scholarly journals A case of X-linked hypophosphatemic rickets: complications and the therapeutic use of cinacalcet

2008 ◽  
Vol 159 (suppl_1) ◽  
pp. S101-S105 ◽  
Author(s):  
Helge Ræder ◽  
Nick Shaw ◽  
Coen Netelenbos ◽  
Robert Bjerknes
Keyword(s):  
Vitamin D ◽  
Sodium Phosphate ◽  
Fibroblast Growth Factor 23 ◽  
Normal Growth ◽  
Current Treatment ◽  
Phosphate Transporter ◽  
Hypophosphatemic Rickets ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Bone Deformities

In hypophosphatemic rickets, there are both inherited and acquired forms, where X-linked dominant hypophosphatemic rickets (XLH) is the most prevalent genetic form and caused by mutations in the phosphate-regulating endopeptidase (PHEX) gene. XLH is associated with growth retardation and bone deformities. The renal tubular cells have an important role in calcium and phosphate metabolism, where the 1α-hydroxylase enzyme metabolizes the conversion of 25 (OH)-vitamin D to potent 1,25 (OH)2-vitamin D, whereas the sodium–phosphate transporter controls tubular phosphate reabsorption. The pathophysiological defect in XLH is speculated to cause an increase in a circulating phosphate regulating hormone termed phosphatonin (fibroblast growth factor 23 is the primary phosphatonin candidate), which leads to inhibition of 1α-hydroxylase, and simultaneously to inhibition of the sodium–phosphate transporter domain NPT2c leading to parathyroid hormone-independent phosphaturia. Hence, current treatment of XLH is 1,25 (OH)2-vitamin D or the vitamin D analog alfacalcidol and elementary phosphorus. Unfortunately, patients with XLH may develop nephrocalcinosis, secondary or tertiary hyperparathyroidism, and in some situations also hypertension and cardiovascular abnormalities. We describe a patient with XLH caused by a novel missense mutation in the PHEX gene, who on treatment with alfacalcidol and oral phosphate had normal growth and minimal bone deformities, but who subsequently developed moderate nephrocalcinosis, significant hyperparathyroidism, hypercalcemia, renal failure, and hypertension. We also report the use of the calcimimetic drug cinacalcet in the successful treatment of hypercalcemia and hyperparathyroidism.

scholarly journals Variable Clinical Presentation of Children With Hereditary Hypophosphatemic Rickets With Hypercalciuria: A Case Series

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A708-A708
Author(s):  
Stephanie Christensen ◽  
Peter J Tebben ◽  
David Sas ◽  
Ana Creo
Keyword(s):  
Vitamin D ◽  
Sodium Phosphate ◽  
Serum Phosphorus ◽  
Hypophosphatemic Rickets ◽  
Urinary Stones ◽  
Dihydroxyvitamin D ◽  
Presenting Symptoms ◽  
Renal Tubular Cells ◽  
1,25 Dihydroxyvitamin D ◽  
Low Serum

Abstract Background: Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH) is a rare condition of phosphate wasting due to variants in the SLC34A3 gene, encoding the sodium-phosphate cotransporter 2c (NaPi2c) at the brush border of proximal renal tubular cells (1). While labs are characterized by low serum phosphorus, high 1,25 dihydroxyvitamin D and inappropriately high levels of urine phosphate and calcium, the presenting symptoms can vary widely. Little remains known about specific phenotype-genotype correlations, especially in children. Clinical Cases: We report three new cases of HHRH in an unrelated 12 year-old male, 9 year-old female and 14 year-old male. All three patients were found to have low serum phosphorus for age (2.9-3.2 mg/dL), normocalcemia (9.4-9.9 mg/dL), low to low-normal parathyroid hormone (7-15 pg/mL), elevated 1,25 dihydroxyvitamin D (91-178 pg/mL), and hypercalciuria (4.5-7.6 mg/kg/day). Urine phosphorus was inappropriately elevated given the degree of their hypophosphatemia. Despite having similar lab findings, however, their clinical presentations were varied. The 12 year-old male presented with lower extremity pain, which was previously ascribed to patellofemoral pain syndrome. He had no history of renal symptoms, though a renal ultrasound later identified stones bilaterally. Conversely, the 9 year-old female and 14 year-old male presented with recurrent urinary stones and no bone symptoms. Genetic analyses identified 4 novel SLC34A3 gene mutations. Of interest, the 12 year-old male and 9 year-old female each shared a variant (c.575C-T (p.Ser192Leu)) despite having disparate symptoms. All three patients were treated with phosphorus supplementation and were advised to discontinue Vitamin D, if this had previously been prescribed. Conclusion: These three cases highlight the variability of presenting signs and symptoms among individuals with HHRH. Obtaining an accurate diagnosis is critical, as the addition of Vitamin D can seriously worsen symptoms in HHRH though it is a commonly used treatment for other disorders of phosphate wasting and bone demineralization. To aid in clinical decision making, we present a stepwise approach to the diagnosis of hypophosphatemic diseases. References: (1) Lorenz-Depiereux, B., Benet-Pages, A., Eckstein, G., Tenenbaum-Rakover, Y., Wagenstaller, J., Tiosano, D., Gershoni-Baruch, R., Albers, N., Lichtner, P., Schnabel, D., Hochberg, Z., Strom, T. Hereditary Hypophosphatemic Rickets with Hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. Am. J. Hum. Genetic. 2006;78:193-201.

