Nomogram for Derivation of Renal Threshold Phosphate Concentration

Walton, R. J.; Bijvoet, O. L. M.

doi:10.1016/s0140-6736(75)92736-1

Cited by 747 publications

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“…Samples for urea nitrogen, phosphate, sodium, and creatinine were obtained from 24-hour urinary collections. The tubular reabsorption of phosphate, fractional excretion of P, and serum phosphate were used as measures of renal phosphate handling (21). Sodium fractional excretion and n-protein catabolic rate were also evaluated.…”

Section: Methodsmentioning

confidence: 99%

Acute Effects of Very-Low-Protein Diet on FGF23 Levels

Iorio¹,

Micco²,

Torraca³

et al. 2012

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives High levels of fibroblast growth factor 23 are associated with mortality, CKD progression, and calcification in CKD patients. The aim of this pilot study is to assess whether a very-low-protein diet (0.3 g/kg per day) with a consequent low intake of phosphorus would reduce fibroblast growth factor 23 compared with a low-protein diet (0.6 g/kg per day) in CKD patients not yet on dialysis.Design, setting, participants, & measurements A prospective, randomized, controlled crossover study was performed in which 32 patients were randomized into two groups. Group A (16 patients) received a very-lowprotein diet (0.3 g/kg body wt per day) supplemented with ketoanalogues during the first week and a lowprotein diet during the second week, and group B (16 patients) received a low-protein diet during the first week and a very-low-protein diet during the second week. Fibroblast growth factor 23, seric, and urinary phosphate levels were measured at baseline and the end of each study period.Results After only 1 week of the very-low-protein diet, reductions in fibroblast growth factor 23 levels (33.5%), serum phosphate (12%), and urinary phosphate (34%) with the very-low-protein diet compared with the lowprotein diet were observed. Serum and urinary phosphate levels and protein intake were significant determinants of fibroblast growth factor 23 (95% confidence interval=1.04-1.19, 1.12-1.37, and 1.51-2.23, respectively).Conclusions A very-low-protein diet supplemented with ketoanalogues reduced fibroblast growth factor 23 levels in CKD patients not yet on dialysis.

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Section: Methodsmentioning

confidence: 99%

Acute Effects of Very-Low-Protein Diet on FGF23 Levels

Iorio¹,

Micco²,

Torraca³

et al. 2012

Clinical Journal of the American Society of Nephrology

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“…Urinary excretions were expressed as ratio with the urinary creatinine (mg/g). We evaluated renal phosphate handling deriving the phosphate threshold concentration (TmP/GFR) from the nomogram by Walton et al [11]. Osteocalcin was tested by immunoradiometric assay (Immutopics Inc., San Clemente, CA, USA.…”

Section: Methodsmentioning

confidence: 99%

Long-term Treatment of Acromegaly with Lanreotide: Evidence of Increased Serum Parathormone Concentration

et al. 2004

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Abstract. The somatostatin analogue lanreotide is effective in reducing growth hormone levels in patients with acromegaly. Acromegaly is characterized by calcium homeostasis alterations. The aim of our study was to evaluate the effects of lanreotide on bone turnover markers in a group of acromegalic patients and to verify a possible increase of intact parathormone (iPTH) levels in a transient or persistent way. Serum GH, IGF-I and serum and urinary markers of bone metabolism were measured before treatment and on months 3 and 24. In short-term treatment (3 months), lanreotide significantly decreased GH, IGF-I, serum calcium, osteocalcin and alkaline phosphatase levels, but increased iPTH level (49 ± 16.7 vs pre-treatment 28.3 ± 7.6 ng/L, p<0.001). During long-term study (24 months) GH and IGF-I were significantly still low; serum calcium and alkaline phosphatase levels returned to pre-treatment levels. iPTH level was significantly still higher compared with pre-treatment (46.4 ± 9.2 vs 28.3 ± 7.6 ng/L, p<0.05). No changes were seen in serum albumin, creatinine and vitamin D during short and long term treatment. The changes of most bone markers during lanreotide treatment can be explained by the decrease of GH and IGF-I. The increase of iPTH concentration suggests that lanreotide has ulterior and long-standing actions on calcium homeostasis: intestinal malabsorption of calcium due to the lanreotide could contribute to this "secondary" hyperparathyroidism. The clinical relevance of these long-standing effects needs to be further investigated.

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“…In a typical patient with TIO, low serum phosphate, normal to low calcium, normal PTH, low or inappropriately normal 1, 25-dihydroxyvitamin D, normal 25-hydroxyvitamin D, normal creatinine, normal electrolyte, elevated alkaline phosphatase (bone alkaline phosphatase), and elevated FGF-23 concentrations will be seen. There will be evidence of phosphate wasting in the form of increased urinary phosphate excretion per 24 hours, increased fractional excretion of phosphorus and a reduced tubular maximum for phosphate/ glomerular filtration rate (TMP/GFR) (44)(45)(46)(47). Bone biopsy (11) performed after tetracycline labeling of bone will show increased osteoid relative to mineralized bone and a reduced mineral appositional rate ( Figure 2) (7).…”

Section: Investigations For Diagnosis Physical Examinationmentioning

confidence: 99%

Tumor-induced Osteomalacia

Raj¹,

Chen²,

Sheldon³

et al. 2009

Encyclopedia of Molecular Mechanisms of Disease

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Clinical description and evaluation Disease phenotypeTumor-induced osteomalacia (TIO) is a rare syndrome (about 350 such cases have been described), characterized by hypophosphatemia, increased urinary losses of phosphate as a result of reduced tubular phosphate reabsorption, reduced or inappropriately normal concentrations of 1,25-dihydroxyvitamin D, normal parathyroid hormone concentrations, rickets or osteomalacia which are caused by substances (generally, fibroblast growth factor-23, FGF-23, and more rarely other peptides) elaborated by mesenchymal tumors (1-8). Patients manifest symptoms of osteomalacia or rickets with bone pain and proximal muscle weakness. Sometimes the causal tumors are readily visible or palpable on physical examination, but more often the tumors are small and very difficult to detect. Removal of the tumor results in reversal of the biochemical abnormalities, thereby demonstrating that the tumors produce a substance which alters phosphate homeostasis.Key biochemical abnormalities seen in the syndrome of TIO are shown in Table 1. As shown, these include hypophosphatemia, normal or low serum calcium concentrations, normal parathyroid hormone concentrations, normal 25-hydroxyvitamin D concentrations, inappropriately low 1,25-dihydroxyvitamin D concentrations, normal renal function, elevated fractional excretion of phosphorus or a low TMP/GFR and generally elevated serum FGF-23 concentrations. Most, but not all, patients with TIO have elevations in serum FGF-23 concentrations (9, 10). Patients generally have osteomalacia or rickets noted on skeletal radiography ( Figure 1A) although the findings can often be quite subtle or absent.

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Nomogram for Derivation of Renal Threshold Phosphate Concentration

Cited by 747 publications

References 0 publications

Acute Effects of Very-Low-Protein Diet on FGF23 Levels

Acute Effects of Very-Low-Protein Diet on FGF23 Levels

Long-term Treatment of Acromegaly with Lanreotide: Evidence of Increased Serum Parathormone Concentration

Tumor-induced Osteomalacia

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