Nephrocalcinosis in children who received high-dose vitamin D.

BACKGROUND: Vitamin D supplements are readily available as over-the-counter preparations. However, although rare, cases of vitamin D overdose still occur and are associated with nephrocalcinosis and life-threatening hypercalcemia. Errors in manufacturing of nutritional supplements may be a cause of vitamin D intoxication in children. This study aimed to identify factors associated with vitamin D overdose-related nephrocalcinosis in children due to manufacturing errors in supplements. METHODS: This retrospective study reviewed medical charts of pediatric patients with non-registered supplement-related vitamin D overdose at a tertiary referral hospital between 2006 and 2011. Clinical and laboratory characteristics of patients with or without nephrocalcinosis were evaluated. Receiver operating characteristics curve and area under the receiver operating characteristics curve were used to determine the most predictive value of each characteristic. RESULTS: A total of 44 patients (males: 29; age: 7-62 months) were included. Age ≤ 16.5 months, body weight ≤ 10.25 kg, body height ≤ 78.5 cm, body surface area (BSA) ≤ 0.475 m2, 25-hydroxyvitamin D3 ≥ 143 ng/mL, and calcium ≥ 10.65 mg/dL were predictive of developing nephrocalcinosis with a sensitivity and specificity of > 60%. Univariant analysis revealed that BSA was the most significant anthropometric prognostic factor (odds ratio: 12.09; 95% confidence interval: 2.61-55.72; P = 0.001). CONCLUSIONS: Children with smaller BSAs were more vulnerable to high-dose vitamin D3-related nephrocalcinosis. Physicians and parents should be aware of the potential adverse effects of vitamin D overdose in children. A higher resolution version of the Graphical abstract is available as Supplementary information.

Effects of bodybuilding supplements on the kidney: A population-based incidence study of biopsy pathology and clinical characteristics among middle eastern men.

BACKGROUND: The incidence of kidney diseases among bodybuilders is unknown. METHODS: Between January 2011 and December 2019, the Iraqi Kurdistan 15 to 39 year old male population averaged 1,100,000 with approximately 56,000 total participants and 25,000 regular participants (those training more than 1 year). Annual age specific incidence rates (ASIR) with (95% confidence intervals) per 100,000 bodybuilders were compared with the general age-matched male population. RESULTS: Fifteen male participants had kidney biopsies. Among regular participants, diagnoses were: focal segmental glomerulosclerosis (FSGS), 2; membranous glomerulonephritis (MGN), 2; post-infectious glomeruonephritis (PIGN), 1; tubulointerstitial nephritis (TIN), 1; and nephrocalcinosis, 2. Acute tubular necrosis (ATN) was diagnosed in 5 regular participants and 2 participants training less than 1 year. Among regular participants, anabolic steroid use was self-reported in 26% and veterinary grade vitamin D injections in 2.6%. ASIR for FSGS, MGN, PIGN, and TIN among regular participants was not statistically different than the general population. ASIR of FSGS adjusted for anabolic steroid use was 3.4 (- 1.3 to 8.1), a rate overlapping with FSGS in the general population at 2.0 (1.2 to 2.8). ATN presented as exertional muscle injury with myoglobinuria among new participants. Nevertheless, ASIR for ATN among total participants at 1.4 (0.4 to 2.4) was not significantly different than for the general population at 0.3 (0.1 to 0.5). Nephrocalcinosis was only diagnosed among bodybuilders at a 9-year cumulative rate of one per 314 vitamin D injectors. CONCLUSIONS: Kidney disease rates among bodybuilders were not significantly different than for the general population, except for nephrocalcinosis that was caused by injections of veterinary grade vitamin D compounds.

Involvement of estrogen in phosphorus-induced nephrocalcinosis through fibroblast growth factor 23.

Excessive phosphorus intake adversely affects bone and mineral metabolism. Estrogen is one of the factors affecting fibroblast growth factor 23 (FGF23), a phosphorus-regulating hormone. However, the interaction between excess phosphorus and estrogen status has not been fully elucidated. This study investigated the involvement of estrogen in the effects of high phosphorus intake on bone metabolism and ectopic calcification in ovariectomized (OVX) rats. The interaction between high phosphorus diet and OVX was not observed in bone mineral density and aortic calcium. In contrast, high phosphorus intake markedly increased renal calcium concentration in sham rats, whereas the effect was attenuated in OVX rats, which was reversed by a selective estrogen-receptor modulator treatment. A strong positive correlation between renal calcium and serum FGF23 was observed. In addition, fibroblast growth factor receptor 1 (FGFR1: a predominant receptor of FGF23) inhibitor treatment partially decreased renal calcium concentrations in rats with high phosphorus intake. In conclusion, the effect of high phosphorus intake on bone metabolism and aortic calcification did not depend on the estrogen status; in contrast, high phosphorus intake synergistically induced nephrocalcinosis in the presence of estrogenic action on the bone. Furthermore, FGF23 was involved in the nephrocalcinosis induced by high phosphorus intake partially through FGFR1 signaling.

