Zusammenfassung
Der Serumphosphatspiegel wird in engen Grenzen durch Vitamin D, Parathormon und fibroblast growth factor-23 (FGF-23) reguliert. Von zentraler Bedeutung dabei ist die Phosphatrückresorption in proximalen Tubulusepithelien durch die Transporter NPT2a und c. Störungen der hormonellen Regulation oder der Transporter können sowohl eine Hypo- als auch eine Hyperphosphatämie verursachen. Zusätzlich können Verschiebungen zwischen intra- und extrazellulärem Raum sowie niedrige oder hohe intestinale Phosphataufnahme Änderungen des Serumphosphats bewirken. Eine schwere Hypophosphatämie führt zur zellulären Energiedepletion mit entsprechenden Symptomen. Die Therapie erfolgt üblicherweise durch orale Zufuhr. Eine parenterale Phosphatgabe sollte schweren Fällen vorbehalten und engmaschig überwacht werden. Eine schwere Hyperphosphatämie kann bei massiver Zytolyse oder exzessiver intestinaler Aufnahme entstehen. Die Symptome erklären sich durch eine konsekutive Hypokalzämie. Eine weitere gefürchtete Komplikation ist die akute Phosphatnephropathie mit Nierenversagen. Die schwere Hyperphosphatämie wird rasch und effektiv mittels Hämodialyse behandelt. Rezente Daten legen nahe, dass hochnormale Phosphatwerte mit einem erhöhten kardiovaskulären Risiko assoziiert sind.
Abstract
Serum phosphate levels are tightly regulated by vitamin D, parathyroid hormone (PTH), and fibroblast growth factor-23 (FGF-23). In particular PTH and FGF-23 decrease renal phosphate reabsorption by proximal tubular epithelial cells via phosphate transporters NPT2a and c. Disturbances of hormone regulation or carrier function may cause hypo- or hyperphosphatemia. In addition, phosphate shifts between the intracellular and extracellular space or decreased or increased gastrointestinal phosphate uptake may cause these disturbances. Severe hypophosphatemia causes energy depletion of cells with consecutive symptoms. Hypophosphatemia is treated by oral phosphate supplementation. Intravenous phosphate therapy should be restricted to symptomatic cases. Severe hyperphosphatemia may occur with massive cytolysis or ingestion of excessive amounts of phosphate. Complications include hypocalcemia and renal failure due to acute phosphate nephropathy. If necessary, severe hyperphosphatemia needs to be treated by hemodialysis. Recent evidence suggests that high normal phosphate levels may be associated with increased cardiovascular risk.
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Aktualisierung von: Lhotta K (2011) Störungen des Phosphathaushaltes. J Klin Endokrinol Stoffw 4(4):20–23
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Lhotta, K. Störungen des Phosphathaushalts. J. Klin. Endokrinol. Stoffw. 12, 7–13 (2019). https://doi.org/10.1007/s41969-019-0054-y
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DOI: https://doi.org/10.1007/s41969-019-0054-y