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Article: Calcitonin, the forgotten hormone: does it deserve to be forgotten?

Felsenfeld, Arnold J / Levine, Barton S

2015 Volume 8, Issue 2, Page(s) 180–187

Abstract: Calcitonin is a 32 amino acid hormone secreted by the C-cells of the thyroid gland. Calcitonin has been preserved during the transition from ocean-based life to land dwellers and is phylogenetically older than parathyroid hormone. Calcitonin secretion is ...

Abstract	Calcitonin is a 32 amino acid hormone secreted by the C-cells of the thyroid gland. Calcitonin has been preserved during the transition from ocean-based life to land dwellers and is phylogenetically older than parathyroid hormone. Calcitonin secretion is stimulated by increases in the serum calcium concentration and calcitonin protects against the development of hypercalcemia. Calcitonin is also stimulated by gastrointestinal hormones such as gastrin. This has led to the unproven hypothesis that postprandial calcitonin stimulation could play a role in the deposition of calcium and phosphate in bone after feeding. However, no bone or other abnormalities have been described in states of calcitonin deficiency or excess except for diarrhea in a few patients with medullary thyroid carcinoma. Calcitonin is known to stimulate renal 1,25 (OH)2 vitamin D (1,25D) production at a site in the proximal tubule different from parathyroid hormone and hypophosphatemia. During pregnancy and lactation, both calcitonin and 1,25D are increased. The increases in calcitonin and 1,25D may be important in the transfer of maternal calcium to the fetus/infant and in the prevention and recovery of maternal bone loss. Calcitonin has an immediate effect on decreasing osteoclast activity and has been used for treatment of hypercalcemia. Recent studies in the calcitonin gene knockout mouse have shown increases in bone mass and bone formation. This last result together with the presence of calcitonin receptors on the osteocyte suggests that calcitonin could possibly affect osteocyte products which affect bone formation. In summary, a precise role for calcitonin remains elusive more than 50 years after its discovery.
Language	English
Publishing date	2015-03-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2655800-2
ISSN	2048-8513 ; 2048-8505
ISSN (online)	2048-8513
ISSN	2048-8505
DOI	10.1093/ckj/sfv011
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Article ; Online: Approach to treatment of hypophosphatemia.

Felsenfeld, Arnold J / Levine, Barton S

American journal of kidney diseases : the official journal of the National Kidney Foundation

2012 Volume 60, Issue 4, Page(s) 655–661

Abstract: Hypophosphatemia can be acute or chronic. Acute hypophosphatemia with phosphate depletion is common in the hospital setting and results in significant morbidity and mortality. Chronic hypophosphatemia, often associated with genetic or acquired renal ... ...

Abstract	Hypophosphatemia can be acute or chronic. Acute hypophosphatemia with phosphate depletion is common in the hospital setting and results in significant morbidity and mortality. Chronic hypophosphatemia, often associated with genetic or acquired renal phosphate-wasting disorders, usually produces abnormal growth and rickets in children and osteomalacia in adults. Acute hypophosphatemia may be mild (phosphorus level, 2-2.5 mg/dL), moderate (1-1.9 mg/dL), or severe (<1 mg/dL) and commonly occurs in clinical settings such as refeeding, alcoholism, diabetic ketoacidosis, malnutrition/starvation, and after surgery (particularly after partial hepatectomy) and in the intensive care unit. Phosphate replacement can be given either orally, intravenously, intradialytically, or in total parenteral nutrition solutions. The rate and amount of replacement are empirically determined, and several algorithms are available. Treatment is tailored to symptoms, severity, anticipated duration of illness, and presence of comorbid conditions, such as kidney failure, volume overload, hypo- or hypercalcemia, hypo- or hyperkalemia, and acid-base status. Mild/moderate acute hypophosphatemia usually can be corrected with increased dietary phosphate or oral supplementation, but intravenous replacement generally is needed when significant comorbid conditions or severe hypophosphatemia with phosphate depletion exist. In chronic hypophosphatemia, standard treatment includes oral phosphate supplementation and active vitamin D. Future treatment for specific disorders associated with chronic hypophosphatemia may include cinacalcet, calcitonin, or dypyrimadole.
MeSH term(s)	Acute Disease ; Chronic Disease ; Comorbidity ; Dietary Supplements ; Humans ; Hypophosphatemia/epidemiology ; Hypophosphatemia/physiopathology ; Hypophosphatemia/therapy ; Male ; Middle Aged ; Vitamin D/administration & dosage
Chemical Substances	Vitamin D (1406-16-2)
Language	English
Publishing date	2012-10
Publishing country	United States
Document type	Case Reports ; Journal Article ; Review
ZDB-ID	604539-x
ISSN	1523-6838 ; 0272-6386
ISSN (online)	1523-6838
ISSN	0272-6386
DOI	10.1053/j.ajkd.2012.03.024
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Zs.A 1669: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 468: Show issues