Hypoparathyroidism: Less Severe Hypocalcemia With Treatment With Vitamin D2 Compared With Calcitriol.

Context: Options for chronic treatment of hypoparathyroidism include calcitriol, recombinant human parathyroid hormone, and high-dose vitamin D (D2). D2 is used in a minority of patients because of fear of prolonged hypercalcemia and renal toxicity. There is a paucity of recent data about D2 use in hypoparathyroidism. Objective: Compare renal function, hypercalcemia, and hypocalcemia in patients with hypoparathyroidism treated chronically with either D2 (D2 group) or calcitriol. Design, Setting, and Patients: A retrospective study of patients with hypoparathyroidism treated at the University of Maryland Hospital. Participants were identified by a billing record search with diagnosis confirmed by chart review. Thirty patients were identified; 16 were treated chronically with D2, 14 with calcitriol. Data were extracted from medical records. Main Outcome Measures: Serum creatinine and calcium, hospitalizations, and emergency department (ED) visits for hypercalcemia and hypocalcemia. Results: D2 and calcitriol groups were similar in age (58.9 ± 16.7 vs 50.9 ± 22.6 years, P = 0.28), sex, and treatment duration (17.8 ± 14.2 vs 8.5 ± 4.4 years, P = 0.076). Hospitalization or ED visits for hypocalcemia occurred in none of the D2 group vs four of 14 in the calcitriol group (P = 0.03); three in the calcitriol group had multiple ED visits. There were no differences between D2 and calcitriol groups in hospitalizations or ED visits for hypercalcemia, serum creatinine or calcium, or kidney stones. Conclusion: We found less morbidity from hypocalcemia in hypoparathyroid patients treated chronically with D2 compared with calcitriol and found no difference in renal function or morbidity from hypercalcemia. Treatment with D2 should be considered in patients with hypoparathyroidism, particularly in those who experience recurrent hypocalcemia.

[Magnesium, calcium and potassium: "no one was born alone"]. / Magnesio, calcio e potassio: "Nessuno nasce solo o è nato per sé solo".

In contrast to other ions, magnesium is treated as an orphan by the body: there are no hormones that have a substantial role in regulating urinary magnesium excretion, and bone, the principal reservoir of magnesium, does not readily exchange with circulating magnesium.The Mg ++ is often overlooked by physicians in the differential diagnosis because it is considered insignificant, but its role is crucial for cells function, first of all neurons and cardiomyocytes. A condition of hypocalcemia associated with hypokalemia, especially in the presence of chronic renal failure, should raise suspicion of a lack of Mg ++.We report the case of an old man of 77 year with kidney transplant for 13 years, treated with cyclosporine, and sodium mycophenolate and steroid who, for about a month, accused impaired balance and walking instability, who fell accidentally down with wrist fracture.Blood tests showed hypocalcemia and hypokalemia, and so we required dosage of serum and urinary magnesium. A significant reduction in the ion plasma concentration was seen, associated to a fraction of excretion inappropriately high in relation to the degree of hypomagnesemia.The cause of this important renal loss is likely attributable to cyclosporine, a drug that has as a side effect the inhibition of the reabsorption of Mg ++ in the distal convoluted tubule. then, oral supplementation was started (244 mg of Mg ++ ion / day), with subsequent normalization, after a few days, not only of magnesiemia, but also in serum calcium and potassium levels, and improvement of neurological symptoms.Hypomagnesaemia is common in patients with renal transplantation in therapy with calcineurin inhibitors ICN, due to the effects of such drugs on the TRPM6 transporter present in the kidney distal convoluted tubule. To prevent complications caused by chronic and severe depletion of magnesium in this particular population, we recommend periodic monitoring of magnesium plasma levels.

[Analysis of Factors Influencing the Development of Hypomagnesemia in Patients Receiving Cetuximab Therapy for Head and Neck Cancer].