scholarly journals Pleiotropic Actions of FGF23

2017 ◽  
Vol 45 (7) ◽  
pp. 904-910 ◽  
Author(s):  
Reinhold G. Erben
Keyword(s):  
Vitamin D ◽  
Fibroblast Growth Factor 23 ◽  
Renal Tubules ◽  
Hormone Production ◽  
Membrane Expression ◽  
Fgf Receptor ◽  
Local Inhibition ◽  
Organ Systems ◽  
Key Enzyme ◽  
Renal Tubular

Fibroblast growth factor-23 (FGF23) is a bone-derived hormone, mainly produced by osteoblasts and osteocytes in response to increased extracellular phosphate and circulating vitamin D hormone. Endocrine FGF23 signaling requires co-expression of the ubiquitously expressed FGF receptor 1 (FGFR1) and the co-receptor α-Klotho (Klotho). In proximal renal tubules, FGF23 suppresses the membrane expression of the sodium–phosphate cotransporters Npt2a and Npt2c which mediate urinary reabsorption of filtered phosphate. In addition, FGF23 suppresses proximal tubular expression of 1α-hydroxylase, the key enzyme responsible for vitamin D hormone production. In distal renal tubules, FGF23 signaling activates with-no-lysine kinase 4, leading to increased renal tubular reabsorption of calcium and sodium. Therefore, FGF23 is not only a phosphaturic but also a calcium- and sodium-conserving hormone, a finding that may have important implications for the pathophysiology of chronic kidney disease. Besides these endocrine, Klotho-dependent functions of FGF23, FGF23 is also an auto-/paracrine suppressor of tissue-nonspecific alkaline phosphatase transcription via Klotho-independent FGFR3 signaling, leading to local inhibition of mineralization through accumulation of pyrophosphate. In addition, FGF23 may target the heart via an FGFR4-mediated Klotho-independent signaling cascade. Taken together, there is emerging evidence that FGF23 is a pleiotropic hormone, linking bone with several other organ systems.

VITAMIN D DEPENDENCY: AN INHERITED POSTNATAL SYNDROME WITH SECONDARY HYPERPARATHYROIDISM

PEDIATRICS ◽  
1970 ◽  
Vol 46 (6) ◽  
pp. 871-880
Author(s):  
C. Arnaud ◽  
R. Maijer ◽  
T. Reade ◽  
C. R. Scriver ◽  
D. T. Whelan
Keyword(s):  
Vitamin D ◽  
Autosomal Recessive ◽  
Hypophosphatemic Rickets ◽  
First Year ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Recessive Trait ◽  
Daily Allowance ◽  
Renal Tubular ◽  
First Year Of Life