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Article ; Online: Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease.

Felsenfeld, Arnold J / Levine, Barton S / Rodriguez, Mariano

Seminars in dialysis

2015 Volume 28, Issue 6, Page(s) 564–577

Abstract: Calcium, phosphorus, and magnesium homeostasis is altered in chronic kidney disease (CKD). Hypocalcemia, hyperphosphatemia, and hypermagnesemia are not seen until advanced CKD because adaptations develop. Increased parathyroid hormone (PTH) secretion ... ...

Abstract	Calcium, phosphorus, and magnesium homeostasis is altered in chronic kidney disease (CKD). Hypocalcemia, hyperphosphatemia, and hypermagnesemia are not seen until advanced CKD because adaptations develop. Increased parathyroid hormone (PTH) secretion maintains serum calcium normal by increasing calcium efflux from bone, renal calcium reabsorption, and phosphate excretion. Similarly, renal phosphate excretion in CKD is maintained by increased secretion of fibroblast growth factor 23 (FGF23) and PTH. However, the phosphaturic effect of FGF23 is reduced by downregulation of its cofactor Klotho necessary for binding FGF23 to FGF receptors. Intestinal phosphate absorption is diminished in CKD due in part to reduced levels of 1,25 dihydroxyvitamin D. Unlike calcium and phosphorus, magnesium is not regulated by a hormone, but fractional excretion of magnesium increases as CKD progresses. As 60-70% of magnesium is reabsorbed in the thick ascending limb of Henle, activation of the calcium-sensing receptor by magnesium may facilitate magnesium excretion in CKD. Modification of the TRPM6 channel in the distal tubule may also have a role. Besides abnormal bone morphology and vascular calcification, abnormalities in mineral homeostasis are associated with increased cardiovascular risk, increased mortality and progression of CKD.
MeSH term(s)	Calcium/metabolism ; Disease Progression ; Glomerular Filtration Rate/physiology ; Humans ; Kidney/physiopathology ; Magnesium/metabolism ; Metabolic Diseases/etiology ; Metabolic Diseases/metabolism ; Phosphorus/metabolism ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/physiopathology
Chemical Substances	Phosphorus (27YLU75U4W) ; Magnesium (I38ZP9992A) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2015-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1028193-9
ISSN	1525-139X ; 0894-0959
ISSN (online)	1525-139X
ISSN	0894-0959
DOI	10.1111/sdi.12411
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Article: Metabolic acidosis-induced hypercalcemia in an azotemic patient with primary hyperparathyroidism.

Rastegar, Mandana / Levine, Barton S / Felsenfeld, Arnold J

Clinical kidney journal

2014 Volume 7, Issue 3, Page(s) 299–302

Abstract: A 58-year-old man with Stage 3b chronic kidney disease and primary hyperparathyroidism treated with cinacalcet was admitted for acute cholecystitis. A cholecystostomy tube was placed, estimated glomerular filtration rate decreased, metabolic acidosis ... ...

Abstract	A 58-year-old man with Stage 3b chronic kidney disease and primary hyperparathyroidism treated with cinacalcet was admitted for acute cholecystitis. A cholecystostomy tube was placed, estimated glomerular filtration rate decreased, metabolic acidosis developed and ionized calcium increased from 1.33 to 1.76 mM despite cinacalcet administration. A sodium bicarbonate infusion corrected the metabolic acidosis restoring ionized calcium to normal despite no improvement in renal function. The correlation between the increase in serum bicarbonate and decrease in ionized calcium was r = -0.93, P < 0.001. In summary, severe hypercalcemia was attributable to metabolic acidosis increasing calcium efflux from bone while renal failure decreased the capacity to excrete calcium.
Language	English
Publishing date	2014-05-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2655800-2
ISSN	2048-8513 ; 2048-8505
ISSN (online)	2048-8513
ISSN	2048-8505
DOI	10.1093/ckj/sfu041
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Article ; Online: Serum calcium and bone: effect of PTH, phosphate, vitamin D and uremia.