Cetuximab was approved in Japan as the only clinically available molecular targeted drug for the treatment of head and neck cancer. Hypomagnesemia associated with cetuximab is considered one of the most serious adverse events. However, the factors influencing the development of hypomagnesemia are not clear, although the drug was previously approved for the treatment of patients with colorectal cancer. Thus, we studied the factors involved in the development of hypomagnesemia in patients receiving cetuximab therapy for head and neck cancer. Patients' background data and laboratory values before starting cetuximab therapy did not affect the development of hypomagnesemia. Among patients who had never been treated with cisplatin (NT group), 36.4% developed hypomagnesemia. In contrast, all patients who had previously been treated with cisplatin (T group) developed hypomagnesemia (p=0.034). Magnesium is reabsorbed by transient receptor potential subfamily melastatin 6 (TRPM6) in the distal convoluted tubule. The expression level of TRPM6 is controlled by the epidermal growth factor (EGF) pathway. Cetuximab is an EGF receptor inhibitor and reduces the expression of TRPM6. Additionally, recent studies have shown that the expression of TRPM6 is reduced by cisplatin. Therefore, we considered that the serum magnesium level was cumulatively reduced by cetuximab and cisplatin. In conclusion, the T group was more likely to develop hypomagnesemia than the NT group, and therefore the serum magnesium level in the T group requires careful monitoring so that magnesium supplementation can be provided to patients when the level decreases.

Lots of steroids and vitamins, tons of complications. Hypercalcemia and nephrocalcinosis as important complications of performance-enhancing drugs / Montones de esteroides y vitaminas, toneladas de complicaciones. Hipercalcemia y nefrocalcinosis como complicaciones importantes de los fármacos para mejorar el rendimiento

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[Nephrocalcinosis associated with the use of anabolic steroid]. / Nefrocalcinose associada ao uso de esteroide anabolizante.

UNLABELLED: The anabolic steroid have been used as a therapeutic tool in various clinical conditions. However, indiscriminate use associated with other nutritional supplements has generated serious adverse effects. CASE REPORT: Male, 21 years old, admitted with nausea, fatigue, appetite loss, headache and hypertension. Blood tests showed Cr: 3.9 mg% U: 100 mg% and Total Calcium 14 mg/dl. Ultrasonography and renal biopsy were consistent with nephrocalcinosis. There has been gradual improvement in renal function and calcium levels after vigorous hydration and furosemide. However, after 1 year, renal calcium deposits persist, corticomedullary ratio reduced in ultrasound and stable creatinine of 1.4 mg/dl. Previous cases showed acute tubular necrosis and interstitial nephritis with little calcium deposits in the renal interstitium. In this case we found severe nephrocalcinosis associated with nephrosclerosis. Our objective is to report the occurrence of acute kidney Injury with nephrocalcinosis associated with use of anabolic steroid and provide a review of the matter.

Nefrocalcinose associada ao uso de esteroide anabolizante / Nephrocalcinosis associated with the use of anabolic steroid

Os esteroides anabolizantes têm sido usados como arma terapêutica em diversas condições clínicas. Entretanto, o uso abusivo e indiscriminado, associado a outros suplementos nutricionais, tem gerado efeitos adversos graves. Relato do caso: Sexo masculino, 21 anos, admitido com náuseas, astenia, hiporexia, cefaleia e hipertensão arterial. Exames no sangue evidenciaram Cr: 3,9 mg/dl U:100 mg/dl e Cálcio total 14 mg/dl. Ultrassonografia e biópsia renal compatíveis com nefrocalcinose. Houve melhora gradativa da função renal e da calcemia após hidratação vigorosa e furosemida. Entretanto, após 1 ano, persistiram depósitos renais de cálcio e relação córticomedular reduzida ao ultrassom e creatinina estável em 1,4 mg/dl. Casos anteriores evidenciaram necrose tubular aguda e nefrite intersticial com poucos depósitos de cálcio no interstício renal. Nesse caso, encontramos nefrocalcinose acentuada associada à nefroesclerose. O objetivo deste estudo é relatar a ocorrência de injúria renal aguda com nefrocalcinose associada ao uso de esteroide anabolizante e oferecer uma revisão do assunto. .

