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Hypophosphatemia

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6 papers 0 to 25 followers
https://www.readbyqxmd.com/read/22863286/approach-to-treatment-of-hypophosphatemia
#1
REVIEW
Arnold J Felsenfeld, Barton S Levine
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...
October 2012: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
https://www.readbyqxmd.com/read/21490240/tumor-induced-osteomalacia
#2
REVIEW
William H Chong, Alfredo A Molinolo, Clara C Chen, Michael T Collins
Tumor-induced osteomalacia (TIO) is a rare and fascinating paraneoplastic syndrome in which patients present with bone pain, fractures, and muscle weakness. The cause is high blood levels of the recently identified phosphate and vitamin D-regulating hormone, fibroblast growth factor 23 (FGF23). In TIO, FGF23 is secreted by mesenchymal tumors that are usually benign, but are typically very small and difficult to locate. FGF23 acts primarily at the renal tubule and impairs phosphate reabsorption and 1α-hydroxylation of 25-hydroxyvitamin D, leading to hypophosphatemia and low levels of 1,25-dihydroxy vitamin D...
June 2011: Endocrine-related Cancer
https://www.readbyqxmd.com/read/20177401/recent-advances-in-renal-phosphate-handling
#3
REVIEW
Emily G Farrow, Kenneth E White
Phosphate is critical for the maintenance of skeletal integrity, is a necessary component of important biomolecules, and is central to signal transduction and cell metabolism. It is becoming clear that endocrine communication between the skeleton, kidney, and the intestine is involved in maintaining appropriate serum phosphate concentrations, and that the kidney is the primary site for minute-to-minute regulation of phosphate levels. The identification of genetic alterations in Mendelian disorders of hypophosphatemia and hyperphosphatemia has led to the isolation of novel genes and the identification of new roles for existing proteins--such as fibroblast growth factor 23 and its processing systems, the co-receptor alpha-klotho, and phosphate transporters--in the control of renal phosphate handling...
April 2010: Nature Reviews. Nephrology
https://www.readbyqxmd.com/read/19669798/regulation-of-phosphate-transport-by-fibroblast-growth-factor-23-fgf23-implications-for-disorders-of-phosphate-metabolism
#4
REVIEW
Jyothsna Gattineni, Michel Baum
There are a number of hypophosphatemic disorders due to renal phosphate wasting that cannot be explained by elevated levels of parathyroid hormone. The circulating factors responsible for the phosphaturia have been designated as phosphatonins. Studies of patients with tumor-induced osteomalacia and other genetic diseases of phosphate metabolism have resulted in the identification of a number of hormones that regulate phosphate homeostasis, including matrix extracellular phosphoglycoprotein (MEPE), secreted frizzled-related protein 4 (sFRP-4), dentin matrix protein 1 (DMP1), fibroblast growth factor 7 (FGF7), fibroblast growth factor 23 (FGF23), and Klotho...
April 2010: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
https://www.readbyqxmd.com/read/17568018/hypophosphatemia-clinical-consequences-and-management
#5
REVIEW
Steven M Brunelli, Stanley Goldfarb
Current evidence regarding the clinical consequences of hypophosphatemia is not straightforward. Given the potentially different implications of hypophosphatemia among various patient groups, this commentary touches on patients with low serum phosphate after acute hospitalization, those with chronic ambulatory hypophosphatemia, and those with hypophosphatemia in the setting of advanced renal disease. Finally, this commentary examines the evidence regarding how best to replete phosphorous in the hypophosphatemic patient...
July 2007: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/9644637/dipyridamole-decreases-renal-phosphate-leak-and-augments-serum-phosphorus-in-patients-with-low-renal-phosphate-threshold
#6
D Prié, F B Blanchet, M Essig, J P Jourdain, G Friedlander
It has been shown that an acute infusion of dipyridamole increased renal phosphate reabsorption in rats and humans. A prospective study was performed to determine whether chronic treatment by dipyridamole given orally could decrease renal phosphate leak and increase serum phosphorus in patients with idiopathic low renal phosphate threshold (TmPO4/GFR < 0.77 mM). Sixty-four patients with low TmPO4/GFR were included and treated with dipyridamole (75 mg, 4 times daily) for more than 12 mo. Serum phosphorus, TmPO4/GFR, parathyroid hormone, serum calcium, and 1,25-dihydroxyvitamin D were measured sequentially before treatment, and after 3, 6 to 9, and 12 mo of treatment...
July 1998: Journal of the American Society of Nephrology: JASN
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