Levine, Barton S / Rodríguez, Mariano / Felsenfeld, Arnold J

Nefrologia : publicacion oficial de la Sociedad Espanola Nefrologia

2014 Volume 34, Issue 5, Page(s) 658–669

Abstract: Hyperparathyroidism develops in chronic kidney disease (CKD). A decreased calcemic response to parathyroid hormone (PTH) contributes to the development of hyperparathyroidism and is presumed due to reduced calcium efflux from bone. Contributing factors ... ...

Abstract	Hyperparathyroidism develops in chronic kidney disease (CKD). A decreased calcemic response to parathyroid hormone (PTH) contributes to the development of hyperparathyroidism and is presumed due to reduced calcium efflux from bone. Contributing factors to the decreased calcemic response to PTH in CKD include: 1) hyperphosphatemia; 2) decreased serum calcitriol; 3) downregulation of the PTH1 receptor; 4) large, truncated amino-terminal PTH fragments acting at the carboxy-PTH receptor; and 5) uremic toxins. Also, prolonged high dose calcitriol administration may decrease the exchangeable pool of bone calcium independent of PTH. The goal of the review is to provide a better understanding of how the above cited factors affect calcium efflux from bone in CKD. In conclusion, much remains to be learned about the role of bone in the regulation of serum calcium.
MeSH term(s)	Bone and Bones/metabolism ; Calcium/blood ; Calcium/metabolism ; Humans ; Parathyroid Hormone/pharmacology ; Parathyroid Hormone/physiology ; Phosphates/pharmacology ; Phosphates/physiology ; Uremia/metabolism ; Vitamin D/pharmacology ; Vitamin D/physiology
Chemical Substances	Parathyroid Hormone ; Phosphates ; Vitamin D (1406-16-2) ; Calcium (SY7Q814VUP)
Language	Spanish
Publishing date	2014
Publishing country	Spain
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632512-9
ISSN	1989-2284 ; 0211-6995
ISSN (online)	1989-2284
ISSN	0211-6995
DOI	10.3265/Nefrologia.pre2014.Jun.12379
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Zs.B 2773: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 56: Show issues

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Article ; Online: Silver jubilee: 25 years of the first demonstration of the direct effect of phosphate on the parathyroid cell.

Bover, Jordi / Trinidad, Pedro / Jara, Aquiles / Soler-Majoral, Jordi / Martín-Malo, Alejandro / Torres, Armando / Frazão, João / Ureña, Pablo / Dusso, Adriana / Arana, Carolt / Graterol, Fredzzia / Romero-González, Gregorio / Troya, Maribel / Samaniego, Diana / D'Marco, Luis / Valdivielso, José Manuel / Fernández, Elvira / Arenas, María Dolores / Torregrosa, Vicente /

Navarro-González, Juan F / Lloret, María Jesús / Ballarín, J A / Bosch, Ricardo J / Górriz, José L / de Francisco, Agl / Gutiérrez, Orlando / Ara, Jordi / Felsenfeld, Arnold / Canalejo, Antonio / Almadén, Yolanda

Nefrologia

2023 Volume 42, Issue 6, Page(s) 645–655

Abstract: Although phosphorus is an essential element for life, it is not found in nature in its native state but rather combined in the form of inorganic phosphates ( ... ...

Abstract	Although phosphorus is an essential element for life, it is not found in nature in its native state but rather combined in the form of inorganic phosphates (PO
MeSH term(s)	Humans ; Parathyroid Glands ; Phosphates ; Parathyroid Hormone ; Hyperparathyroidism, Secondary/complications ; Renal Insufficiency, Chronic/complications
Chemical Substances	Phosphates ; Parathyroid Hormone
Language	English
Publishing date	2023-03-14
Publishing country	Spain
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2837917-2
ISSN	2013-2514 ; 2013-2514
ISSN (online)	2013-2514
ISSN	2013-2514
DOI	10.1016/j.nefroe.2023.02.008
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Article: An unusual case of hyperphosphatemia in a vitamin D-deficient patient with tuberculosis.