The anabolic steroid have been used as a therapeutic tool in various clinical conditions. However, indiscriminate use associated with other nutritional supplements has generated serious adverse effects. Case report: Male, 21 years old, admitted with nausea, fatigue, appetite loss, headache and hypertension. Blood tests showed Cr: 3.9 mg% U: 100 mg% and Total Calcium 14 mg/dl. Ultrasonography and renal biopsy were consistent with nephrocalcinosis. There has been gradual improvement in renal function and calcium levels after vigorous hydration and furosemide. However, after 1 year, renal calcium deposits persist, corticomedullary ratio reduced in ultrasound and stable creatinine of 1.4 mg/dl. Previous cases showed acute tubular necrosis and interstitial nephritis with little calcium deposits in the renal interstitium. In this case we found severe nephrocalcinosis associated with nephrosclerosis. Our objective is to report the occurrence of acute kidney Injury with nephrocalcinosis associated with use of anabolic steroid and provide a review of the matter. .

Iatrogenic vitamin D toxicity in an infant--a case report and review of literature.

Public concern over vitamin D deficiency has led to widespread use of over the counter (OTC) vitamin D (-D3 or -D2) supplements, containing up to 10,000 IU/unit dose (400 IU=10µg). Overzealous use of such supplements can cause hypercalcemia due to vitamin D toxicity. Infants are particularly vulnerable to toxicity associated with vitamin D overdose. OTC supplements are not subject to stringent quality control regulations from FDA and high degree of variability in vitamin D content in OTC pills has been demonstrated. Other etiologies of vitamin D induced hypercalcemia include hyperparathyroidism, granulomatous malignancies like sarcoidosis and mutations in the CYP24A1 gene. The differential diagnosis of hypercalcemia should include iatrogenic and genetic etiologies. C24-hydroxylation and C3-epimerization are two important biochemical pathways via which 25-hydroxyvitamin D3 (25(OH)D3) is converted to its metabolites, 24,25-dihydroxyvitamin D3 (24,25(OH)2D3) or its C3 epimer, 3-epi-25-OH-D3 respectively. Mutations in the CYP24A1 gene cause reduced serum 24,25(OH)2D3 to 25(OH)D3 ratio (<0.02), elevated serum 1,25-dihydroxyvitamin D (1,25(OH)2D3), hypercalcemia, hypercalciuria and nephrolithiasis. Studies in infants have shown that 3-epi-25(OH)D3 can contribute 9-61.1% of the total 25(OH)D3. Therefore, measurements of parathyroid hormone (PTH) and vitamin D metabolites 25(OH)D3, 1,25(OH)2D3, 3-epi-25(OH)D3 and 24,25(OH)2D3 are useful to investigate whether the underlying cause of vitamin D toxicity is iatrogenic versus genetic. Here we report a case of vitamin D3 associated toxicity in a 4-month-old female who was exclusively breast-fed and received an oral liquid vitamin D3 supplement at a dose significantly higher than recommended on the label. The vitamin D3 content of the supplement was threefold higher (6000 IU of D/drop) than listed on the label (2000 IU). Due to overdosing and higher vitamin D3 content, the infant received ∼50,000 IU/day for two months resulting in severe hypercalcemia, hypercalciuria and nephrocalcinosis. We also review the relevant literature on vitamin D3 toxicity in this report.

Vitamin D supplementation and risk of toxicity in pediatrics: a review of current literature.

CONTEXT: Although vitamin D toxicity is rare in children, increased use of vitamin D formulations, re-examination of optimal vitamin D levels, and use of higher doses lend potential for an increased incidence of vitamin D toxicity. EVIDENCE ACQUISITION: A PubMed search was conducted through May 2013 for cases of vitamin D intoxication and vitamin D trials in pediatrics. Safety data were collected and reviewed. EVIDENCE SYNTHESIS: A small number of pediatric studies tested vitamin D doses at or above the currently recommended upper tolerable intake. In children and adolescents, vitamin D excess was rare and usually asymptomatic. Recent cases of intoxication relate to errors in manufacturing, formulation, or prescription; involve high total intake in the range of 240,000 to 4,500,000 IU; and present with severe hypercalcemia, hypercalciuria, or nephrocalcinosis. However, mild hypercalcemia and hypervitaminosis using currently recommended doses have been reported in infants with rickets. CONCLUSIONS: Although rare, cases of vitamin D intoxication that present with dramatic life-threatening symptoms still occur in children. Moreover, recent studies in infants raise a potential need for monitoring vitamin D levels when doses at or above the currently recommended upper range are used. Further studies are needed to clarify these findings. The Drugs and Therapeutics Committee of the Pediatric Endocrine Society suggests obtaining serum 25-hydroxyvitamin D levels in infants and children who receive long-term vitamin D supplementation at or above the upper level intake that is currently recommended.