Three French-Canadian children in a large inbred pedigree each developed hypocalcemic, hypophosphatemic rickets in the latter half of their first year of life; there were also manifestations of generalized renal tubular dysfunction. These abnormalities, which mimic advanced Vitamin D deficiency, disappeared only when Vitamin D2 or D3 was given at about 100 times the recommended daily allowance; this indicated the diagnosis of Vitamin D dependency. Enamel hypoplasia was a prominent clinical finding; only those teeth which calcify postnatally were affected, indicating that the condition found does not affect Vitamin D-dependent nutrition in utero. The level of parathyroid hormone was elevated in serum before treatment; it fell to normal either after treatment with Vitamin D, or during intravenous infusion with a calcium solution sufficient to produce hypercalcemia. Vitamin D dependency appeared to be inherited as an autosomal recessive trait in this pedigree, but we could observe no phenotypic signs in presumably obligate heterozygotes. One of the three cases in the pedigree arose from outbreeding, suggesting that the mutant allele is probably not particularly rare in the population under our surveillance.

scholarly journals The Receptor-Dependent Actions of 1,25-Dihydroxyvitamin D Are Required for Normal Growth Plate Maturation in NPt2a Knockout Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (10) ◽  
pp. 4607-4612 ◽  
Author(s):  
Susanne U. Miedlich ◽  
Eric D. Zhu ◽  
Yves Sabbagh ◽  
Marie B. Demay
Keyword(s):  
Vitamin D ◽  
Growth Plate ◽  
Fibroblast Growth Factor 23 ◽  
Normal Growth ◽  
Chondrocyte Apoptosis ◽  
Apoptotic Pathway ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Hypertrophic Chondrocyte

Rickets is a growth plate abnormality observed in growing animals and humans. Rachitic expansion of the hypertrophic chondrocyte layer of the growth plate, in the setting of hypophosphatemia, is due to impaired apoptosis of these cells. Rickets is observed in humans and mice with X-linked hypophosphatemia that is associated with renal phosphate wasting secondary to elevated levels of fibroblast growth factor-23. Rickets is also seen in settings of impaired vitamin D action, due to elevated PTH levels that increase renal phosphate excretion. However, mice with hypophosphatemia secondary to ablation of the renal sodium-dependent phosphate transport protein 2a (Npt2a), have not been reported to develop rickets. Because activation of the mitochondrial apoptotic pathway by phosphate is required for hypertrophic chondrocyte apoptosis in vivo, investigations were undertaken to address this paradox. Analyses of the Npt2a null growth plate demonstrate expansion of the hypertrophic chondrocyte layer at 2 wk of age, with resolution of this abnormality by 5 wk of age. This is temporally associated with an increase in circulating levels of 1,25-dihydroxyvitamin D. To address whether the receptor-dependent actions of this steroid hormone are required for normalization of the growth plate phenotype, the Npt2a null mice were mated with mice lacking the vitamin D receptor or were rendered vitamin D deficient. These studies demonstrate that the receptor-dependent actions of 1,25-dihydroxyvitamin D are required for maintenance of a normal growth plate phenotype in the Npt2a null mice.

scholarly journals ASARM peptides: PHEX-dependent and -independent regulation of serum phosphate

2011 ◽  
Vol 300 (3) ◽  
pp. F783-F791 ◽  
Author(s):  
Valentin David ◽  
Aline Martin ◽  
Anne-Marie Hedge ◽  
Marc K. Drezner ◽  
Peter S. N. Rowe
Keyword(s):  
Vitamin D ◽  
Fibroblast Growth Factor 23 ◽  
Inverse Correlation ◽  
Fractional Excretion ◽  
Serum Phosphate ◽  
Hypophosphatemic Rickets ◽  
Separate Experiment ◽  
Constitutive Overexpression ◽  
Fractional Excretion Of Phosphate