Lee, Roland H / Felsenfeld, Arnold J / Levine, Barton S

NDT plus

2011 Volume 4, Issue 4, Page(s) 264–269

Language	English
Publishing date	2011-04-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2410383-4
ISSN	1753-0784
ISSN	1753-0784
DOI	10.1093/ndtplus/sfr029
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Zs.A 6587: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 562: Show issues

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Article ; Online: PTH, FGF-23 and early CKD.

Rodriguez, Mariano / Felsenfeld, Arnold J

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2008 Volume 23, Issue 11, Page(s) 3391–3393

MeSH term(s)	Calcium/blood ; Chronic Disease ; Fibroblast Growth Factors/blood ; Glomerular Filtration Rate/physiology ; Humans ; Hyperparathyroidism, Secondary/etiology ; Hyperparathyroidism, Secondary/physiopathology ; Kidney Diseases/blood ; Kidney Diseases/complications ; Kidney Diseases/physiopathology ; Parathyroid Hormone/blood ; Phosphates/blood ; Postprandial Period/physiology
Chemical Substances	Parathyroid Hormone ; Phosphates ; fibroblast growth factor 23 ; Fibroblast Growth Factors (62031-54-3) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2008-11
Publishing country	England
Document type	Editorial
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfn438
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Zs.A 2198: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 329: Show issues

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Article ; Online: Assessment of Inorganic Phosphate Intake by the Measurement of the Phosphate/Urea Nitrogen Ratio in Urine.

Pendón-Ruiz de Mier, María Victoria / Vergara, Noemí / Rodelo-Haad, Cristian / López-Zamorano, María Dolores / Membrives-González, Cristina / López-Baltanás, Rodrigo / Muñoz-Castañeda, Juan Rafael / Caravaca, Francisco / Martín-Malo, Alejandro / Felsenfeld, Arnold J / De la Torre, Eugenio J / Soriano, Sagrario / Santamaría, Rafael / Rodríguez, Mariano

Nutrients

2021 Volume 13, Issue 2

Abstract: In chronic kidney disease (CKD) patients, it would be desirable to reduce the intake of inorganic phosphate (P) rather than limit the intake of P contained in proteins. Urinary excretion of P should reflect intestinal absorption of P(inorganic plus ... ...

Abstract	In chronic kidney disease (CKD) patients, it would be desirable to reduce the intake of inorganic phosphate (P) rather than limit the intake of P contained in proteins. Urinary excretion of P should reflect intestinal absorption of P(inorganic plus protein-derived). The aim of the present study is to determine whether the ratio of urinary P to urinary urea nitrogen (P/UUN ratio) helps identify patients with a high intake of inorganic P.A cross-sectional study was performed in 71 patients affected by metabolic syndrome with CKD (stages 2-3) with normal serum P concentration. A 3-day dietary survey was performed to estimate the average daily amount and the source of P ingested. The daily intake ofPwas1086.5 ± 361.3mg/day; 64% contained in animal proteins, 22% in vegetable proteins, and 14% as inorganic P. The total amount of P ingested did not correlate with daily phosphaturia, but it did correlate with the P/UUN ratio (
MeSH term(s)	Adult ; Aged ; Animals ; Cross-Sectional Studies ; Diet ; Eating ; Female ; Humans ; Male ; Middle Aged ; Phosphates/administration & dosage ; Phosphates/urine ; Rats ; Rats, Wistar ; Urea/urine
Chemical Substances	Phosphates ; Urea (8W8T17847W)
Language	English
Publishing date	2021-01-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu13020292
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Article ; Online: Milk alkali syndrome and the dynamics of calcium homeostasis.

Felsenfeld, Arnold J / Levine, Barton S

Clinical journal of the American Society of Nephrology : CJASN

2006 Volume 1, Issue 4, Page(s) 641–654

MeSH term(s)	Aged ; Animals ; Calcium/metabolism ; Homeostasis ; Humans ; Hypercalcemia/metabolism ; Male ; Middle Aged
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2006-07
Publishing country	United States
Document type	Case Reports ; Journal Article ; Review
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.01451005
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