Prophylactic effect of coconut water (Cocos nucifera L.) on ethylene glycol induced nephrocalcinosis in male wistar rat.

PURPOSE: Many medicinal plants have been employed during ages to treat urinary stones though the rationale behind their use is not well established. Thus, the present study was proposed to evaluate the effect of coconut water as a prophylactic agent in experimentally induced nephrolithiasis in a rat model. MATERIALS AND METHODS: The male Wistar rats were divided randomly into three groups. Animals of group I (control) were fed standard rat diet. In group II, the animals were administrated 0.75% ethylene glycol in drinking water for the induction of nephrolithiasis. Group III animals were administrated coconut water in addition to ethylene glycol. All the treatments were continued for a total duration of seven weeks. RESULTS AND CONCLUSION: Treatment with coconut water inhibited crystal deposition in renal tissue as well as reduced the number of crystals in urine. Furthermore, coconut water also protected against impaired renal function and development of oxidative stress in the kidneys. The results indicate that coconut water could be a potential candidate for phytotherapy against urolithiasis.

Prophylactic effect of coconut water (Cocos nucifera L.) on ethylene glycol induced nephrocalcinosis in male wistar rat

Purpose Many medicinal plants have been employed during ages to treat urinary stones though the rationale behind their use is not well established. Thus, the present study was proposed to evaluate the effect of coconut water as a prophylactic agent in experimentally induced nephrolithiasis in a rat model. Materials and Methods The male Wistar rats were divided randomly into three groups. Animals of group I (control) were fed standard rat diet. In group II, the animals were administrated 0.75% ethylene glycol in drinking water for the induction of nephrolithiasis. Group III animals were administrated coconut water in addition to ethylene glycol. All the treatments were continued for a total duration of seven weeks. Results and Conclusion Treatment with coconut water inhibited crystal deposition in renal tissue as well as reduced the number of crystals in urine. Furthermore, coconut water also protected against impaired renal function and development of oxidative stress in the kidneys. The results indicate that coconut water could be a potential candidate for phytotherapy against urolithiasis. .

Development of an animal model of nephrocalcinosis via selective dietary sodium and chloride depletion.

BACKGROUND: Nephrocalcinosis (NC) is an important clinical problem seen in critically ill preterm neonates treated with loop diuretics. No reliable animal models are available to study the pathogenesis of NC in preterm infants. The purpose of this study was to develop a reproducible and clinically relevant animal model of NC for these patients and to explore the impact of extracellular fluid (ECF) volume contraction induced by sodium and chloride depletion in this process. METHODS: Three-week-old weanling Sprague-Dawley rats were fed diets deficient in either chloride or sodium or both. A subgroup of rats from each dietary group was injected daily with furosemide (40 mg/kg i.p.). RESULTS: Rats fed a control diet, with or without furosemide, or a chloride-depleted diet alone, did not develop NC. By contrast, 50% of the rats injected with furosemide and fed the chloride-depleted diet developed NC. Moreover, 94% of the rats fed the combined sodium- and chloride-depleted diet developed NC, independently of furosemide use. NC was associated with the development of severe ECF volume contraction; hypochloremic, hypokalemic, metabolic alkalosis; increased phosphaturia; and growth retardation. CONCLUSION: Severe ECF volume contraction induced by chronic sodium and chloride depletion appears to play an important role in the pathogenesis of NC.

Recent safety concerns with proton pump inhibitors.

There have been recent concerns about the safety of proton pump inhibitors (PPIs). We focus here on 3 specific concerns-the possible interaction between PPIs and clopidogrel, the postulated link between PPI use and fractures, and the possibility that long-term PPI use might lead to hypomagnesemia. There is evidence for an in vitro interaction between clopidogrel and at least some PPIs. The Food and Drug Administration (FDA) has warned against the use of certain PPIs by patients on clopidogrel. However, a randomized controlled trial that compared clopidogrel alone with the combination of clopidogrel and omeprazole found no increase in adverse cardiovascular outcomes and a reduction in the rate of adverse gastrointestinal outcomes attributable to omeprazole. PPI use may be a weak risk factor for certain fractures, but the quality of evidence is relatively poor and there is a strong possibility of confounding. The mechanism whereby PPI use might increase fracture risk is unknown. Currently, no additional measures concerning calcium supplementation or bone mineral density monitoring are recommended for patients on a PPI. The FDA has suggested monitoring serum magnesium levels in patients on PPI therapy. The mechanism and frequency of PPI-induced hypomagnesemia are unclear. PPI treatment should not be withheld from patients who genuinely require it, but the PPI should be taken in the lowest effective dose and only for as long as clinically indicated. The same is, of course, true for all medicines. The benefits of PPI therapy greatly outweigh the risks.

