Hypophosphatemia: an evidence-based approach to its clinical consequences and management

Abstract

Optimal cellular function is dependent on maintenance of a normal serum phosphorus concentration. Serum phosphorus concentration is affected by several determinants, the most important of which is regulation of phosphorus reabsorption by the kidney. The majority of this reabsorption (80%) occurs in the proximal tubule and is mediated by an isoform of the sodium-phosphate cotransporter (NaPi-II). Parathyroid hormone, via a variety of intracellular signaling cascades leading to NaPi-IIa internalization and downregulation, is the main regulator of renal phosphate reabsorption. Shift of phosphorus from extracellular to intracellular compartments, decreased gastrointestinal absorption, and increased urinary losses, are the primary mechanisms of hypophosphatemia, which affects approximately 2% of hospitalized patients. Hypophosphatemia has been implicated as a cause of rhabdomyolysis, respiratory failure, hemolysis and left ventricular dysfunction. With the exception of ventilated patients, there is little evidence that moderate hypophosphatemia has significant clinical consequences in humans, and aggressive intravenous phosphate replacement is unnecessary. By contrast, patients with severe hypophosphatemia should be treated. Intravenous repletion may be considered, especially for patients who have clinical sequelae of hypophosphatemia.

Serum Levels of Intact Parathyroid Hormone, Calcium, and Phosphorus and Risk of Mortality in Hemodialysis Patients

“…As low serum phosphorus level is observed in patients with a poor nutritional status and major comorbidities, observation of poor outcomes is justified in these cases and low phosphorus level can be a strong indicator of mortality. In fact, the association in these patients is even more obvious than cases with normal or high serum phosphorus level (26). However, some large-scale studies (1,3) have shown that after adjustment for markers of malnutrition/inflammation, low serum phosphorus level (< 3 mg/dL) was still associated with a higher mortality rate in HD patients.…”

New Insights on Left Displaced Abomasum in Dairy Cows

“…The significant reduction in serum phosphorous concentration may be secondary to phosphorus redistribution as a result of metabolic alkalosis that induces intracellular phosphorus entry, thus decreasing serum phosphorus concentration Amanzadeh and Reilly (2006) and Mahmoud et al (2016). While, the serum magnesium level in LDA affected cows was non-significantly altered these results agree with De Cardoso et al (2008), Mokhber Dezfouli et al (2013) and Mahmoud et al (2016).…”

Hypophosphatemia in patients with chronic HBV

“…Condizioni associate ad alcalosi respiratoria sono l'intossicazione da salicilati, la ventilazione meccanica, il coma epatico, la sepsi, i colpi di calore e le ustioni [11]. Aumentati livelli sierici di insulina promuovono il trasporto di glucosio e fosforo all'interno del muscolo scheletrico e del fegato.…”

“…Anche i bifosfonati possono provocare ipofosfatemia ma di solito è modesta, transitoria e secondaria all'aumento del PTH, che causa una brusca riduzione della calcemia [4]. Tra i disordini genetici in grado di provocare aumentata escrezione renale di fosforo ricordiamo l'Xlinked ipofosfatemia e il rachitismo ipofosfatemico familiare, legate rispettivamente a una mutazione inattivante una zinco metallo-endopeptidasi e a una mutazione attivante il FGF-23; sono caratterizzate da giovane età, bassa statura, dolore osseo, evidenza radiologica di rachitismo, perdita renale di fosforo, e deficit di vitamina D [11].…”