHRH is underdiagnosed, due to its similarity to other hypophosphatemic syndromes in clinical, radiological and most biochemical parameters. Therefore, it is recommended that urinary calcium excretion and serum 1,25-di-hydroxyvitamin D concentrations be measured in every patient with hypophosphatemic rickets/and or osteomalacia before the initiation of any therapy. The correct diagnosis of HHRN is of immense therapeutic implications. Phosphate therapy alone could cause a complete remission in HHRH, while the addition of active vitamin D metabolites, as is recommended in hypophosphatemic vitamin D resistant rickets, could cause deterioration in the patient’s condition.

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“…Serum phosphate concentrations in healthy children and adolescents are normally distributed (Kruse et al 1982), as expected of a complex metrical trait ). An age-related fall in renal phosphate reabsorptive function explains the corresponding decline in serum phosphate concentrations (Kruse et al 1982).…”

Section: Renal Control Of Phosphate Homeostasismentioning

confidence: 99%

“…An age-related fall in renal phosphate reabsorptive function explains the corresponding decline in serum phosphate concentrations (Kruse et al 1982). Renal phosphate reabsorption is achieved by several processes distributed along the proximal nephron and across epithelial cells forming the proximal nephron segments .…”

Section: Renal Control Of Phosphate Homeostasismentioning

confidence: 99%

X‐linked hypophosphataemia: A homologous phenotype in humans and mice with unusual organ‐specific gene dosage

Scriver

Tenenhouse

1992

J of Inher Metab Disea

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XLH (X-linked hypophosphataemia, gene symbol HYP, McKusick 307800, 307810) and its murine counterparts (Hyp and Gy) map to a conserved segment on the X-chromosome (Xp 22.31-p.21.3, human; distal X, mouse). Gene dosage has received relatively little attention in the long history of research on this disease, which began over 50 years ago. Bone and teeth are sites of the principal disease manifestations in XLH (rickets, osteomalacia, interglobular dentin). Newer measures of quantitative XLH phenotypes reveal gene dose effects in bone and teeth with heterozygous values distributed between those in mutant hemizygotes and normal homozygotes. On the other hand, serum phosphate concentrations (which are low in the mutant phenotype and thereby contribute to bone and tooth phenotypes) do not show gene dosage. In Hyp mice serum values in mutant hemizygotes, mutant homozygotes and heterozygotes are similar. Phosphate homeostasis reflects its renal conservation. Renal absorption of phosphate on a high-affinity, Na+ ion-gradient coupled system in renal brush border membrane is impaired and gene dosage is absent at this level; the mutant phenotype is fully dominant. Synthesis and degradation of 1,25(OH)2D are also abnormal in XLH (and Hyp), but gene dosage in these parameters has not yet been measured. An (unidentified) inhibitory trans-acting product of the X-linked locus, affecting phosphate transport and vitamin D metabolism, acting perhaps through cytosolic protein kinase C, could explain the renal phenotype. But why would it have a normal gene dose effect in bone and teeth? Since the locus may have duplicated (to form Hyp and Gy), and shows evidence of variable expression in different organs (inner ear, bone/teeth, kidney), it may have been recruited during evolution to multiple functions.

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Renal threshold phosphate concentration (TmPO4/GFR).

Cited by 101 publications

References 11 publications

Direct Measurement of TP/GFR: A Simple and Reliable Parameter of Renal Phosphate Handling

Direct Measurement of TP/GFR: A Simple and Reliable Parameter of Renal Phosphate Handling

A New Kindred with Hereditary Hypophosphatemic Rickets with Hypercalciuria: Implications for Correct Diagnosis and Treatment

X‐linked hypophosphataemia: A homologous phenotype in humans and mice with unusual organ‐specific gene dosage

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