[Modest risk of phosphate nephropathy by bowel cleansing]. / Beskeden risiko for fosfatnefropati ved colonudrensning.

Acute phosphate nephropathy is a rare, but serious adverse event associated with the use of sodium phosphate for bowel cleansing. It may lead to permanent renal impairment and a need for dialysis. The aetiology is hyperphosphataemia caused by intestinal absorption of the cleanser. Risk factors include: advanced age, existing kidney disease, decreased intravascular volume, and medications affecting renal perfusion or function such as diuretics, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, and possibly nonsteroidal anti-inflammatory drugs.

Exposure to furosemide as the strongest risk factor for nephrocalcinosis in preterm infants.

BACKGROUND: The objective of this study was to determine which of the many risk factors for nephrocalcinosis (NC) in preterm infants are most relevant. METHODS: In 55 neonates born before 32 completed weeks of gestation, parameters relevant to NC were analyzed. Median birthweight was 1010 g (range 500-2070 g). Fifteen (27%) asymptomatic children had ultrasonographic NC. RESULTS: In multivariate analysis the strongest independent risk factor was furosemide therapy above 10 mg per kg bodyweight cumulative dose, with a 48-fold increased risk of NC (odds ratio confidence interval 4.0-585, P < 0.01). The risk of NC was 1.65-fold higher per 100 g lower weight (1.07-2.56, P= 0.02) and 4.5-fold higher per mmol/l of urinary calcium concentration (1.14-17.7, P= 0.03). Many other risk factors were only significant in univariate analysis (gestational age, mechanical ventilation, infection, broncho-pulmonary dysplasia, blood transfusions, intraventricular hemorrhage, surfactant therapy, vasopressors, phenobarbital or caffeine, duration of hospital stay), indicating an indirect effect only. Other parameters of calcium and phosphate homeostasis were not significant, possibly due to standardized supplementation. CONCLUSION: We suggest that in preterm infants, furosemide should be prescribed with caution and close monitoring of calcium excretions is advisable. Some guidelines for infant respiratory distress syndrome now favor calcium-sparing thiazides if diuretics are considered.

Calcimimetics as an adjuvant treatment for familial hypophosphatemic rickets.

BACKGROUND AND OBJECTIVES: The treatment for X-linked hypophosphatemia (XLH) with phosphate and calcitriol can be complicated by secondary hyperparathyroidism and nephrocalcinosis. Furthermore, vitamin D and phosphate stimulate FGF23 production, the pathogenic factor causing XLH. We investigated in XLH patients: 1) whether treatment with the calcimimetic agent, cinacalcet, will block the rise in parathyroid hormone (PTH) caused by phosphate administration; and 2) whether treatment with oral phosphate and calcitriol increases FGF23 levels. DESIGN, SETTING, PARTICIPANTS, AND MEASUREMENTS: Eight subjects with XLH were given a single oral dose of phosphate, followed the next day by combined treatment with phosphate and cinacalcet. Serum measurements of ionized calcium (Ca), phosphate, creatinine, intact PTH, 1,25(OH)(2)D, FGF23, and tubular threshold for phosphate/glomerular filtration rate (TP/GFR) were assessed in response to short-term treatment with phosphate and cinacalcet and compared with long-term administration of phosphate and calcitriol. RESULTS: Oral phosphate load increased serum phosphate, decreased ionized calcium, and increased PTH. Twenty-four hours later, FGF23 significantly increased and 1,25(OH)(2)D decreased. The concomitant administration of phosphate and cinacalcet resulted in further decrease in serum Ca(2+) but suppression of PTH and greater increase in serum phosphate and TP/GFR. Chronic treatment with phosphate and calcitriol resulted in a smaller increment in serum phosphate and high serum FGF23. CONCLUSIONS: Traditional therapy of XLH with phosphate and calcitriol elevates FGF23 and has the potential to stimulate PTH. Short-term treatment with cinacalcet suppresses PTH, leading to increase in TP/GFR and serum phosphate. Thus, long-term clinical studies are needed to investigate whether cinacalcet may be a useful adjuvant in the treatment of XLH, allowing the use of lower doses of phosphate and calcitriol.