Increased acidic serine aspartate-rich MEPE-associated motif (ASARM) peptides cause mineralization defects in X-linked hypophosphatemic rickets mice (HYP) and “directly” inhibit renal phosphate uptake in vitro. However, ASARM peptides also bind to phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX) and are a physiological substrate for this bone-expressed, phosphate-regulating enzyme. We therefore tested the hypothesis that circulating ASARM peptides also “indirectly” contribute to a bone-renal PHEX-dependent hypophosphatemia in normal mice. Male mice ( n = 5; 12 wk) were fed for 8 wk with a normal phosphorus and vitamin D3 diet (1% Pi diet) or a reduced phosphorus and vitamin D3 diet (0.1% Pi diet). For the final 4 wk, transplantation of mini-osmotic pumps supplied a continuous infusion of either ASARM peptide (5 mg·day−1·kg−1) or vehicle. HYP, autosomal recessive hypophosphatemic rickets (ARHR), and normal mice (no pumps or ASARM infusion; 0.4% Pi diet) were used in a separate experiment designed to measure and compare circulating ASARM peptides in disease and health. ASARM treatment decreased serum phosphate concentration and renal phosphate cotransporter (NPT2A) mRNA with the 1% Pi diet. This was accompanied by a twofold increase in serum ASARM and 1,25-dihydroxy vitamin D3 [1,25 (OH)2D3] levels without changes in parathyroid hormone. For both diets, ASARM-treated mice showed significant increases in serum fibroblast growth factor 23 (FGF23; +50%) and reduced serum osteocalcin (−30%) and osteopontin (−25%). Circulating ASARM peptides showed a significant inverse correlation with serum Pi and a significant positive correlation with fractional excretion of phosphate. We conclude that constitutive overexpression of ASARM peptides plays a “component” PHEX-independent part in the HYP and ARHR hypophosphatemia. In contrast, with wild-type mice, ASARM peptides likely play a bone PHEX-dependent role in renal phosphate regulation and FGF23 expression. They may also coordinate FGF23 expression by competitively modulating PHEX/DMP1 interactions and thus bone-renal mineral regulation.

scholarly journals AB0922 BUROSUMAB (ANTI-FGF23 MONOCLONAL ANTIBODY) IN THE TREATMENT OF A PATIENT WITH RECURRENT TUMOR INDUCED OSTEOMALACIA.

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1762.3-1762
Author(s):  
C. Crotti ◽  
F. Zucchi ◽  
P. Messa ◽  
R. Caporali ◽  
M. Varenna
Keyword(s):  
Monoclonal Antibody ◽  
Vitamin D ◽  
Great Trochanter ◽  
Fibroblast Growth Factor 23 ◽  
Well Being ◽  
Hypophosphatemic Rickets ◽  
Imaging Evaluation ◽  
Left Femur ◽  
Pet Ct ◽  
Fgf 23

Background:Tumor-induced Osteomalacia (TIO) is a rare paraneoplastic syndrome caused by tumoral overproduction of fibroblast growth factor 23 (FGF23), resulting in hyperphospaturia, hypophosphatemia and osteomalacia. Surgery is the only curative treatment, but tumor can locally recur, even after years from primary surgery. Furthermore, some tumors cannot be removed by surgery due to their location.Objectives:To describe a case of a 53-year-old woman affected by recurrent TIO after three surgical attempts of removal treated with Burosumab.Methods:We describe the case of a 53 years old woman with TIO treated with Burosumab, an anti-FGF-23 monoclonal antibody at present approved for X-linked hypophosphatemic rickets only.Results:A 46-year-old Caucasian female was referred to our Bone Unit after experiencing several fractures in different sites. She reported being in good health until three years prior consultation. At the time of symptoms onset, she experienced a progressive muscle pain, enabling her to stand for a long period. During imaging evaluation for atraumatic fracture of right great trochanter, the MRI abdomen and18FDG- PET-CT showed a metabolic pre-sacral lesion. She unsuccessfully underwent to an exploratory laparotomy of that lesion. Then, she suffered from atraumatic intertrochanteric fracture of right femur, surgically treated, and after 3 months, she had an insufficiency dyaphiseal fracture of the left femur, surgically treated. Furthermore, she experienced several ribs fractures. At the time of first evaluation, lab works showed: serum-Phosophate (PS) 1.2 mg/dL (reference range (RR) 2.5-4.5 mg/dL), urinary-phosphate of 24h (PU) 842 mg/24h, alkaline phosphatase (ALP) 565 UI (RR<300), 1,25(OH)2vitamin D327 ng/L (RR 25-86.5), PTH 24 (RR<75 pg/mL), intact-FGF-23 117 (RR 25-45 pg/mL), normal serum and 24h-urinary Calcium. Patient underwent to68Ga-DOTATATE-PET-CT that showed a pre-sacral lesion, who was studied with MRI and CT before surgery. In 2013 patient underwent surgical excision of the pre-sacral region. After 18 months of well-being, patient complained worsening of articular pain and muscle weakness, and further ribs fractures. Another68Ga-DOTATATE-PET-CT reported a relapse of the previous pre-sacral lesion (32x12x47 mm) with an increase of FGF-23levels (54.6 pg/mL). Even the subsequent surgery was not able to remove the tumor. Since 2015, patient was maintained in phosphorus supplements and 1,25(OH)2vitamin D3, but PS levels never normalized. We asked for compassionate use of Burosumab and, after ethical committee approval, in September 2019 she was started on Burosumab, at a dose of 30 mg per month (0.3 mg/kg). At baseline, she had PS 1.2 mg/dL, PU 1874 mg/24h, TRP 25.96%. After two months, she improved in pain symptom (VAS reduction from 65 to 12 mm), which allow her to walk and stand without crutches. She did not normalize her PS levels (1.3 mg/dL), while PU reduced to 1000 mg/24h. We titred Burosumab dose at 40 mg per month (0.6 mg/kg) and patient is still under therapy, waiting for next blood works.Conclusion:This is the first European patient affected by TIO treated with Burosumab. Burosumab could be a promising therapy in the medical treatment of TIO refractory or not eligible for definitive surgery. Further data are needed to standardize the proper dose regimen.Disclosure of Interests:Chiara Crotti: None declared, Francesca Zucchi: None declared, Piergiorgio Messa: None declared, Roberto Caporali Consultant of: AbbVie; Gilead Sciences, Inc.; Lilly; Merck Sharp & Dohme; Celgene; Bristol-Myers Squibb; Pfizer; UCB, Speakers bureau: Abbvie; Bristol-Myers Squibb; Celgene; Lilly; Gilead Sciences, Inc; MSD; Pfizer; Roche; UCB, Massimo Varenna: None declared

scholarly journals SAT-373 A Case of X Linked Hypophosphatemic Rickets Due to DE Novo Phex Gene Mutation

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Ahmed Badran ◽  
Renee Bargman
Keyword(s):  
Vitamin D ◽  
Growth Factor ◽  
Vitamin D Deficiency ◽  
Fibroblast Growth Factor ◽  
Gene Mutation ◽  
De Novo ◽  
Fibroblast Growth Factor 23 ◽  
Hypophosphatemic Rickets ◽  
Fibroblast Growth ◽  
Phex Gene

Abstract Introduction Rickets is a condition that can affect bones of infants and children. It is characterized by growth plate demineralization and can occur secondary to, most commonly, vitamin D deficiency or various problems with vitamin D, Calcium or Phosphate metabolism. Hypophosphatemic rickets (HR) is a type of rickets that is inherited by X linked dominant pattern mainly however it can be also inherited by autosomal dominant and recessive patterns in rare cases. X linked dominant type (XLH) affects about 1 in 20,000 newborns. Each of the other hereditary forms of HR has been identified in only a few families. Clinical features of XLH is similar to other types of rickets including metaphyseal widening, palpable rachitic rosaries, frontal prominence, malformation of the horizontal depression along the lower border of the chest, insufficient weight gain and leg bowing. Case presentation: A 10-month-old infant presented to endocrinology with vitamin D deficiency, low serum phosphorus and hyperparathyroidism. Physical examination showed macrocephaly with frontal bossing, widening of the wrists and rachitic rosaries. His lab results showed low 25 OH vitamin D (11 ng/ml) (N:20-50 ng/ml), low phosphorus (PO4) (3.3 mg/dl) (N:4-6.5 mg/dl), high PTH (113 pg/ml) (N: 20-65pg/ml), high alkaline phosphatase (ALP) (836 IU/L) (N: 135-518 IU/L) and normal calcium (Ca2+) (9.6 mg/dl) (N:9-11 mg/dl). Vitamin D treatment was started however his follow up lab results showed persistent hypophosphatemia for age (2.8mg/dl) and elevated ALP (600IU/l) despite normalization of vitamin D (38 ng/ml). Additional lab tests were done showing high PO4 excretion (19.5 mg/dl)(N:1:3.5 mg/dl), Ca/Cr ratio 0.005 (N &lt;0.14), inappropriately normal FGF23 level (129 RU/ml) (N: &gt;124 RU/mL). Genetic testing showed de novo mutation in PHEX gene (871C&gt;T) which is consistent with XLH. PHEX gene mutation is the most common mutation associated with XLH. Normally this gene can directly or indirectly regulate a protein called fibroblast growth factor 23 (produced from FGF23 gene). This protein normally inhibits renal reabsorption of phosphate into the bloodstream. Gene mutations increase the production or reduce the breakdown of fibroblast growth factor 23 leading to an overactivation of this protein and reduction of phosphate reabsorption by the kidneys, resulting in hypophosphatemia. The patient was maintained on Burosomab (0.4 mg/kg biweekly); a recombinant human monoclonal antibody (IgG1) that binds to and inhibits the activity of fibroblast growth factor 23 (FGF23) and increases the phosphate reabsorption in the renal tubules. Conclusion: XLH due to PHEX gene mutation should be considered in rachitic children who have persistently low phosphate levels despite treating vitamin D deficiency.

Npt2a and Npt2c in mice play distinct and synergistic roles in inorganic phosphate metabolism and skeletal development

2009 ◽  
Vol 297 (3) ◽  
pp. F671-F678 ◽  
Author(s):  
Hiroko Segawa ◽  
Akemi Onitsuka ◽  
Junya Furutani ◽  
Ichiro Kaneko ◽  
Fumito Aranami ◽  
...  
Keyword(s):  
Bone Mineralization ◽  
Skeletal Development ◽  
Single Gene ◽  
Hypophosphatemic Rickets ◽  
Minor Role ◽  
Double Knockout ◽  
Renal Tubular Cells ◽  
Bone Phenotype ◽  
Adult Mice ◽  
Renal Tubular

Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a rare autosomal recessively inherited disorder, characterized by hypophosphatemia, short stature, rickets and/or osteomalacia, and secondary absorptive hypercalciuria. HHRH is caused by a defect in the sodium-dependent phosphate transporter (NaPi-IIc/Npt2c/NPT2c), which was thought to have only a minor role in renal phosphate (Pi) reabsorption in adult mice. In fact, mice that are null for Npt2c (Npt2c−/−) show no evidence for renal phosphate wasting when maintained on a diet with a normal phosphate content. To obtain insights and the relative importance of Npt2a and Npt2c, we now studied Npt2a−/−Npt2c+/+, Npt2a+/−Npt2c−/−, and Npt2a−/−Npt2c−/− double-knockout (DKO). DKO mice exhibited severe hypophosphatemia, hypercalciuria, and rickets. These findings are different from those in Npt2a KO mice that show only a mild phosphate and bone phenotype that improve over time and from the findings in Npt2c KO mice that show no apparent abnormality in the regulation of phosphate homeostasis. Because of the nonreddundant roles of Npt2a and Npt2c, DKO animals showed a more pronounced reduction in Pi transport activity in the brush-border membrane of renal tubular cells than that in the mice with the single-gene ablations. A high-Pi diet after weaning rescued plasma phosphate levels and the bone phenotype in DKO mice. Our findings thus showed in mice that Npt2a and Npt2c have independent roles in the regulation of plasma Pi and bone mineralization.

scholarly journals Two Cases of Hypophosphatemia with Increased Renal Phosphate Excretion in Legionella Pneumonia

2016 ◽  
Vol 6 (1) ◽  
pp. 40-45 ◽  
Author(s):  
Shuhei Watanabe ◽  
Keiji Kono ◽  
Hideki Fujii ◽  
Kentaro Nakai ◽  
Shunsuke Goto ◽  
...  
Keyword(s):  
Vitamin D ◽  
Fibroblast Growth Factor 23 ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Fibroblast Growth ◽  
Phosphate Excretion ◽  
Legionella Pneumonia ◽  
Vitamin D Levels ◽  
Renal Tubular ◽  
Renal Phosphate Excretion

We encountered 2 cases of hypophosphatemia due to Legionella pneumonia. Both cases showed increased urinary phosphate excretion and renal tubular dysfunction, which ameliorated with recovery from Legionella pneumonia. Serum fibroblast growth factor-23 level was suppressed, whereas serum 1,25(OH)2 vitamin D and parathyroid hormone levels were normal. Delayed elevation of serum 1,25(OH)2 vitamin D levels was observed with improvement in renal tubular function. These findings suggested hypophosphatemia might be mediated by renal tubular dysfunction.

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